House Café

The House Café set up its premier branch in the year 2002 by converting an old Nişantaşı flat into a café. In short time, adding giant salads, main dishes and pizzas to its menu, the café started serving a restaurant menu pleasing even to the gourmets. With its seasonal menu that allows only the fresh ingredients and large selection of coffee choices, The House Café provides its guests with a friendly and comfortable environment to dine and chat.
Today, The House Café operates in 10 separate branches, located in prime locations including Teşvikiye, Tünel, Ortaköy, Etiler, Caddebostan, İstiklal Avenue and İstinye Park. While increasing in number of branches, The House Café also gives priority to its institutionalization conducted from its head office in Balat. With 30 employees, the new 3-floor management office houses general management, accounts, finance, buying, cost analysis, public relations and human resources departments.
Featured in various local and international publications, The House Café branches and head office interior concept and designs are the works of the award-wining design outfit, Autoban. Chosen as "Best Young Designers" by Wallpaper Magazine in 2004 and "Upcoming Designers" by Blueprint Magazine in 2005, Autoban team carefully preserves the original features of the historic buildings that usually house the branches and maintain a balance by adding modern touches to the interiors. The old-meets-new approach continues all throughout the décor from the lighting units to the chairs.

Individual differences in semantic short-term

Brain and Language 68, 218–224 (1999)
Article ID brln.1999.2085, available online at http://www.idealibrary.com on
Decomposition: To What Extent? The Case of Turkish
Ays¸e Gu¨rel
McGill University, Montre´al, Que´bec, Canada
It has been proposed that in agglutinative languages, lexical access of morphologically
complex words must involve decomposition rather than full listing (Frauenfelder
& Schreuder, 1992; Hankamer, 1989). We tested this proposal in Turkish
using a simple lexical decision task. Results show that multimorphemic words that
consist of frequent affixes are processed as fast as monomorphemic words. This
finding suggests that in languages with rich morphology, not all multimorphemic
words are accessed in a decomposed form. To the extent that morphemes are in
frequent use, they may induce whole-word rather than decompositional lexical access.
ã 1999 Academic Press
Key Words: Turkish; lexical access; morphological decomposition; whole-word
access.
INTRODUCTION
Lexical access and representation of complex words has widely been discussed
in the psycholinguistic literature. Existing models of lexical access
of multimorphemic words range from morphological decomposition (Taft &
Forster, 1975) to full-listing (Butterworth, 1983). While the decompositional
account assumes that a morphologically complex form is parsed into its constituent
morphemes prior to lexical access, the full-listing view maintains
that the morphological structure of a complex form has no independent representation,
suggesting that no parsing is involved in word recognition. There
are also hybrid models which include features of both decomposition and
full-listing models (Caramazza, Laudanna, & Romani, 1988; Frauenfelder &
This research was in part supported by an MCRI grant from the Social Sciences and Humanities
Research Council of Canada to Gonia Jarema, Eva Kehayia, and Gary Libben. I thank
all the members of the Mental Lexicon Project, especially Eva Kehayia, Chris Grindrod, Gerald
Rosenau, and Kyrana Tsapkini for their invaluable help in the design and the statistical analysis
of this experiment. I also thank the conference participants in Edmonton for their helpful
suggestions.
Address correspondence and reprint requests to Ays¸e Gu¨rel, Department of Linguistics,
McGill University, 1001 Sherbrooke Street West, Montre´al, Que´bec, H3A 1G5 Canada. Email:
agurel@po-box.mcgill.ca.
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DECOMPOSITION IN TURKISH 219
Schreuder, 1992). Among the hybrid models, Augmented Addressed Morphology
(AAM) (Caramazza et al., 1988) postulates that an input can activate
simultaneously both a whole-word representation and constituent morphemes.
When a word is familiar to the subject, whole-word representation
is activated. When the word is novel, however, morpheme activation takes
place. The Morphological Race Model (MRM) proposed by Frauenfelder
and Schreuder (1992) also assumes the existence of two routes which are in
competition. However, in their view, even familiar words can be accessed
through decomposition depending on factors such as transparency and frequency.
According to this model, while the parsing route wins in the recognition
of transparent low-frequency words, the direct route wins in the recognition
of high-frequency opaque words.
The above-mentioned models have been tested using only a few languages
(for the most part English). However, it has recently been acknowledged
that cross-language studies, particularly those using languages with a rich
morphology (such as Turkish and Finnish), allow for experimental confirmation
of the proposed models of lexical access (Laine, Niemi, Koivuselka¨-
Sallinen, Ahlse´n, & Hyo¨na¨, 1995). It has been suggested that due to the
storage efficiency in highly inflected, agglutinative languages like Turkish,
lexical access of morphologically complex words must involve decomposition
rather than full-listing (Hankamer, 1989). A similar claim has come
from Frauenfelder and Schreuder (1992) who suggest that in Turkish, the
morphological parsing route rather than the direct access route must win the
race in the analysis of most complex words. However, they also predict that
depending on the frequency of the root-plus-affix combination, a word can
be recognized by the direct route.
In order to test the above predictions, we investigated word recognition
of morphologically simple and complex words in Turkish using a simple
lexical decision task measuring reaction time (RT). In this study, we also
looked at whether stems that include pseudomorphemes (i.e., units which
are homographic and homophonous with real morphemes) are more difficult
to process than simple nondecomposable stems. There are many Turkish
words (i.e., stems) that can induce ambiguous parsings. That is, assuming a
left-to-right parsing for Turkish (Hankamer, 1989), an input stem that is presented
in isolation can have several alternative parsings. For example, the
word dilim is ambiguous in the absence of any contextual information. Thus,
depending on the access strategy, it can have different readings: it means
‘‘slice,’’ if accessed as a whole or it means ‘‘my tongue,’’ if parsed as
dil 1 im (‘‘tongue’’ 1 first-person singular possessive). We assume that if
every morphemelike representation in a word is activated in word recognition,
then the processing will take longer and this, in turn, will lead to longer
RTs for these pseudomorphemic items.
Given these features of the language, we investigated the following questions:
(1) to what extent does lexical access of multimorphemic words in
220 AYS¸E GU¨ REL
Turkish involve morphological decomposition? and (2) will all possible
substrings of a word be parsed in word recognition? We hypothesize that
(1) if decomposition takes place during word recognition, we anticipate
longer RTs for all multimorphemic words and (2) if every possible morpheme
or morphemelike structure is activated in word recognition, we anticipate
longer RTs not only for multimorphemic but also for pseudomorphemic
items.
METHOD
Participants
Thirty-one native speakers of Turkish, with an average age of 26 years (range 18–36) and
an average number of 19 years of education (range 12–25) participated in this study.
Procedure
Subjects were given a simple visual lexical decision task run on a Power Macintosh using
PsyScope 1.1. Subjects saw a string of letters presented on the computer screen and were
asked to press the ‘‘yes’’ key if they recognized the item as a word of Turkish and the ‘‘no’’
key if they did not. The main experiment was run in a single test of 576 trials. A practice
trial of 10 stimuli preceded the main test. Each stimulus was preceded by a mask (######)
lasting 150 ms followed by a 200-ms interval until the target items appeared on the screen.
The item remained on the screen until the subject pressed ‘‘yes’’ or ‘‘no.’’
Stimuli
The stimuli comprised 130 words, 273 nonwords, and 173 fillers. The nonwords were constructed
by changing the first phoneme of the real-word stimuli. Nonwords included both
simple and inflected types, affixed with a legal suffix of Turkish. Fillers consisted of verbs,
adjectives, and adverbs, both simple and inflected.
The experimental stimuli comprised monomorphemic and multimorphemic items. Monomorphemic
items included nondecomposable and pseudomorphemic items.
Nondecomposable items (NDC) are words that cannot be decomposed in any way (e.g.,
pencere, ‘‘window’’).
Pseudomorphemic items were of three types. (1) pseudostem (PS): this group included
words such as dalga (‘‘wave’’), which consist of a meaningful stem plus a syllable which
has no meaning in Turkish. For example, dal (‘‘branch’’), the first syllable of the word, is
followed by a meaningless syllable, ga. (2) Pseudostem-stem (PSS): this category included
pseudomorphemic items which appear to contain two stems. For example, the first and second
syllables of the word bakkal (‘‘grocery’’) are also meaningful stems in Turkish: bak (‘‘look’’)
and kal (‘‘stay’’). (3) Pseudostem-affix (PSA): this category consisted of pseudostems which
have a stem followed by a legal suffix in Turkish. These were homographic and homophonous
with the possessive suffix in Turkish [e.g., dilim (‘‘slice’’), dil (‘‘tongue’’), and im (the firstperson
singular possessive)].
Multimorphemic items contained one- and two-suffix words inflected for case (ablative,
locative) and number [e.g., stem-ablative (S-AB): deprem-den (‘‘from the earthquake’’); stemlocative
(S-LOC): masa-da (‘‘on the table’’); stem-plural (S-PL): emir-ler (‘‘orders’’); stemplural-
ablative (S-PL-AB): oda-lar-dan (‘‘from the rooms’’); and stem-plural-locative
(S-PL-LOC): resim-ler-de (‘‘in the pictures’’)]. These morphemes differ in frequency in both
DECOMPOSITION IN TURKISH 221
FIG. 1. Mean RTs for one-suffix, two-suffix, and monomorphemic words.
written and spoken Turkish: the ablative suffix has the lowest frequency. This is followed by
the locative suffix. The plural morpheme has the highest frequency (Pierce, 1960).
Multimorphemic and monomorphemic items were matched only for stem frequency. In the
frequency count of Turkish (Pierce, 1960), the stem and the morpheme frequency are given
separately. Therefore, the surface frequency was not available. Nondecomposable items were
matched with one-suffix words for length. Length here can be defined in terms of either the
number of syllables or the number of letters. In either case, one-suffix words were matched
with nondecomposable items in length. Nondecomposable words of three to four syllables in
Turkish are generally of low frequency. Therefore matching these items with one-suffix words
for frequency was not possible. Pseudomorphemic words were inevitably shorter than nondecomposable
monomorphemic items.
Results and Discussion
The error rate across categories ranged from 0.5 to 3.4%. The RTs that
were 62 standard deviations above and below each group mean were
deemed outliers and thus were eliminated from further analysis. Errors and
outliers constituted 6.8% of total responses. The results show that as a whole,
multimorphemic words (687 ms) yield longer RTs than monomorphemic
words (615 ms) (p , .0001). A repeated-measures ANOVA revealed that
overall there is a significant difference among one-suffix, two-suffix, and
monomorphemic words [F(2, 30) 5 24.11, p , .0001]. Post hoc comparisons
using the Fisher’s LSD method showed that monomorphemic words
yield significantly shorter RTs than one-suffix (p,.05) and two suffix words
(p , .005) (see Fig. 1).
Comparisons of the monomorphemic group to each category of the onesuffix
group reveal an important effect of the suffix frequency. A repeatedmeasures
ANOVA for these comparisons revealed a significant difference
[F(3, 30) 5 9.8, p , .0001]. As shown in Fig. 2, a Fisher’s LSD post hoc
analysis showed that the words with the ablative suffix (S-AB) yield significantly
longer RTs than monomorphemic words (p , .005). The interesting
finding is that the difference between words with the locative case marker
(S-LOC), the second most frequent suffix, and monomorphemic words is
not statistically significant. Furthermore, there is no significant difference in
222 AYS¸E GU¨ REL
FIG. 2. Mean RTs for each category in the one-suffix group and monomorphemic words;
S-AB vs MONO, p , .005; S-LOC vs MONO, ns; S-PL vs MONO, ns.
RT for words with the frequent plural suffix (S-PL) and monomorphemic
words. That is, words with the plural morpheme are accessed as fast as monomorphemic
words.
The individual analysis within one-suffix words shows an effect of frequency
of suffixes in lexical access. A repeated-measures ANOVA revealed
a significant difference among the categories in this group [F(2, 30) 5 7.01,
p , .005]. As Fig. 3 shows, words with the ablative suffix, which has the
lowest frequency, yield the longest RT. This is followed by the words with
the locative suffix. The words which contained the plural morpheme, however,
yield significantly faster RTs. A Fisher’s LSD post hoc analysis showed
that words with the ablative suffix yield significantly longer RTs than the
words inflected with the plural morpheme (p , .05).
Within monomorphemic words, a repeated-measures ANOVA yielded a
significant difference [F(3, 30) 5 7.9, p , .0001]. However, a Fisher’s LSD
post hoc analysis did not show any significant difference between the nonde-
FIG. 3. Mean RTs for each category in the one-suffix group; S-AB vs S-LOC, ns; S-AB
vs S-PL, p , .05; S-LOC vs S-PL, ns.
DECOMPOSITION IN TURKISH 223
FIG. 4. Mean RTs for nondecomposable (NDC) and pseudomorphemic words (PS, PSS,
and PSA).
composable group and any of the categories in the pseudomorphemic group
(Fig. 4). In this analysis, the only difference that was close to reaching significance
was between NDC and PS (p 5 .07). However, it was not statistically
significant.
As mentioned earlier, in a left-to-right parsing in Turkish, there may be
several alternative parsings in the lexical access of certain words and this is
expected to cause a delay in processing, and, in turn, longer RTs. However,
it seems that not every ‘‘possible’’ substring of a word is parsed. If this had
been the case, we would have obtained longer RTs for pseudomorphemic
items.
A comparison among multimorphemic words reveals a significant interaction
between the number of suffixes and the speed of word recognition. We
find that overall, two-suffix words yield significantly longer RTs than onesuffix
words (p , .05). A repeated-measures ANOVA for the multimorphemic
group yielded a significant difference [F(4, 30) 5 6.03, p , .0005].
However, as can be seen in Fig. 5, the two-suffix group (both S-PL-AB and
S-PL-LOC) are accessed as fast as one-suffix words (S-AB and S-LOC). A
Fisher’s LSD post hoc analysis revealed that the only significant difference
is between one-suffix words with the plural morpheme (S-PL) and two-suffix
words with the plural plus ablative morpheme (S-PL-AB) (p , .05). This
suggests that the plural morpheme in two-suffix words does not contribute
any extra processing load to the access of these words; it is accessed as part
of the stem.
CONCLUSION
This study has shown that not all multimorphemic words are accessed in
a decomposed form in Turkish. Words with frequent suffixes seem to be
accessed through a whole-word access procedure. Depending on the frequency
of the suffix, a word can be accessed via the direct access route or
the parsing route. The higher frequency of a suffix makes processing easier
and faster. It appears, then, that in a highly inflected language like Turkish,
224 AYS¸E GU¨ REL
FIG. 5. Mean RTs for multimorphemic words; S-AB vs. S-PL-AB, ns; S-AB vs S-PLLOC,
ns; S-LOC vs S-PL-AB, ns; S-LOC vs S-PL-LOC, ns; S-PL vs S-PL-AB, p , .05;
S-PL vs S-PL-LOC, ns.
the recognition of morphologically complex words is not as ‘‘costly’’ as it
may be in languages with little inflection (such as English), at least for words
that contain frequent suffixes. In other words, lexical access in languages
with complex morphology involves the direct route where possible in order
to save time in processing. This suggests that the parser in Turkish needs to
be much more effective than the parser in English in order to handle the
complexity of word forms during lexical access.
REFERENCES
Butterworth, B. 1983. Lexical representation. In B. Butterworth (Ed.), Language production
(Vol. 2). New York: Academic Press.
Caramazza, A., Laudanna, A., & Romani, C. 1988. Lexical access and inflectional morphology.
Cognition, 28, 297–332.
Frauenfelder, U. H., & Schreuder, R. 1992. Constraining psycholinguistic models of morphological
processing and representation: The role of productivity. In G. E. Booij & J. van
Marle (Eds.), Yearbook of morphology 1991. Dordrecht: Kluwer.
Hankamer, J. 1989. Morphological parsing and the lexicon. In W. Marslen-Wilson (Ed.), Lexical
representation and process. Cambridge, MA: The MIT Press.
Laine, M., Niemi, J., Koivuselka¨-Sallinen, P., & Hyo¨na¨, J. 1995. Morphological processing
of polymorphemic nouns in a highly inflected language. Cognitive Neuropsychology,
12(5), 457–502.
Pierce, J. 1960. A frequency count of Turkish words. Ankara: Milli Egitim Mudurlugu.
Taft, M., & Forster, K. I. 1975. Lexical storage and retrieval of prefixed words. Journal of
Verbal Learning and Verbal Behavior, 14, 638–647.

Brain, Language, and Environment

Brain and Language 71, 4–6 (2000)
doi:10.1006/brln.1999.2196, available online at http://www.idealibrary.com on
Brain, Language, and Environment
Martin L. Albert and Lisa Tabor Connor
Harold Goodglass Aphasia Research Center, Department of Neurology, Boston University
School of Medicine and Research Service of the Department of Veterans Affairs Medical
Center, Boston; and Language in the Aging Brain Laboratory, Boston University
School of Medicine
and
Loraine K. Obler
Harold Goodglass Aphasia Research Center, Department of Neurology, Boston University
School of Medicine and Research Service of the Department of Veterans Affairs Medical
Center, Boston; Language in the Aging Brain Laboratory, Boston University School of
Medicine; and CUNY Graduate Center, Program in Speech and Hearing Sciences
Research results from seemingly unrelated domains are converging on an
aspect of human behavior that will be of critical interest to cognitive neuroscientists
in the next century: the intimate interaction of brain, language, and
environment. Our principal argument is that brain–language relations cannot
be fully understood absent an understanding of the reciprocal influences of
the environment on brain–language relations and brain–language relations
on the environment. We predict that future research in the cognitive neuroscience
of language will, of necessity, include this new domain of theoretical
relevance—the mutual influence, that is, the dynamic interaction, of the neurally
based rules of linguistic grammar and the neurally based rules of social
interaction, which we call the ‘‘social grammar.’’ The present paper provides
evidence from the following sources to support our prediction: language
learning, theory of mind, behavioral neurology, and sociolinguistics.
The most obvious example of the influence of environment on language
is in the learning of one’s first language. The social context in which one
learns a first language obviously influences what one learns. (For example,
Address correspondence and reprint requests to Martin L. Albert, M.D., Ph.D., Harold
Goodglass Aphasia Research Center, Boston University School of Medicine and Boston Veterans
Affairs Medical Center, 150 South Huntington Avenue, Boston, MA 02130. E-mail:
malbert@bu.edu.
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MILLENNIUM ISSUE 5
children in English-speaking environments learn English; children in Japanese-
speaking environments learn Japanese.) Moreover the language context
interacts with brain development to set neural constraints on the ability to
comprehend and produce other languages. Werker et al. (1995) have noted
demonstrable loss in the ability to discriminate nonnative phonemic distinctions
as early as the first year of life. Furthermore, if a second language is
acquired after age 4, a limitation in the appreciation of aspects of that language’s
morphosyntax is evident by nonnative proficiency as an adult (Johnson
& Newport, 1989). Training can minimize such distinctions between
nonnative and native performance, however. For example, McCandliss and
colleagues (1999) have developed a program to enable Japanese speakers to
distinguish /l/ and /r/. That such training can be effective is further evidence
for the influence of environment on language.
Another set of examples of the mutual dependence of social behavior and
brain–language relations comes from research in the cognitive neuroscience
of ‘‘theory of mind.’’ Theory of mind refers to the ability to understand
someone else’s intent (Premack & Woodruff, 1978). Impairments in the ability
to produce or comprehend indirect requests, humor, sarcasm, or other
aspects of idiomatic or metaphoric language use, as can occur following right
hemispheric damage (Brownell et al., 1986), can seriously disrupt the ability
to understand a speaker’s intent, disturb normal social conversation, and interfere
with normal social interaction.
A dramatic clinical example of the intimate interaction of brain, language,
and environment comes from a different realm of behavioral analysis: a
single case study recently completed of an association between language
and the ‘‘environmental dependency’’ syndrome (Tanaka et al., 1999). The
environmental dependency syndrome refers to a peculiar pattern of actions
linked to frontal lobe dysfunction in which patients display an exaggerated
dependency on the environment for behavioral cues (Lhermitte, 1986). We
examined an 84-year-old woman with an acute left frontal lobe infarction
who entered the hospital with striking imitation behavior. After two weeks
her imitation behavior disappeared, but an equally striking new behavior
emerged. In the presence of others, she would call out the names of objects
in the room, and also call out the actions and gestures of people in the room,
even though she was not asked to do so, and even though she was asked to
stop. She appeared altogether unable to prevent herself from speaking aloud
in response to specific environmental cues.
The argument we are making in this paper, which we believe will find its
place in future research in the cognitive neuroscience of language, echoes
arguments made previously in Russian research. An extensive series of studies,
starting decades ago with Vygotsky and extending through Luria to
Bakhtin, elegantly summarized by Wertsch (1998), demonstrates how language
as a cultural tool influences expectations of social groups, ultimately
setting constraints on understanding. In turn, these constraints contribute to
6 MILLENNIUM ISSUE
the development of social rules which, themselves, influence language use.
Military propaganda and commercial advertising are the best known representatives
of this influence. Wertsch concludes that the proper study of ‘‘the
relationship between mind and sociocultural setting’’ is not only to look at
the extremes (neurobiology, on one hand; society, on the other) but also ‘‘to
employ a unit of analysis that focuses precisely on how these forces come
into dynamic contact.’’ We are here making the same argument for the study
of brain, language, and environment, and we suggest that the tools (theoretical,
methodological, technological) are at hand, and the time is ripe, for the
development of this field of research.
Earlier in this paper we spoke of the ‘‘social grammar.’’ By social grammar
we mean the internalized, neurally conditioned set of rules that order
and constrain interactions between and among individuals and their environment(
s). As a child grows into adulthood, a neurally based social grammar
develops whereby cognitive and emotional systems are conditioned by environmental
cues, and the cognitive capacity to control the environment and
plan ahead emerges. A research theme we believe likely to be found on the
research agenda of cognitive neuroscientists in the future is the study of the
dynamic interaction between the social grammar and the linguistic grammar.
REFERENCES
Brownell, H., Potter, H., & Birhle, A. 1986. Inferences deficits in right brain damaged patients.
Brain and Language 27, 310–321.
Johnson, J. S., & Newport, E. L. 1989. Critical period effects in second language learning:
The influence of maturational state on the acquisition of English as a second language.
Cognitive Psychology 21, 60–99.
Lhermitte, F. 1986. Human autonomy of the frontal lobes. Part II: Patient behavior in complex
and social situations: The ‘‘environmental dependency syndrome.’’ Annals of Neurology
19, 335–343.
McCandliss, B., Fiez, J., Conway, M., & McClelland, J. 1999. Eliciting adult plasticity for
Japanese adults struggling to identify English /r/ and /l/: Insights from a Hebbian model
and a new training procedure. Paper presented at Annual Meeting of Cognitive Neuroscience
Society, Washington, DC.
Premack, D., & Woodruff, G. 1978. Does the chimpanzee have a theory of mind? Behavioral
and Brain Sciences 1, 515–526.
Tanaka, Y., Albert, M. L., Hara, H., Miyashita, T., & Otani, N. 1999. Forced hyperphasia
and the environmental dependency syndrome, Journal of Neurology, Neurosurgery, and
Psychiatry, in press.
Werker, J. F.,& Desjardins, R. N. 1995. Listening to speech in the first year of life. Experiential
influences on phoneme perception. Current Directions in Psychological Science 4, 76–
81.
Wertsch, J. 1998. Mind as action. New York: Oxford University Press.

Cancer

Cancer /ˈkænsər/ ( listen) (medical term: malignant neoplasm) is a class of diseases in which a group of cells display uncontrolled growth (division beyond the normal limits), invasion (intrusion on and destruction of adjacent tissues), and sometimes metastasis (spread to other locations in the body via lymph or blood). These three malignant properties of cancers differentiate them from benign tumors, which are self-limited, and do not invade or metastasize. Most cancers form a tumor but some, like leukemia, do not. The branch of medicine concerned with the study, diagnosis, treatment, and prevention of cancer is oncology.

Cancer affects people at all ages with the risk for most types increasing with age.[1] Cancer caused about 13% of all human deaths in 2007[2] (7.6 million).[3]

Cancers are caused by abnormalities in the genetic material of the transformed cells.[4] These abnormalities may be due to the effects of carcinogens, such as tobacco smoke, radiation, chemicals, or infectious agents. Other cancer-promoting genetic abnormalities may randomly occur through errors in DNA replication, or are inherited, and thus present in all cells from birth. The heritability of cancers is usually affected by complex interactions between carcinogens and the host's genome.

Genetic abnormalities found in cancer typically affect two general classes of genes. Cancer-promoting oncogenes are typically activated in cancer cells, giving those cells new properties, such as hyperactive growth and division, protection against programmed cell death, loss of respect for normal tissue boundaries, and the ability to become established in diverse tissue environments. Tumor suppressor genes are then inactivated in cancer cells, resulting in the loss of normal functions in those cells, such as accurate DNA replication, control over the cell cycle, orientation and adhesion within tissues, and interaction with protective cells of the immune system.

Definitive diagnosis requires the histologic examination of a biopsy specimen, although the initial indication of malignancy can be symptomatic or radiographic imaging abnormalities. Most cancers can be treated and some forced into remission, depending on the specific type, location, and stage. Once diagnosed, cancer is usually treated with a combination of surgery, chemotherapy and radiotherapy. As research develops, treatments are becoming more specific for different varieties of cancer. There has been significant progress in the development of targeted therapy drugs that act specifically on detectable molecular abnormalities in certain tumors, and which minimize damage to normal cells. The prognosis of cancer patients is most influenced by the type of cancer, as well as the stage, or extent of the disease. In addition, histologic grading and the presence of specific molecular markers can also be useful in establishing prognosis, as well as in determining individual treatments.

Contents [hide]
1 Classification
2 Signs and symptoms
3 Causes
3.1 Mutation: chemical carcinogens
3.2 Mutation: ionizing radiation
3.3 Infection
3.4 Hormonal imbalances
3.5 Immune system dysfunction
3.6 Heredity
3.7 Other causes
4 Pathophysiology
5 Prevention
5.1 Modifiable ("lifestyle") risk factors
5.2 Diet
5.3 Vitamins
5.4 Chemoprevention
5.5 Genetic testing
5.6 Vaccination
5.7 Screening
6 Diagnosis
6.1 Pathology
7 Management
8 Prognosis
8.1 Emotional impact
9 Epidemiology
10 History
11 Research
12 Glossary
13 Notes
14 References
15 External links

Classification
Further information: List of cancer types
Cancers are classified by the type of cell that resembles the tumor and, therefore, the tissue presumed to be the origin of the tumor. These are the histology and the location, respectively. Examples of general categories include:

Carcinoma: Malignant tumors derived from epithelial cells. This group represents the most common cancers, including the common forms of breast, prostate, lung and colon cancer.
Sarcoma: Malignant tumors derived from connective tissue, or mesenchymal cells.
Lymphoma and leukemia: Malignancies derived from hematopoietic (blood-forming) cells
Germ cell tumor: Tumors derived from totipotent cells. In adults most often found in the testicle and ovary; in fetuses, babies, and young children most often found on the body midline, particularly at the tip of the tailbone; in horses most often found at the poll (base of the skull).
Blastic tumor or blastoma: A tumor (usually malignant) which resembles an immature or embryonic tissue. Many of these tumors are most common in children.
Malignant tumors (cancers) are usually named using -carcinoma, -sarcoma or -blastoma as a suffix, with the Latin or Greek word for the organ of origin as the root. For instance, a cancer of the liver is called hepatocarcinoma; a cancer of the fat cells is called liposarcoma. For common cancers, the English organ name is used. For instance, the most common type of breast cancer is called ductal carcinoma of the breast or mammary ductal carcinoma. Here, the adjective ductal refers to the appearance of the cancer under the microscope, resembling normal breast ducts.

Benign tumors (which are not cancers) are named using -oma as a suffix with the organ name as the root. For instance, a benign tumor of the smooth muscle of the uterus is called leiomyoma (the common name of this frequent tumor is fibroid). Unfortunately, some cancers also use the -oma suffix, examples being melanoma and seminoma.

Signs and symptoms

Symptoms of cancer metastasis depend on the location of the tumor.Roughly, cancer symptoms can be divided into three groups:

Local symptoms: unusual lumps or swelling (tumor), hemorrhage (bleeding), pain and/or ulceration. Compression of surrounding tissues may cause symptoms such as jaundice (yellowing the eyes and skin).
Symptoms of metastasis (spreading): enlarged lymph nodes, cough and hemoptysis, hepatomegaly (enlarged liver), bone pain, fracture of affected bones and neurological symptoms. Although advanced cancer may cause pain, it is often not the first symptom.
Systemic symptoms: weight loss, poor appetite, fatigue and cachexia (wasting), excessive sweating (night sweats), anemia and specific paraneoplastic phenomena, i.e. specific conditions that are due to an active cancer, such as thrombosis or hormonal changes.
Every symptom in the above list can be caused by a variety of conditions (a list of which is referred to as the differential diagnosis). Cancer may be a common or uncommon cause of each item.

Causes
Cancer is a diverse class of diseases which differ widely in their causes and biology. Any organism, even plants, can acquire cancer. Nearly all known cancers arise gradually, as errors build up in the cancer cell and its progeny (see mechanisms section for common types of errors).

Anything which replicates (living cells) will probabilistically suffer from errors (mutations). Unless error correction and prevention is properly carried out, the errors will survive, and might be passed along to daughter cells. Normally, the body safeguards against cancer via numerous methods, such as: apoptosis, helper molecules (some DNA polymerases), possibly senescence, etc. However these error-correction methods often fail in small ways, especially in environments that make errors more likely to arise and propagate. For example, such environments can include the presence of disruptive substances called carcinogens, or periodic injury (physical, heat, etc.), or environments that cells did not evolve to withstand, such as hypoxia[5] (see subsections). Cancer is thus a progressive disease, and these progressive errors slowly accumulate until a cell begins to act contrary to its function in the organism.

The errors which cause cancer are often self-amplifying, eventually compounding at an exponential rate. For example:

A mutation in the error-correcting machinery of a cell might cause that cell and its children to accumulate errors more rapidly
A mutation in signaling (endocrine) machinery of the cell can send error-causing signals to nearby cells
A mutation might cause cells to become neoplastic, causing them to migrate and disrupt more healthy cells
A mutation may cause the cell to become immortal (see telomeres), causing them to disrupt healthy cells forever
Thus cancer often explodes in something akin to a chain reaction caused by a few errors, which compound into more severe errors. Errors which produce more errors are effectively the root cause of cancer, and also the reason that cancer is so hard to treat: even if there were 10,000,000,000 cancerous cells and one killed all but 10 of those cells, those cells (and other error-prone precancerous cells) could still self-replicate or send error-causing signals to other cells, starting the process over again. This rebellion-like scenario is an undesirable survival of the fittest, where the driving forces of evolution work against the body's design and enforcement of order. In fact, once cancer has begun to develop, this same force continues to drive the progression of cancer towards more invasive stages, and is called clonal evolution.[6]

Research about cancer causes often falls into the following categories:

Agents (e.g. viruses) and events (e.g. mutations) which cause or facilitate genetic changes in cells destined to become cancer.
The precise nature of the genetic damage, and the genes which are affected by it.
The consequences of those genetic changes on the biology of the cell, both in generating the defining properties of a cancer cell, and in facilitating additional genetic events which lead to further progression of the cancer.
Mutation: chemical carcinogens
Further information: Carcinogen

The incidence of lung cancer is highly correlated with smoking. Source:NIH.Cancer pathogenesis is traceable back to DNA mutations that impact cell growth and metastasis. Substances that cause DNA mutations are known as mutagens, and mutagens that cause cancers are known as carcinogens. Particular substances have been linked to specific types of cancer. Tobacco smoking is associated with many forms of cancer,[7] and causes 90% of lung cancer.[8] Prolonged exposure to asbestos fibers is associated with mesothelioma.[9]

Many mutagens are also carcinogens, but some carcinogens are not mutagens. Alcohol is an example of a chemical carcinogen that is not a mutagen.[10] Such chemicals may promote cancers through stimulating the rate of cell division. Faster rates of replication leaves less time for repair enzymes to repair damaged DNA during DNA replication, increasing the likelihood of a mutation.

Decades of research has demonstrated the link between tobacco use and cancer in the lung, larynx, head, neck, stomach, bladder, kidney, oesophagus and pancreas.[11] Tobacco smoke contains over fifty known carcinogens, including nitrosamines and polycyclic aromatic hydrocarbons.[12] Tobacco is responsible for about one in three of all cancer deaths in the developed world,[7] and about one in five worldwide.[12] Indeed, lung cancer death rates in the United States have mirrored smoking patterns, with increases in smoking followed by dramatic increases in lung cancer death rates and, more recently[when?], decreases in smoking followed by decreases in lung cancer death rates in men. However, the numbers of smokers worldwide is still rising, leading to what some organizations have described as the tobacco epidemic.[13]

Mutation: ionizing radiation
Sources of ionizing radiation, such as radon gas, can cause cancer. Prolonged exposure to ultraviolet radiation from the sun can lead to melanoma and other skin malignancies.[14] It is estimated that 2% of future cancers will be due to current CT scans.[15]

Non-ionizing radio frequency radiation from mobile phones and other similar RF sources has also been proposed as a cause of cancer, but there is currently little established evidence of such a link.[16]

Infection
Some cancers can be caused by infection.[17] This is especially true in animals such as birds, but also in humans, with viruses responsible for up to 20% of human cancers worldwide.[18] These include human papillomavirus (cervical carcinoma), human polyomaviruses (mesothelioma, brain tumors), Epstein-Barr virus (B-cell lymphoproliferative disease and nasopharyngeal carcinoma), Kaposi's sarcoma herpesvirus (Kaposi's Sarcoma and primary effusion lymphomas), hepatitis B and hepatitis C viruses (hepatocellular carcinoma), Human T-cell leukemia virus-1 (T-cell leukemias), and Helicobacter pylori (gastric carcinoma).[18]

Experimental and epidemiological data imply a causative role for viruses and they appear to be the second most important risk factor for cancer development in humans, exceeded only by tobacco usage.[19] The mode of virally induced tumors can be divided into two, acutely transforming or slowly transforming. In acutely transforming viruses, the virus carries an overactive oncogene called viral-oncogene (v-onc), and the infected cell is transformed as soon as v-onc is expressed. In contrast, in slowly transforming viruses, the virus genome is inserts near a proto-oncogene in the host genome. The viral promoter or other transcription regulation elements then cause overexpression of that proto-oncogene. This induces uncontrolled cell division. Because the site of insertion is not specific to proto-oncogenes and the chance of insertion near any proto-oncogene is low, slowly transforming viruses will cause tumors much longer after infection than the acutely transforming viruses.

Hepatitis viruses, including hepatitis B and hepatitis C, can induce a chronic viral infection that leads to liver cancer in 0.47% of hepatitis B patients per year (especially in Asia, less so in North America), and in 1.4% of hepatitis C carriers per year. Liver cirrhosis, whether from chronic viral hepatitis infection or alcoholism, is associated with the development of liver cancer, and the combination of cirrhosis and viral hepatitis presents the highest risk of liver cancer development. Worldwide, liver cancer is one of the most common, and most deadly, cancers due to a huge burden of viral hepatitis transmission and disease.

Advances in cancer research have made a vaccine designed to prevent cancer available. In 2006, the U.S. Food and Drug Administration approved a human papilloma virus vaccine, called Gardasil. The vaccine protects against four HPV types, which together cause 70% of cervical cancers and 90% of genital warts. In March 2007, the US Centers for Disease Control and Prevention (CDC) Advisory Committee on Immunization Practices (ACIP) officially recommended that females aged 11–12 receive the vaccine, and indicated that females as young as age 9 and as old as age 26 are also candidates for immunization.

In addition to viruses, researchers have noted a connection between bacteria and certain cancers. The most prominent example is the link between chronic infection of the wall of the stomach with Helicobacter pylori and gastric cancer.[20][21] Although only a minority of those infected with Helicobacter go on to develop cancer, since this pathogen is quite common it is probably responsible for most of these cancers.[22]

Hormonal imbalances
Some hormones can act in a similar manner to non-mutagenic carcinogens in that they may stimulate excessive cell growth.[clarification needed]

Immune system dysfunction
HIV is associated with a number of malignancies, including Kaposi's sarcoma, non-Hodgkin's lymphoma, and HPV-associated malignancies such as anal cancer and cervical cancer. AIDS-defining illnesses have long included these diagnoses. The increased incidence of malignancies in HIV patients points to the breakdown of immune surveillance as a possible etiology of cancer.[23] Certain other immune deficiency states (e.g. common variable immunodeficiency and IgA deficiency) are also associated with increased risk of malignancy.[24]

Heredity
Most forms of cancer are sporadic, meaning that there is no inherited cause of the cancer. There are, however, a number of recognised syndromes where there is an inherited predisposition to cancer, often due to a defect in a gene that protects against tumor formation. Famous examples are:

certain inherited mutations in the genes BRCA1 and BRCA2 are associated with an elevated risk of breast cancer and ovarian cancer
tumors of various endocrine organs in multiple endocrine neoplasia (MEN types 1, 2a, 2b)
Li-Fraumeni syndrome (various tumors such as osteosarcoma, breast cancer, soft tissue sarcoma, brain tumors) due to mutations of p53
Turcot syndrome (brain tumors and colonic polyposis)
Familial adenomatous polyposis an inherited mutation of the APC gene that leads to early onset of colon carcinoma.
Hereditary nonpolyposis colorectal cancer (HNPCC, also known as Lynch syndrome) can include familial cases of colon cancer, uterine cancer, gastric cancer, and ovarian cancer, without a preponderance of colon polyps.
Retinoblastoma, when occurring in young children, is due to a hereditary mutation in the retinoblastoma gene.
Down syndrome patients, who have an extra chromosome 21, are known to develop malignancies such as leukemia and testicular cancer, though the reasons for this difference are not well understood.
Other causes
Excepting the rare transmissions that occur with pregnancies and only a marginal few organ donors, cancer is generally not a transmissible disease. The main reason for this is tissue graft rejection caused by MHC incompatibility.[25] In humans and other vertebrates, the immune system uses MHC antigens to differentiate between "self" and "non-self" cells because these antigens are different from person to person. When non-self antigens are encountered, the immune system reacts against the appropriate cell. Such reactions may protect against tumour cell engraftment by eliminating implanted cells. In the United States, approximately 3,500 pregnant women have a malignancy annually, and transplacental transmission of acute leukaemia, lymphoma, melanoma and carcinoma from mother to fetus has been observed.[25] The development of donor-derived tumors from organ transplants is exceedingly rare. The main cause of organ transplant associated tumors seems to be malignant melanoma, that was undetected at the time of organ harvest.[26] though other cases exist[27] In fact, cancer from one organism will usually grow in another organism of that species, as long as they share the same histocompatibility genes,[28] proven using mice; however this would never happen in a real-world setting except as described above.

In non-humans, a few types of transmissible cancer have been described, wherein the cancer spreads between animals by transmission of the tumor cells themselves. This phenomenon is seen in dogs with Sticker's sarcoma, also known as canine transmissible venereal tumor,[29] as well as Devil facial tumour disease in Tasmanian devils.

Pathophysiology
Main article: Oncogenesis

Cancers are caused by a series of mutations. Each mutation alters the behavior of the cell somewhat.Cancer is fundamentally a disease of regulation of tissue growth. In order for a normal cell to transform into a cancer cell, genes which regulate cell growth and differentiation must be altered.[30] Genetic changes can occur at many levels, from gain or loss of entire chromosomes to a mutation affecting a single DNA nucleotide. There are two broad categories of genes which are affected by these changes. Oncogenes may be normal genes which are expressed at inappropriately high levels, or altered genes which have novel properties. In either case, expression of these genes promotes the malignant phenotype of cancer cells. Tumor suppressor genes are genes which inhibit cell division, survival, or other properties of cancer cells. Tumor suppressor genes are often disabled by cancer-promoting genetic changes. Typically, changes in many genes are required to transform a normal cell into a cancer cell.[31]

There is a diverse classification scheme for the various genomic changes which may contribute to the generation of cancer cells. Most of these changes are mutations, or changes in the nucleotide sequence of genomic DNA. Aneuploidy, the presence of an abnormal number of chromosomes, is one genomic change which is not a mutation, and may involve either gain or loss of one or more chromosomes through errors in mitosis.

Large-scale mutations involve the deletion or gain of a portion of a chromosome. Genomic amplification occurs when a cell gains many copies (often 20 or more) of a small chromosomal locus, usually containing one or more oncogenes and adjacent genetic material. Translocation occurs when two separate chromosomal regions become abnormally fused, often at a characteristic location. A well-known example of this is the Philadelphia chromosome, or translocation of chromosomes 9 and 22, which occurs in chronic myelogenous leukemia, and results in production of the BCR-abl fusion protein, an oncogenic tyrosine kinase.

Small-scale mutations include point mutations, deletions, and insertions, which may occur in the promoter of a gene and affect its expression, or may occur in the gene's coding sequence and alter the function or stability of its protein product. Disruption of a single gene may also result from integration of genomic material from a DNA virus or retrovirus, and such an event may also result in the expression of viral oncogenes in the affected cell and its descendants.

Prevention
Cancer prevention is defined as active measures to decrease the incidence of cancer.[32] Greater than 30% of cancer is preventable via avoiding risk factors including: tobacco, overweight or obesity, low fruit and vegetable intake, physical inactivity, alcohol, sexually transmitted infection, air pollution.[33] This can be accomplished by avoiding carcinogens or altering their metabolism, pursuing a lifestyle or diet that modifies cancer-causing factors and/or medical intervention (chemoprevention, treatment of pre-malignant lesions). The epidemiological concept of "prevention" is usually defined as either primary prevention, for people who have not been diagnosed with a particular disease, or secondary prevention, aimed at reducing recurrence or complications of a previously diagnosed illness.

Modifiable ("lifestyle") risk factors
See also: Alcohol and cancer
The vast majority of cancer risk factors are environmental or lifestyle-related, leading to the claim that cancer is a largely preventable disease.[34] Examples of modifiable cancer risk factors include alcohol consumption (associated with increased risk of oral, esophageal, breast, and other cancers), smoking (although 20% of women with lung cancer have never smoked, versus 10% of men[35]), physical inactivity (associated with increased risk of colon, breast, and possibly other cancers), and being overweight / obese (associated with colon, breast, endometrial, and possibly other cancers). Based on epidemiologic evidence, it is now thought that avoiding excessive alcohol consumption may contribute to reductions in risk of certain cancers; however, compared with tobacco exposure, the magnitude of effect is modest or small and the strength of evidence is often weaker. Other lifestyle and environmental factors known to affect cancer risk (either beneficially or detrimentally) include certain sexually transmitted diseases (such as those conveyed by the human papillomavirus), the use of exogenous hormones, exposure to ionizing radiation and ultraviolet radiation from the sun or from tanning beds, and certain occupational and chemical exposures.

Every year, at least 200,000 people die worldwide from cancer related to their workplace.[36] Millions of workers run the risk of developing cancers such as lung cancer and mesothelioma from inhaling asbestos fibers and tobacco smoke, or leukemia from exposure to benzene at their workplaces.[36] Currently, most cancer deaths caused by occupational risk factors occur in the developed world.[36] It is estimated that approximately 20,000 cancer deaths and 40,000 new cases of cancer each year in the U.S. are attributable to occupation.[37]

Diet
Main article: Diet and cancer
The consensus on diet and cancer is that obesity increases the risk of developing cancer. Particular dietary practices often explain differences in cancer incidence in different countries (e.g. gastric cancer is more common in Japan, while colon cancer is more common in the United States. In this example the preceding consideration of Haplogroups are excluded). Studies have shown that immigrants develop the risk of their new country, often within one generation, suggesting a substantial link between diet and cancer.[38] Whether reducing obesity in a population also reduces cancer incidence is unknown.

Despite frequent reports of particular substances (including foods) having a beneficial or detrimental effect on cancer risk, few of these have an established link to cancer. These reports are often based on studies in cultured cell media or animals. Public health recommendations cannot be made based on these studies until they have been validated in an observational (or occasionally a prospective interventional) trial in humans.

Proposed dietary interventions for primary cancer risk reduction generally gain support from epidemiological association studies. Examples of such studies include reports that reduced meat consumption is associated with decreased risk of colon cancer,[39] and reports that consumption of coffee is associated with a reduced risk of liver cancer.[40] Studies have linked consumption of grilled meat to an increased risk of stomach cancer,[41] colon cancer,[42] breast cancer,[43] and pancreatic cancer,[44] a phenomenon which could be due to the presence of carcinogens such as benzopyrene in foods cooked at high temperatures.

A 2005 secondary prevention study showed that consumption of a plant-based diet and lifestyle changes resulted in a reduction in cancer markers in a group of men with prostate cancer who were using no conventional treatments at the time.[45] These results were amplified by a 2006 study. Over 2,400 women were studied, half randomly assigned to a normal diet, the other half assigned to a diet containing less than 20% calories from fat. The women on the low fat diet were found to have a markedly lower risk of breast cancer recurrence, in the interim report of December, 2006.[46]

Recent[when?] studies have also demonstrated potential links between some forms of cancer and high consumption of refined sugars and other simple carbohydrates.[47][48][49][50][51] Although the degree of correlation and the degree of causality is still debated,[52][53][54] some organizations have in fact begun to recommend reducing intake of refined sugars and starches as part of their cancer prevention regimens.[55][56][57]

In November 2007, the American Institute for Cancer Research (AICR), in conjunction with the World Cancer Research Fund (WCRF), published Food, Nutrition, Physical Activity and the Prevention of Cancer: a Global Perspective, "the most current and comprehensive analysis of the literature on diet, physical activity and cancer".[58] The WCRF/AICR Expert Report lists 10 recommendations that people can follow to help reduce their risk of developing cancer, including the following dietary guidelines: (1) reducing intake of foods and drinks that promote weight gain, namely energy-dense foods and sugary drinks, (2) eating mostly foods of plant origin, (3) limiting intake of red meat and avoiding processed meat, (4) limiting consumption of alcoholic beverages, and (5) reducing intake of salt and avoiding mouldy cereals (grains) or pulses (legumes).[59][60]

Some mushrooms offer an anti-cancer effect, which is thought to be linked to their ability to up-regulate the immune system. Some mushrooms known for this effect include, Reishi,[61][62] Agaricus blazei,[63] Maitake,[64] and Trametes versicolor[65]. Research suggests the compounds in medicinal mushrooms most responsible for up-regulating the immune system and providing an anti-cancer effect, are a diverse collection of polysaccharide compounds, particularly beta-glucans. Beta-glucans are known as "biological response modifiers", and their ability to activate the immune system is well documented. Specifically, beta-glucans stimulate the innate branch of the immune system. Research has shown beta-glucans have the ability to stimulate macrophage, NK cells, T cells, and immune system cytokines. The mechanisms in which beta-glucans stimulate the immune system is only partially understood. One mechanism in which beta-glucans are able to activate the immune system, is by interacting with the Macrophage-1 antigen (CD18) receptor on immune cells.[66]

Vitamins
Vitamin supplementation has not been proven effective in the prevention of cancer.[citation needed] The components of food are also proving to be more numerous and varied than previously understood, so patients are increasingly advised to consume fruits and vegetables for maximal health benefits.[67]

Vitamin D
Low levels of vitamin D is correlated with increased cancer risk.[68][69] Whether this relationship is causal is yet to be determined.[70]

Beta carotene
Beta-carotene supplementation has been found to increase slightly, but not significantly risks of lung cancer.[71]

Folic acid
Folic acid supplementation has not been found effective in preventing colon cancer and may increase colon polyps.[72]

Chemoprevention
The concept that medications could be used to prevent cancer is an attractive one, and many high-quality clinical trials support the use of such chemoprevention in defined circumstances.

Daily use of tamoxifen, a selective estrogen receptor modulator (SERM), typically for 5 years, has been demonstrated to reduce the risk of developing breast cancer in high-risk women by about 50%. A recent[when?] study reported that the selective estrogen receptor modulator raloxifene has similar benefits to tamoxifen in preventing breast cancer in high-risk women, with a more favorable side effect profile.[73]

Raloxifene is a SERM like tamoxifen; it has been shown (in the STAR trial) to reduce the risk of breast cancer in high-risk women equally as well as tamoxifen. In this trial, which studied almost 20,000 women, raloxifene had fewer side effects than tamoxifen, though it did permit more DCIS to form.[73]

Finasteride, a 5-alpha-reductase inhibitor, has been shown to lower the risk of prostate cancer, though it seems to mostly prevent low-grade tumors.[74] The effect of COX-2 inhibitors such as rofecoxib and celecoxib upon the risk of colon polyps have been studied in familial adenomatous polyposis patients[75] and in the general population.[76][77] In both groups, there were significant reductions in colon polyp incidence, but this came at the price of increased cardiovascular toxicity.

Genetic testing
Genetic testing for high-risk individuals is already available for certain cancer-related genetic mutations. Carriers of genetic mutations that increase risk for cancer incidence can undergo enhanced surveillance, chemoprevention, or risk-reducing surgery. Early identification of inherited genetic risk for cancer, along with cancer-preventing interventions such as surgery or enhanced surveillance, can be lifesaving for high-risk individuals.

Gene Cancer types Availability
BRCA1, BRCA2 Breast, ovarian, pancreatic Commercially available for clinical specimens
MLH1, MSH2, MSH6, PMS1, PMS2 Colon, uterine, small bowel, stomach, urinary tract Commercially available for clinical specimens

Vaccination
Prophylactic vaccines have been developed to prevent infection by oncogenic infectious agents such as viruses, and therapeutic vaccines are in development to stimulate an immune response against cancer-specific epitopes.[78]

As reported above, a preventive human papillomavirus vaccine exists that targets certain sexually transmitted strains of human papillomavirus that are associated with the development of cervical cancer and genital warts. The only two HPV vaccines on the market as of October 2007 are Gardasil and Cervarix.[78] There is also a hepatitis B vaccine, which prevents infection with the hepatitis B virus, an infectious agent that can cause liver cancer.[78] A canine melanoma vaccine has also been developed.[79][80]

Screening
Main article: Cancer screening
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Cancer screening is an attempt to detect unsuspected cancers in an asymptomatic population. Screening tests suitable for large numbers of healthy people must be relatively affordable, safe, noninvasive procedures with acceptably low rates of false positive results. If signs of cancer are detected, more definitive and invasive follow up tests are performed to confirm the diagnosis.

Screening for cancer can lead to earlier diagnosis in specific cases. Early diagnosis may lead to extended life, but may also falsely prolong the lead time to death through lead time bias or length time bias.

A number of different screening tests have been developed for different malignancies. Breast cancer screening can be done by breast self-examination, though this approach was discredited by a 2005 study in over 300,000 Chinese women. Screening for breast cancer with mammograms has been shown to reduce the average stage of diagnosis of breast cancer in a population. Stage of diagnosis in a country has been shown to decrease within ten years of introduction of mammographic screening programs. Colorectal cancer can be detected through fecal occult blood testing and colonoscopy, which reduces both colon cancer incidence and mortality, presumably through the detection and removal of pre-malignant polyps. Similarly, cervical cytology testing (using the Pap smear) leads to the identification and excision of precancerous lesions. Over time, such testing has been followed by a dramatic reduction of cervical cancer incidence and mortality. Testicular self-examination is recommended for men beginning at the age of 15 years to detect testicular cancer. Prostate cancer can be screened using a digital rectal exam along with prostate specific antigen (PSA) blood testing, though some authorities (such as the US Preventive Services Task Force) recommend against routinely screening all men.

Screening for cancer is controversial in cases when it is not yet known if the test actually saves lives. The controversy arises when it is not clear if the benefits of screening outweigh the risks of follow-up diagnostic tests and cancer treatments. For example: when screening for prostate cancer, the PSA test may detect small cancers that would never become life threatening, but once detected will lead to treatment. This situation, called overdiagnosis, puts men at risk for complications from unnecessary treatment such as surgery or radiation. Follow up procedures used to diagnose prostate cancer (prostate biopsy) may cause side effects, including bleeding and infection. Prostate cancer treatment may cause incontinence (inability to control urine flow) and erectile dysfunction (erections inadequate for intercourse). Similarly, for breast cancer, there have recently[when?] been criticisms that breast screening programs in some countries cause more problems than they solve. This is because screening of women in the general population will result in a large number of women with false positive results which require extensive follow-up investigations to exclude cancer, leading to having a high number-to-treat (or number-to-screen) to prevent or catch a single case of breast cancer early.

Cervical cancer screening via the Pap smear has the best cost-benefit profile of all the forms of cancer screening from a public health perspective as, largely caused by a virus, it has clear risk factors (sexual contact), and the natural progression of cervical cancer is that it normally spreads slowly over a number of years therefore giving more time for the screening program to catch it early. Moreover, the test is easy to perform and relatively cheap.

For these reasons, it is important that the benefits and risks of diagnostic procedures and treatment be taken into account when considering whether to undertake cancer screening.

Use of medical imaging to search for cancer in people without clear symptoms is similarly marred with problems. There is a significant risk of detection of what has been recently[when?] called an incidentaloma - a benign lesion that may be interpreted as a malignancy and be subjected to potentially dangerous investigations. Recent[when?] studies of CT scan-based screening for lung cancer in smokers have had equivocal results, and systematic screening is not recommended as of July 2007. Randomized clinical trials of plain-film chest X-rays to screen for lung cancer in smokers have shown no benefit for this approach.

Canine cancer detection has shown promise, but is still in the early stages of research.

Diagnosis

Chest x-ray showing lung cancer in the left lung.Most cancers are initially recognized either because signs or symptoms appear or through screening. Neither of these lead to a definitive diagnosis, which usually requires the opinion of a pathologist, a type of physician (medical doctor) who specializes in the diagnosis of cancer and other diseases. People with suspected cancer are investigated with medical tests. These commonly include blood tests, X-rays, CT scans and endoscopy.

Pathology
A cancer may be suspected for a variety of reasons, but the definitive diagnosis of most malignancies must be confirmed by histological examination of the cancerous cells by a pathologist. Tissue can be obtained from a biopsy or surgery. Many biopsies (such as those of the skin, breast or liver) can be done in a doctor's office. Biopsies of other organs are performed under anesthesia and require surgery in an operating room.

The tissue diagnosis given by the pathologist indicates the type of cell that is proliferating, its histological grade, genetic abnormalities, and other features of the tumor. Together, this information is useful to evaluate the prognosis of the patient and to choose the best treatment. Cytogenetics and immunohistochemistry are other types of testing that the pathologist may perform on the tissue specimen. These tests may provide information about the molecular changes (such as mutations, fusion genes, and numerical chromosome changes) that has happened in the cancer cells, and may thus also indicate the future behavior of the cancer (prognosis) and best treatment.

Snoring

Snoring is the vibration of respiratory structures and the resulting sound, due to obstructed air movement during breathing while sleeping. In some cases the sound may be soft, but in other cases, it can be rather loud and quite unpleasant. Generally speaking, the structures involved are the uvula and soft palate. The irregular airflow is caused by a passageway blockage and usually due to one of the following:

Throat weakness, causing the throat to close during sleep
Mispositioned jaw, often caused by tension in the muscles
Fat gathering in and around the throat
Obstruction in the nasal passageway
The tissues at the top of airways touching each other causing vibrations
Relaxants such as alcohol or drugs relaxing throat muscles
Sleeping on one's back, which may result in the tongue dropping to the back of the mouth.
Statistics on snoring are often contradictory, but at least 30% of adults and perhaps as many as 50% of people in some demographics snore.[1] One survey of 5,713 Italian residents identified habitual snoring in 24% of men and 13.8% of women, rising to 60% of men and 40% of women aged 60 to 65 years; this suggests an increased susceptibility to snoring as age increases.[2]

Contents [hide]
1 Impacts
2 Diagnosis
3 Treatment
3.1 Dental appliances
3.2 Positive airway pressure
3.3 Surgery
3.4 Pharmacological treatment
3.5 Natural remedies
3.6 Antidepressants
4 Coping as partner
5 See also
6 References
7 External links

[edit] Impacts
Snoring is known to cause sleep deprivation to snorers and those around them, as well as daytime drowsiness, irritability, lack of focus and decreased libido.[3] It has also been suggested that it can cause significant psychological and social damage to sufferers.[4] Multiple studies reveal a positive correlation between loud snoring and risk of heart attack (about +34% chance) and stroke (about +67% chance).[5]

Though snoring is often considered a minor affliction, snorers can sometimes suffer severe impairment of lifestyle. The between-subjects trial by Armstrong et al. discovered a statistically significant improvement in marital relations after snoring was surgically corrected. This was confirmed by evidence from Gall et al.[6], Cartwright and Knight[7] and Fitzpatrick et al.[8]

New studies associate loud "snoring" with the development of carotid artery atherosclerosis[9] and the risk of stroke. Researchers hypothesize that loud snoring creates turbulence in carotid artery blood flow closest to the airway. Generally speaking, increased turbulence irritates blood cells and has previously been implicated as a cause of atherosclerosis.

[edit] Diagnosis

Snoring...Usually, snoring is recognized by a friend or partner who observes the patient sleeping. Besides the "noise" of snoring, more complex conditions such as sleep apnea can be consistent with the symptom of snoring. A sleep study can identify such issues. Patients can also assess their own condition to determine the likelihood of such problems based on the severity of their sleeping difficulties.

[edit] Treatment
Almost all treatments for snoring revolve around clearing the blockage in the breathing passage. This is the reason snorers are advised to lose weight (to stop fat from pressing on the throat), stop smoking (smoking weakens and clogs the throat) and sleep on their side (to prevent the tongue from blocking the throat).[10] A number of other treatment options are also available, ranging from over-the-counter aids such as nasal strips or nose clips, lubricating sprays, and "anti-snore" clothing and pillows, to such unusual activities as playing the didgeridoo.[11] However, snoring is a recognized medical problem and people who snore should always seek professional medical advice before relying on techniques that may mask symptoms (i.e. snoring) but not treat the underlying condition.

[edit] Dental appliances
Specially made dental appliances called mandibular advancement splints, which advance the lower jaw slightly and thereby pull the tongue forward, are a common mode of treatment for snoring. Typically, a dentist specializing in sleep apnea dentistry is consulted. Such appliances have been proven to be effective in reducing snoring and sleep apnea in cases where the apnea is mild to moderate. Mandibular advancement splints are often tolerated much better than CPAP machines. Possible but rare side effects include gradual movement of the teeth, temporomandibular joint disorder, excess salivation and gum irritation.

Over-the-counter mandibular advancement splints provide the same benefits if fitted correctly.[citation needed] They are usually made from an EVA polymer and are similar in appearance to protective mouth-guards worn for sports. One disadvantage of the cheaper devices compared to the professionally fitted devices is the difficulty in setting up the correct jaw position. An over-advanced jaw results in jaw joint pain, whilst an under-advanced jaw produces no therapeutic effect. The professionally fitted devices generally incorporate an adjustment mechanism so that jaw advancement can be easily increased or decreased after fitting. To adjust the "do it yourself" appliances it is necessary to reheat them and mold them again in the desired new position. Alternatively, given the low cost, a new splint can be used.

In the United States, mandibular advancement splints are currently considered class 2 medical devices and cannot be legally sold without a prescription. Americans are, however, allowed to purchase these devices outside the United States and import them for personal use. In Australia, manufacturers can obtain approval from the TGA (Therapeutic Goods Administration) allowing the devices to be sold via normal retail channels without the involvement of a doctor.

[edit] Positive airway pressure
Main article: Positive airway pressure
A continuous positive airway pressure (CPAP) machine is often used to control sleep apnea and the snoring associated with it. To keep the airway open, a shoebox-sized device pumps a controlled stream of air through a flexible hose to a mask worn over the nose, mouth, or both.[12]

[edit] Surgery
Surgery is also available as a method of correcting social snoring. Some procedures, such as uvulopalatopharyngoplasty, attempt to widen the airway by removing tissues in the back of the throat, including the uvula and pharynx. These surgeries are quite invasive, however, and there are risks of adverse side effects. The most dangerous risk is that enough scar tissue could form within the throat as a result of the incisions to make the airway more narrow than it was prior to surgery, diminishing the airspace in the velopharynx. Scarring is an individual trait, so it is difficult for a surgeon to predict how much a person might be predisposed to scarring. Some patients have reported the development of severe sleep apnea as a result of damage to their airway caused by pharnygeal surgery.[citation needed] Currently, the American Medical Association does not approve of the use of lasers to perform operations on the pharynx or uvula.

Radiofrequency ablation (RFA) is a relatively new surgical treatment for snoring. This treatment applies radiofrequency energy and heat (between 77°C to 85°C) to the soft tissue at the back of the throat, such as the soft palate and uvula, causing scarring of the tissue beneath the skin. After healing, this results in stiffening of the treated area. The procedure takes less than one hour, is usually performed on an outpatient basis, and usually requires several treatment sessions. Radiofrequency ablation is frequently effective in reducing the severity of snoring, but, often does not completely eliminate snoring.[13][14]

Bipolar radiofrequency ablation, a technique used for coblation tonsillectomy, is also used for the treatment of snoring.

The Pillar Procedure is a relatively new treatment for obstructive sleep apnea and snoring. In the procedure, three small fibrous strips are inserted into the soft palate. After this brief and painless outpatient operation, which usually lasts no more than an hour, the soft palate is more rigid and snoring and apnea are reduced.

[edit] Pharmacological treatment
A combination of pseudoephedrine and domperidone shows excellent results (about 95%) in the treatment of severe snoring. The preparation is sold over the counter in some countries.[15]

[edit] Natural remedies
There are various natural methods alleged to alleviate snoring. These can be in the form of herbal pills, acupressure devices or specialized acupuncture.

Change of bed position – There are occasions wherein snoring is the result of wrong sleeping position. Sometimes, sleeping with too many pillows can stretch and narrow the air passage. Use one pillow to avoid it. Also, lying on the back can cause snoring. So, a change in sleeping position can be a good help.

All natural anti snoring spray are also available. These can come in over-the-counter products available at pharmacies.

[edit] Antidepressants
Most antidepressant drugs have a side effect of inhibiting deep sleep. [citation needed]

[edit] Coping as partner
Earplugs may facilitate good sleep for people sharing the same bedroom with someone who snores. External earmuffs are not designed to sleep with. Other alternatives include white noise generators.

Martin Keamy

First Sergeant Martin Christopher Keamy is a recurring fictional character played by Kevin Durand in the fourth season and sixth season of the American ABC television series Lost. Keamy is introduced in the fifth episode of the fourth season as a crew member aboard the freighter called the Kahana that is offshore the island where most of Lost takes place.[1] In the second half of the season, Keamy served as a primary antagonist. He is the leader of a mercenary team hired by billionaire Charles Widmore (played by Alan Dale) that is sent to the island on a mission to capture Widmore's enemy Ben Linus (Michael Emerson) from his home, then torch the island.[2]

Unlike Lost's ensemble of characters who, according to the writers, each have good and bad intentions,[3] the writers have said that Keamy is evil and knows it.[4] Durand was contacted for the role after one of Lost's show runners saw him in the 2007 film 3:10 to Yuma. Like other Lost actors, Durand was not informed of his character's arc when he won the role.[5] Throughout Durand's nine-episode stint as a guest star in the fourth season, little was revealed regarding Keamy's life prior to his arrival on the island and Durand cited this as a reason why the audience "loved to hate" his villainous character.[6] Critics praised the writers for breaking Lost tradition and creating a seemingly heartless character, while Durand's performance and appearance were also reviewed positively. Keamy returned in the final season for a tenth appearance.

Contents [hide]
1 Arc
1.1 Alternate Timeline
2 Personality
3 Development
4 Reception
5 References

[edit] Arc
Originally from Las Vegas, Nevada,[7] Martin Keamy was a First Sergeant of the United States Marine Corps, serving with distinction from 1996 to 2001. In the three years before the events of Lost in 2004, he worked with various mercenary organizations in Uganda.[8] In fall 2004, Keamy is hired by Widmore to lead a mercenary team to the island via freighter then helicopter and extract Ben for a large sum of money.[9] Once he captures Ben, Keamy has orders to kill everyone on the island (including the forty-plus survivors of the September 22, 2004 crash of Oceanic Airlines Flight 815: the protagonists of the series) by torching it.[2]

Keamy boards the freighter Kahana in Suva, Fiji sometime between December 6 and December 10.[10] On the night of December 25, helicopter pilot Frank Lapidus (Jeff Fahey) flies Keamy and his mercenary team,[11] which consists of Omar (Anthony Azizi),[7] Lacour, Kocol, Redfern and Mayhew, to the island.[9] On December 27, the team ambushes several islanders in the jungle, taking Ben's daughter Alex Linus (Tania Raymonde) hostage and killing her boyfriend Karl (Blake Bashoff) and her mother Danielle Rousseau (Mira Furlan).[10] The team infiltrates the Barracks compound where Ben resides, blowing up the house of 815 survivor Claire Littleton (Emilie de Ravin) and fatally shooting three 815 survivors (played by extras). Keamy attempts to negotiate for Ben's surrender in exchange for the safe release of Alex. Believing that he is bluffing, Ben does not comply, and Keamy shoots Alex dead.[8] Ben retaliates by summoning the island's smoke monster, which brutally assaults the mercenaries and fatally wounds Mayhew.[12]

Upon returning to the freighter, Keamy unsuccessfully attempts to kill Michael Dawson (Harold Perrineau), whom he has discovered is Ben's spy, then obtains the "secondary protocol" from a safe. The protocol contains instructions from Widmore for finding Ben if he finds out Keamy's intention to torch the island, which he apparently had. The protocol contains details about a 1980s research station called the "Orchid" that was previously run by a group of scientists working for the Dharma Initiative. Keamy is also informed by Captain Gault that Keamy and his mercenary squad may be suffering from some sort of mental sickness, to which Keamy dismisses the notion. Later in the day, Omar straps a dead man's switch to Keamy, rigged to detonate C4 on the freighter if Keamy's heart stops beating. That night, Frank refuses to fly the mercenaries to the island. In a display of power, Keamy slits the throat of the ship's doctor Ray (Marc Vann) and throws him overboard and later outdraws and shoots Captain Gault (Grant Bowler) during a tense standoff. Frank flies the remaining five mercenaries back to the island.[2] On December 30,[13] the team apprehends Ben at the Orchid and takes him to the chopper where they are ambushed and killed by Ben's people[14]—referred to as the "Others" by the 815 survivors[15]—and 815 survivors Kate Austen (Evangeline Lilly) and Sayid Jarrah (Naveen Andrews).[16] After a chase to recapture Ben and a brawl with Sayid, Keamy is shot in the back by Richard Alpert (Nestor Carbonell), who leaves him for dead, unaware of Keamy's bulletproof vest. Later, Keamy descends into the Orchid's underground level via its elevator to stalk Ben, who hides in the shadows. Goading Ben with taunts about his daughter's death, Keamy is ambushed by Ben, who beats him into submission with an expandable baton before stabbing him repeatedly in the neck. Though Locke attempts to save his life for the sake of the freighter, Keamy dies and the dead man's trigger detonates the explosives on the freighter, killing nearly everyone aboard.[14]

[edit] Alternate Timeline
Keamy is a business associate of Mr. Paik, Sun’s (Yunjin Kim) father. Mr. Paik sent Jin (Daniel Dae Kim) to LA to give Keamy a watch and $25,000 which was intended to be Keamy’s reward for killing Jin. However, the money was confiscated at customs in LAX, and Keamy was disappointed to discover it missing. He took Jin to a restaurant and had him tied up in freezer. Shortly after, Omar, one of Keamy’s henchmen, captured Sayid and brought him to the same restaurant Jin was being held at. Keamy explained to Sayid that his brother loaned money from him and failed to pay it back and thus shot him to send a message to keep paying him. After threatening Sayid’s family, Sayid retaliated and shot Keamy in the chest, presumably killing him.

[edit] Personality
"He's a bad guy, that's who the Keamy guy is. I should embrace the presence of a character like Keamy 'cause he makes Ben [a primary antagonist of the series] look like a pussycat. You know, Ben is just like our kooky uncle now, compared to Keamy."

Actor Michael Emerson, who plays Ben[17]During the casting process, Keamy was described as a military type in his late-twenties who does not question orders.[18] Chris Carabott of IGN wrote that "in a show that features characters fraught with uncertainty, Keamy is the polar opposite and his Marine mentality definitely sets him apart. His team has a physical advantage and with the help of Mr. Widmore, they have a tactical advantage as well. Keamy is like a bulldog being thrown into a cage full of kittens (except for [Iraqi military torturer] Sayid)".[19] Jay Glatfelter of The Huffington Post, stated that "Keamy is Crazy! … out of all the bad guys on the Island—past, present, and future—Keamy has to be one of the most dangerous ones. Not because of how big he is, or the weaponry, but his willingness to kill at the drop of a hat. That doesn't bode well for our Losties [protagonists]."[20] Co-show runner/executive producer/writer Carlton Cuse has stated that he and the other writers create "complex" characters because they "are interested in exploring how good and evil can be embodied in the same characters and [the writers are also intrigued] the struggles we all have[,] to overcome the dark parts of our souls";[3] however, he later clarified that there is an exception: "Keamy's bad, he knows he's bad, but he's … a guy that does the job."[4] Damon Lindelof stated that "the great thing about Keamy is that he is like a … merciless survivor. [There]'s this great moment [in the season finale] where he just sort of hackie-sacks [a grenade thrown at him] over to where [his ally] Omar is standing. Omar is certainly an acceptable casualty as far as Keamy is concerned."[21] According to a featurette in the Lost: The Complete Fourth Season – The Expanded Experience DVD set, Keamy likes "heavy weaponry" and "physical fitness" and dislikes "negotiations" and "doctors".[17]

[edit] Development
"Get your ass out here right now or I'm gonna kill your daughter."

Keamy to Ben in "The Shape of Things to Come"A remake of the 1957 film 3:10 to Yuma opened in theaters on September 7, 2007.[22] Lost's co-show runner/executive producer/head writer/co-creator Damon Lindelof enjoyed Kevin Durand's supporting performance as Tucker and checked to see if he was available for a role on Lost. The casting director had Durand read a page of dialogue for the new character Keamy;[5] Durand was offered the role in early October and he traveled to Honolulu in Hawaii—where Lost is filmed on location[23]—by October 17, 2007.[24] A former stand-up comic and rapper from Thunder Bay, Ontario, Canada, with the stage name "Kevy D", Durand had seen only around six episodes of Lost by the time that he won the part. When he was shooting, he was confused by the story, later stating "I didn't want to know anything or be attached to anybody. I'm glad I didn't. But now that I'm on it, I'll watch all of it."[6] Durand revealed his appreciation for the cast, crew and scripts and the fact that he had the chance to act as someone with a similar physical appearance to himself, as he had previously done roles that had not prompted recognition from viewers on the street.[25]

Durand was never informed of his character's arc and only learned more of Keamy's importance to the plot as he received new scripts; thus, he was thrilled when the role was expanded for his third appearance, in "The Shape of Things to Come", when he kills Alex and Durand compared his excitement to that of "a kid in a candy store."[5] He also stated that "you really don't know what's going to happen in the next episode and you get the scripts pretty late, so it is pretty secretive and it's kind of exciting that way [because] you're really forced to get in the moment and say the words and play the guy".[25] Durand was initially met with negative reaction from fans on the street for this action and he defended his murderous character by arguing that it was actually more Ben's fault for failing to negotiate with Keamy; later, fans warmed up to Keamy. Despite the antagonist's increasing popularity and fanbase,[6] it became apparent to Durand that fans were hoping for Keamy's death in what promised to be a showdown in the season finale.[26] Throughout his nine-episode run, Keamy never receives an episode in which his backstory is developed through flashbacks and Durand holds this partially responsible for the negative reaction to his character, saying that the audience "[has not] really seen anything outside of Keamy's mission, so I think they definitely want him put down." Following the season's conclusion, Durand stated that he would not be surprised if his character returned in the fifth season and concluding that "Lost was really fun. If I can have that experience in any genre, I'd take it."[6]

Durand returned for the sixth season episodes "Sundown" and "The Package", following a twenty-two episode absence since his character's death in the fourth season finale. Keamy appears in the "flash sideways" parallel timeline in September 2004 working for Sun Kwon's father Mr. Paik to assassinate her new husband Jin Kwon (Daniel Dae Kim) upon the couple's arrival in Los Angeles. Keamy and his sidekick Omar are also extorting money from Sayid's brother Omer, prompting Sayid to shoot them both, aiding Jin's rescue process.[27]

[edit] Reception
Professional television critics deemed Martin Keamy a welcome addition to the cast. Jeff Jensen of Entertainment Weekly commented that Kevin Durand "is emerging as a real find this season; he plays that mercenary part with a scene-stealing mix of menace and damaged vulnerability."[28] After Jensen posted what he thought were the fifteen best moments of the season, the New York Post's Jarett Wieselman "ha[d] to complain about one glaring omission from EW's list: Martin Keamy. I have loved this character all season long—and not just solely for [his] physical attributes … although those certainly don't hurt."[29] Alan Sepinwall of The Star-Ledger reflected, "He was only on the show for a season and not featured all that much in that season, but Kevin Durand always made an impression as Keamy. Lots of actors might have his sheer physical size, but there's a sense of danger (insanity?) that you can't build at the gym, you know?"[30] IGN's Chris Carabott wrote that "Keamy is one of the more striking new additions to Lost [in the fourth] season … and is a welcome addition to the Lost universe."[19] Maureen Ryan of The Chicago Tribune stated that Keamy has "so much charisma" and she would "rather find out more about [him] than most of the old-school Lost characters".[31] TV Guide's Bruce Fretts agreed with a reader's reaction to Durand's "chilling portrayal" of Keamy and posted it in his weekly column. The reader, nicknamed "huntress", wrote "love him or hate him, nobody is neutral when it comes to Keamy, which is the hallmark of a well-played villain. Even the camera seems to linger on Durand, who conveys malice with just a look or tilt of his head. This role should give Durand's career a well-deserved boost".[32] Following his demise, Whitney Matheson of USA Today noted that "it seems Keamy, Lost's camouflaged baddie, is turning into a bit of a cult figure." A "hilarious" blog containing Keamy digitally edited into various photographs, posters and art titled "Keamy's Paradise" was set up in early June 2008.[33] TV Squad's Bob Sassone thought that the blog was "a great idea" and "funny" and he called Keamy "the Boba Fett of Lost".[34] In 2009, Kevin Durand was nominated for a Saturn Award for Best Guest Starring Role in a Television Series.[35]

Reaction to the antagonist's death was mixed. Kristin Dos Santos of E! criticized the writing for Keamy when he futilely asks Sayid where his fellow 815 survivors are so that he can kill them, but enjoyed his attractive physique, writing that "that guy is deep-fried evil, and he must die horribly for what he did to Alex, but in the meantime, well, he's certainly a well-muscled young man".[36] The Huffington Post's Jay Glatfelter also called for Keamy's death, stating that "nothing would be better to me than him getting run over by Hurley's Dharma Bus", alluding to a scene in the third season finale.[20] Dan Compora of SyFy Portal commented that "Keamy took a bit too long to die. Yes, he was wearing a bullet proof vest so it wasn't totally unexpected, but it was a bit predictable."[37] In a review of the season finale, Erin Martell of AOL's TV Squad declared her disappointment in the conclusion of Keamy's arc, stating that "it's always a shame when the hot guys die, [especially when] Kevin Durand did an amazing job with the character … he'll be missed."[38] In a later article titled "Lost Season Four Highlights", Martell noted Durand's "strong performance" that was "particularly fun to watch" and wrote that "we [the audience] all know that Widmore's the big bad, but Keamy became the face of evil on the island in his stead."[39]

Tick

Tick is the common name for the small arachnids in superfamily Ixodoidea that, along with other mites, constitute the Acarina. Ticks are ectoparasites (external parasites), living by hematophagy on the blood of mammals, birds, and occasionally reptiles and amphibians. Ticks are vectors of a number of diseases, including Lyme disease, Q fever (rare; more commonly transmitted by infected excreta)[1], Colorado tick fever, tularemia, tick-borne relapsing fever, babesiosis, ehrlichiosis and Tick-borne meningoencephalitis, as well as anaplasmosis in cattle and canine jaundice.[2].

Contents [hide]
1 Habitats and behaviors
2 Population control
2.1 Case study of the American Deer Tick
2.2 Other control measures
3 Example species
3.1 Ixodidae family (hardbodied)
3.1.1 Dermacentor
3.1.2 Ixodes
3.1.3 Boophilus/Rhipicephalus
3.1.4 Amblyomma
3.2 Argasidae family (softbodied)
4 Fossil record
5 See also
6 References
7 External links

[edit] Habitats and behaviors
Ticks are blood-feeding parasites that are often found in tall grass where they will wait to attach to a passing host. A tick will attach itself to its host by inserting its chelicerae (cutting mandibles) and hypostome (feeding tube) into the skin. The hypostome is covered with recurved teeth and serves as a hammer.[3]

Physical contact is not the only method of transportation for ticks. Ticks can't jump or fly. Some species stalk the host from ground level, emerging from cracks or crevices located in the woods or even inside a home or kennel, where infestations of "seed ticks" (the six-legged stage of newborn ticks) can attack in numbers up to 30,000 at a time[citation needed]. Weak or elderly dogs, puppies, and cats are particularly endangered and can die from anemia from a sudden influx of seed ticks[citation needed]. Seed ticks also attack horses, cattle, moose, lions and other mammals, causing anemia, various diseases, paralysis and even death. Such infestations can be difficult to detect until thousands have attached themselves to an animal and eradication can be difficult.[4][5]


Mature ticks are harder to see. Frequent grooming and chemicals for control may control the spread of seed ticks and adults.[6]

Changes in temperature and day length are some of the factors signalling a tick to seek a host. Ticks can detect heat emitted or carbon dioxide respired from a nearby host. They will generally drop off the animal when full, but this may take several days. In some cases ticks will live for some time on the blood of an animal. Ticks are more active outdoors in warm weather, but can attack a host at any time.[7]

Ticks can be found in most wooded or forested regions throughout the world. They are especially common in areas where there are deer trails or human tracks. Ticks are especially abundant near water, where warm-blooded animals come to drink, and in meadows wherever shrubs and brush provide woody surfaces and cover.

[edit] Population control
See also: Animal population control
Ticks are a vector for a number of diseases including Lyme disease, Rocky Mountain spotted fever and other Tick-borne disease.

[edit] Case study of the American Deer Tick
The blacklegged or deer tick (Ixodes scapularis) is dependent on the white-tailed deer for reproduction. Larval and nymph stages (immature ticks that cannot reproduce) of the deer tick feed on birds and small mammals. The adult female tick needs a large 3 day blood meal from the deer before she can reproduce and lay her 2000 or more eggs. Deer are the primary host for the adult deer tick and are key to the reproductive success of the tick.[8] See the Connecticut Agricultural Experiment Station and Connecticut Department of Public Health joint publication "Tick Management Handbook" for more details of the tick's life cycle and dependence on deer.[9]

Numerous studies have shown that abundance and distribution of deer ticks are correlated with deer densities.[8][10][11][12]

When the deer population was reduced by 74% at a 248-acre (100 ha) study site in Bridgeport, Connecticut, for example, the number of nymphal ticks collected at the site decreased by 92%.[8] The relationship between deer abundance, tick abundance, and human cases of Lyme disease was well documented in the Mumford Cove Community in Groton, Connecticut, from 1996 to 2004. The deer population in Mumford Cove was reduced from about 77 deer per square mile to about 10 deer per square mile (4 deer per square kilometer) after 2 years of controlled hunting. After the initial reduction the deer population was maintained at low levels. Reducing deer densities to 10 deer per square mile (4 deer per square kilometer) was adequate to reduce by more than 90% the risk of humans contracting Lyme disease in Mumford Cove.[13]

A 2006 study by Penn State's Center for Infectious Disease Dynamics indicated that reducing the deer population in small areas may lead to higher tick densities, resulting in more tick-borne infections in rodents leading to a high prevalence of tick-borne encephalitis and creating a tick hot-spot.[14]

[edit] Other control measures

Male tick size comparison to a match.The parasitic Ichneumon wasp Ixodiphagus hookeri has long been investigated for its potential to control tick populations. It lays its eggs into ticks; the hatching wasps kill their host.

Another natural form of control for ticks is the guineafowl, a bird species which consumes mass quantities of ticks.[15] Just 2 birds can clear 2 acres (8,100 m2) in a single year.

Topical (drops/dust) flea/tick medicines may be toxic to animals and humans. Phenothrin (85.7%) in combination with Methoprene was a popular topical flea/tick therapy for felines. Phenothrin kills adult fleas and ticks. Methoprene is an insect growth regulator that interrupts the insect's life cycle by killing the eggs. However, the U.S. Environmental Protection Agency required at least one manufacturer of these products to withdraw some products and include strong cautionary statements on others, warning of adverse reactions.[16]

A liquid spray, duster or aerosol spray, with either a hand sprayer or a hand spreader, may be used to control tick populations.

[edit] Example species
Two families of ticks are the Ixodidae and the Argasidae.


Engorged tick attached to back of toddler's head. Adult thumb shown for scale.
Head of Ixodes ricinus (sheep tick)
Ixodes hexagonus[edit] Ixodidae family (hardbodied)
[edit] Dermacentor
Dermacentor variabilis, the American dog tick, is perhaps the most well-known of the North American hard ticks. This tick does not carry Lyme disease but can carry Rocky Mountain spotted fever.
[edit] Ixodes
Ixodes scapularis (formerly Ixodes dammini), known as the black-legged tick or deer tick, is common to the eastern part of North America and is known for spreading Lyme disease.
Ixodes pacificus, the Western black-legged tick, lives in the western part of North America and is responsible for spreading Lyme disease and Rocky Mountain spotted fever. It tends to prefer livestock such as cows as its adult host.
Australia tick fauna consists of approximately 75 species, most of which fall into the Ixodidae, hard tick, family. The most medically important tick is the Paralysis tick, Ixodes holocyclus. It is found in a 20-kilometre band that follows the eastern coastline of Australia. Encounters with these parasites are relatively common as this is where much of the human population resides in New South Wales and South-East Queensland. Although most cases of tick bite are uneventful, some can result in life threatening illnesses including paralysis, tick typhus, and severe allergic reactions both in humans and pets.
[edit] Boophilus/Rhipicephalus
The southern cattle tick, Boophilus microplus (Canestrini), causes annual economic losses in the hundreds of millions of dollars to cattle producers throughout the world, and ranks as the most economically important tick globally. This tick also attacks sheep, horses, goats, and a few related species, but cattle are the most important hosts.[17]
[edit] Amblyomma
The Lone Star tick, Amblyomma americanum, is part of the Ixodidae family. The adult females are distinguished by a white dot or "lone star" on its back. The adult males can also be seen with dots and white streaks on the edge of their bodies. This tick has been associated with transmission of Southern Tick Associated Rash Illness (STARI) in humans, which is a disease caused by a Borrelia sp. related to the agent that causes Lyme Disease.
[edit] Argasidae family (softbodied)
Members of this family include Argas and Ornithodoros