Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cancers of the stomach, pancreas, colon and rectum are increasingly regarded as being diet-influenced. Migrants to Australia from England, Scotland, Ireland, Poland, Yugoslavia, Greece, and Italy have come from countries with varied dietary backgrounds and gastrointestinal cancer risks. Age-standardized cancer death rates in migrrants, by country of origin, sex, age, and duration of residence in Australia (less than or equal to 16 years and greater than 16 years), have been calculated for 1962-76, and compared with those of the Australian-born population. All seven migrant source countries, in 1970, had higher rates of stomach cancer than Australia, and the corresponding migrants groups, which initially reflected those higher rates, experienced an approximately 25% risk reduction with increased duration of residence. For cancer of the pancreas, migrants initially had rates well above their "native" rates; with longer stay, the risks generally converged upon that of the Australian-born population. The four "continental" (European) migrant groups, whose native risk of colon cancer is about half that of the Australian population, showed an increased risk with increasing duration of stay. The increase was greater in men than in women, perhaps reflecting their greater dietary acculturation. By contrast, Scottish migrants, with an initially high risk of cigrants showed even larger increases than colon cancer, while in British migrants there was a marked decline towards the "Australian-borne" risk. These various changes in cancer risk are discussed with reference to inter-country dietary differences.
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PMID:Patterns of gastro-intestinal cancer in European migrants to Australia: the role of dietary change. 737 70

This paper investigates the risk of cancer in Polish migrants to Australia, and compares the results with earlier studies, as well as with results of studies of Polish migrants in other countries. Poisson regression models were used to estimate the risk of death in Polish migrants, relative to the Australia-born, as well as the relative risk of cancer in Poland compared to the Australia-born. In migrant males, a significantly lower risk was found for oral cavity and pharynx, larynx, melanoma, prostate and Hodgkin's disease, while a significantly elevated risk was found for stomach, liver, pancreas, kidney and thyroid gland. In migrant females, a risk significantly lower than in Australian-born individuals was found for oral cavity, colon, melanoma, breast and non-Hodgkin's lymphoma. Relative risk significantly higher than in Australia-born was detected for stomach, gall bladder, pancreas, cervix uteri, nervous system and thyroid gland. For some of these cancers, the risk in migrants approximates to that of the Australia-born with increasing duration of stay. Thus, there are progressive increases in risk for colon cancer in males, and breast cancer and melanoma in females, and decreases in risk for stomach and bladder cancers in males, and uterine cancers in females.
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PMID:Cancer mortality among Polish migrants to Australia. 801 6

A mortality cohort study was carried out on 2,291 workers, including 169 women, with chronic occupational CS2 poisoning diagnosed during the years 1970-90. Information on vital status was available for 98.2% as of December 31, 1992. Mortality assessment was based on the standardized mortality ratio using the person-years method. The general population of Poland was the reference population. The number of subjects who died during the period of observation accounted for 658 men and 21 women. The analysis of mortality in male subjects showed statistically significant excess of deaths from the circulatory system diseases (SMR = 139), in this from ischaemic heart disease (SMR = 137), cerebrovascular disease (SMR = 188) and colon cancer (SMR = 233). Over a two-fold increased risk of death from diseases of the nervous system and sense organs, although statistically insignificant, was also observed. Among women a statistically significant risk of death from atherosclerosis was noted (SMR = 286). An elevated risk of death from the circulatory system diseases and from ischaemic disease (IHD) agrees with the results of some other cohort studies carried out in the viscose rayon workers. The increased mortality from malignant neoplasms is an unusual finding in cohorts of workers exposed to CS2. Our own data reported here showed a significantly increased mortality from colon cancer (9 cases). All these cases were noted in workers of the two oldest rayon plants and they require a detailed analysis. Further survey is also needed to elucidate the excess of deaths from the nervous system and sense organs diseases.
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PMID:A mortality study of workers with reported chronic occupational carbon disulfide poisoning. 911 88

The paper presents data on cancer risk, especially pleural mesothelioma and lung cancer, among the workers of asbestos cement plant who living in the vicinity of the plant, were also environmentally exposed to asbestos. In 1959 an asbestos cement factory was founded in the rural area of south-eastern Poland. Apart from chrysotile asbestos, crocidolite was used till 1985 chiefly for the manufacture of pressure pipes. The blue asbestos made up 15% of the mean annual tonnage of the processed asbestos. It was found that soon after asbestos production had started the process wastes were made available to local community, particularly to the workers of that factory. For over twenty years asbestos wastes of all kinds, both wet (process sludge) and dry (from pipe and sheet grinding) were exploited for the hardening of roads, paths, farmyards and sports fields and as construction material components. For the evaluation of cancer risk due to occupational exposure to asbestos a cohort of 1,526 workers employed in this factory was observed till the end of 1996. The cohort availability was 95.6%. Standardized mortality ratio (SMR) was calculated using the man-years method. The reference population was the general population of Poland. The results of the study demonstrated a statistically significant increase in the risk of a) pleural mesothelioma--over an 80-fold excess among males and over a 200-fold one among females; b) lung cancer in females--over a 6-fold excess; c) colon cancer in males--over a 3-fold excess. In the 1990 ten new cases of pleural mesothelioma in the cohort were reported. As compared to other asbestos-cement cohorts in Poland, observed at the same time, this cohort presented a very high risk of pleural mesothelioma. The analysis of 16 cases of pleural mesothelioma found in the cohort from 1987 to 1997 revealed 4 cases with very short employment period (3.5 months-5 years) including two cases with relatively short latency period (11-12 years). In order to find explanation of these findings, additional investigations were made. The epidemiological study indicated that all these persons were at the same time subject to non-occupational exposure associated with massive utilization of commonly available asbestos-cement wastes as road surface material.
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PMID:Environmental exposure to asbestos in asbestos cement workers: a case of additional exposure from indiscriminate use of industrial wastes. 975 96

Incidence rates of colorectal cancer vary around 20-fold between industrialized and developing countries. Colon cancer is one of the most common cancers and very important public health problem in the Western world. Each year about 7000 patients in Poland die from colorectal cancer. Most cases of this cancer are possibly related to lifestyle or environmental factors. It is estimated that about 13% of colorectal cancer is attributable to low physical activity, 12% to diet and about 10-15% to genetic susceptibility. The aim of this work was to analyze the relationship between diet, physical activity and colorectal cancer risk. Current data suggest that lifestyle modification including proper diet, regular physical activity and maintaining an appropriate body weight may lead to 50-75% decrease of colorectal cancer cases. Therefore, effective management should include effective educational programs including dietary and other lifestyle behavior guidelines as well as early diagnostic of colorectal cancer.
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PMID:[Selected risk factors and primary prevention of colorectal cancer]. 1457 20

A single founder allele of the CHEK2 gene has been associated with predisposition to breast and prostate cancer in North America and Europe. The CHEK2 protein participates in the DNA damage response in many cell types and is therefore a good candidate for a multisite cancer susceptibility gene. Three founder alleles are present in Poland. Two of these result in a truncated CHEK2 protein, and the other is a missense substitution of an isoleucine for a threonine. We ascertained the prevalence of each of these alleles in 4,008 cancer cases and 4,000 controls, all from Poland. The majority of the common cancer sites were represented. Positive associations with protein-truncating alleles were seen for cancers of the thyroid (odds ratio [OR] 4.9; P=.0006), breast (OR 2.2; P=.02), and prostate (OR 2.2; P=.04). The missense variant I157T was associated with an increased risk of breast cancer (OR 1.4; P=.02), colon cancer (OR 2.0; P=.001), kidney cancer (OR 2.1; P=.0006), prostate cancer (OR 1.7; P=.002), and thyroid cancer (OR 1.9; P=.04). The range of cancers associated with mutations of the CHEK2 gene may be much greater than previously thought.
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PMID:CHEK2 is a multiorgan cancer susceptibility gene. 1549 28

The NOD2 gene has been associated with susceptibility to Crohn's disease, and more recently with carcinoma of the colon as well. NOD2 is involved in the inflammatory response and the activation of the NFkB pathway. The range of cancer types associated with NOD2 has not been well studied. The 3020insC allele results in a truncated NOD2 protein and is present in approximately 7% of the population. We studied a possible association between the 3020insC allele of the NOD2 gene and breast cancer using 462 cases and 1910 controls from Poland. Patients were diagnosed with invasive breast cancer at are of two Szczecin regional hospitals between 2002 and 2004. Pathology specimens were reviewed for histological subtype and for the presence of ductal carcinoma in situ (DCIS). Overall there was no association between breast cancer and NOD2 (OR = 1.1; p = 0.76), but significant associations were observed between the presence of the allele and early-onset breast cancer (OR = 1.9; p = 0.01) and between the allele and ductal breast cancer with an in situ component (OR = 2.2; p = 0.006).
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PMID:The 3020insC allele of NOD2 predisposes to early-onset breast cancer. 1566 2

Mutations in the CHEK2 gene have been associated with increased risks of breast, prostate and colon cancer. In contrast, a previous report suggests that individuals with the I157T missense variant of the CHEK2 gene might be at decreased risk of lung cancer and upper aero-digestive cancers. To confirm this hypothesis, we genotyped 895 cases of lung cancer, 430 cases of laryngeal cancer and 6391 controls from Poland for four founder alleles in the CHEK2 gene, each of which has been associated with an increased risk of cancer at several sites. The presence of a CHEK2 mutation was protective against both lung cancer [odds ratio (OR) = 0.3; 95% confidence interval (CI) 0.2-0.5; P = 3 x 10(-8)] and laryngeal cancer (OR = 0.6; 95% CI 0.3-0.99; P = 0.05). The basis of the protective effect is unknown, but may relate to the reduced viability of lung cancer cells with a CHEK2 mutation. Lung cancers frequently possess other defects in genes in the DNA damage response pathway (e.g. p53 mutations) and have a high level of genotoxic DNA damage induced by tobacco smoke. We speculate that lung cancer cells with impaired CHEK2 function undergo increased rates of cell death.
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PMID:Constitutional CHEK2 mutations are associated with a decreased risk of lung and laryngeal cancers. 1828 Dec 49

It is important to have accurate knowledge of the range of cancers associated with various CHEK2 mutations, and of the lifetime risks of cancer associated with each. We wished to establish the relationship between family history, mutation type and cancer risk in families with a CHEK2 mutation. We obtained a blood sample and pedigree information from 2012 unselected women with breast cancer, from 2007 men with prostate cancer and from 1934 patients with colon cancer, from hospitals throughout Poland. Genetic testing was carried out for four founder CHEK2 mutations on all 5953 specimens and 533 carriers were identified. We estimated the risk to age 75 for any cancer in the 2544 first-degree relatives to be 22.3%. After adjusting for mutation type, the risk of breast cancer was much higher among relatives of probands with breast cancer than among relatives of patients with prostate or colon cancer (HR=3.6; 95% CI=2.1-6.2; P=0.0001). Similarly, the risk of prostate cancer was higher among relatives of probands with prostate cancer than among relatives of patients with breast or colon cancer (HR=4.4; 95% CI=2.2-8.7; P=0.0001) and the risk of colon cancer was higher among relatives of probands with colon cancer than among relatives of patients with prostate or breast cancer (HR=4.2; 95% CI=2.4-7.8; P=0.0001). These analyses suggest that the risk of cancer in a carrier of a CHEK2 mutation is dependent on the family history of cancer.
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PMID:Cancer risks in first-degree relatives of CHEK2 mutation carriers: effects of mutation type and cancer site in proband. 1940 4

The CHEK2*I157T missense mutation, reported in ethnically diverse, high-risk families, moderately increases breast and colon cancer risk. The present study assessed whether this mutation represents a founder mutation. Participants identified in high risk clinics or from consecutive cancer patients in Israel, Poland, Latvia, and Finland, were either carriers of the CHEK2*I157T mutation or non-carrier family members. Multi-locus genotyping employed two intragenic markers and five CHEK2 gene flanking markers, spanning about 645 kb. Haplotyping was done when families were available for phasing. Overall, 101 individuals (83 I157T*CHEK2 mutation carriers) were genotyped: 16 Finnish individuals from 11 families (14 mutation carriers, two non-carrier family members), 50 Polish individuals (20 families) (35 carriers, 15 non-carriers), 28 unrelated Latvian mutation carriers, and seven Israeli participants (two families) (six mutation carriers, one non-carrier). Overall 36/83 mutation carriers (43%) were diagnosed with breast cancer, 15/83 (18%)-colon cancer, three-ovarian cancer, one-thyroid cancer, and the rest (n = 28) were asymptomatic. A common core haplotype was detected in all I157T*CHEK2 mutation carriers of Israeli, Polish, and Finnish origin between markers D22S275-D22S689 (approximately 258 kb), with a different allele pattern in Latvians. In conclusion, CHEK2*I157T missense mutation is a founder mutation in ethnically diverse populations, but may also be a mutational hotspot.
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PMID:Haplotypes of the I157T CHEK2 germline mutation in ethnically diverse populations. 1960 24


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