Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0345904 (liver cancer)
15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Major variations in cancer by site and sex are being discovered in the People's Republic of China. Nasopharyngeal carcinoma, the most common form in Kwangtung Province, accounted for 43.0% of biopsied cancers in males. Liver cancer is predominant along the coast near Shanghai and appears to be a major cause of mortality in many other parts of the country. The mortality rate of esophageal cancer, the primary cause of all mortality along the eastern slopes of the Taihang Mountains in North China, varies by 100-fold in areas short distances apart; this geographical variation is paralleled by a carcinoma of the gullet in domestic chickens. Several foods, particularly a type of pickled vegetable, contain high concentrations of nitrosamines and nitrites, which are thought to be etiologically important.
Natl Cancer Inst Monogr 1979 Nov
PMID:Observations on cancer etiology in China. 53 32

Among the Melanesian population of Papua New Guinea, cancer of the oral cavity associated with betel nut chewing is the most commonly reported. Liver cancer is also common and is closely associated with chronic hepatitis-B infection. Burkitt's lymphoma occurs along coastal areas with a high rainfall and intense malaria transmission. The descriptive epidemiology of other cancers in Papua New Guinea is also discussed.
Natl Cancer Inst Monogr 1979 Nov
PMID:Cancer in Papua New Guinea. 53 33

We compared age-adjusted mortality rates for cancer of selected sites for Chinese, Japanese, and native Indian residents of British Columbia during the years 1964-73 to the corresponding rates for the white population. Mortality from all cancers of the Chinese did not differ significantly from that of whites. Elevated rates are seen for cancer of the nasopharynx in both sexes, of the liver and esophagus in males, and of the lung in females. Chinese males had a lower mortality than whites from stomach, prostate, and bladder cancer and brain tumors, whereas females had a lower mortality from tumors of the colon, breast, and ovary; both sexes had a lower mortality from leukemia. For Japanese males and females, the mortality rates for all cancers combined were similar to those of the white population. The rates for cancer of the stomach and gallbladder were higher in both sexes; males also showed a higher rate of liver cancer. Prostate and breast cancer mortality rates were lower. Native Indian males had a lower mortality rate from all cancers combined; the difference was significant for stomach, colon, lung, and prostate cancers, and for leukemia. Native Indian females showed a lower rate for ovarian cancer and a higher rate of tumors of the gallbladder and uterine cervix, but their overall cancer mortality was similar to that of whites.
Natl Cancer Inst Monogr 1979 Nov
PMID:Cancer mortality among Chinese, Japanese, and Indians in British Columbia, 1964-73. 53 37

A retrospective mortality study has been carried out on workers employed in the manufacture of chlordane and heptachlor between 1946 and 1976. The study group was comprised of 1403 white males who worked for more than three months at either of the two plants in the United States now producing these compounds. Information on deaths among terminated employees was obtained from the Social Security Administration and supplemented by information collected by another investigator by individual follow-up. There were 113 deaths observed in the group, compared to 157 expected, giving a standardized mortality ratio (SMR) of 72. There was no overall excess of deaths from cancer, even among workers followed twenty or more years after entry into the occupation. There was one death from liver cancer. An excess of deaths from lung cancer (12 observed, 9.0 expected) was not statistically significant and was not distributed by duration of exposure or of latency in any pattern suggesting an etiologic role for chlordane-heptachlor exposure. Although diseases of the circulatory system as a whole showed fewer deaths than expected (SMR 83), there was a statistically significant excess of deaths from cerebrovascular disease (17 observed, 9.3 expected). This excess was not related to duration of exposure or latency and occurred exclusively after termination of employment.
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PMID:Mortality of workers employed in the manufacture of chlordane and heptachlor. 55 68

The results of the dietary aflatoxin-liver cancer study carried out in the Murang'a district of Kenya have been reassessed in relation to disease incidence rates based on a total of seven years of cancer registration and related to the Population Census carried out during the course of the initial study. These newly derived data have been combined with the results of a second similar dietary aflatoxin-liver cancer study which was later carried out in Swaziland. Separate treatment of the male and female data has been considered necessary due to the variation of the sex ratio of the disease incidence in the two areas. The combined results of the two studies show a high degree of positive correlation between the calculated ingestion levels of aflatoxin, expressed as ng/kg bodyweight/day (x) and the adult incidence rates of hepatocellular carcinoma expressed as cases/10(5) adults/year (y) within the two study populations and this is true for both males and females. Based upon an assumed 2 kg/day intake of wet diet and a mean bodyweight of 70 kg, the calculated relationship for adult females is: y = 4.14 log10 x--0.80 (0.05 greater than P4 greater than 0.02, tor = +/- 2.90). With the added assumption of a daily intake of native beer of two liters/day the regression equation for adult males is: y = 21.96 log10 x--11.17 (P5 less than 0.001, tor = +/- 3.42). The regression data are found to be essentially compatible with comparable data recorded by independent workers in Thailand and Mozambique; the latter being the region where the highest rates of liver cancer and of aflatoxin ingestion levels have so far been recorded. A highly significant regression line has also been calculated using crude disease incidence data and aflatoxin exposure levels from all available studies: y = 7.60 log10 x--3.60 (P8 less than 0.001, tor = +/- 3.10).
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PMID:Dietary aflatoxins and human primary liver cancer. 61 2

Some 1,390 male and 1,418 female cancer cases examined histologically in Cameroon--1969-1973--were analysed. The relatively most frequent cancers were: Males: skin 30%, malignant lymphomas 13%, primary liver cancer 11%. Females: skin 20%, uterine cervix 16%, breast 10%. Kaposi's sarcoma comprised 31% of all male skin cancer with a high male-female ratio (157/14). Tumours of the lung and intestinal tract were rare. Ethnic differences were noted with regard to cancer of the liver, skin, buccal cavity, lung and bladder. Possible sources of bias are discussed.
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PMID:Cancer in Cameroon: a relative frequency study. 74 58

Our knowledge of the cellular changes that lead to liver cell carcinoma in humans is limited by proper and necessary ethical restriction on clinical research. We know rather more about risk factors, the most important of which is cirrhosis, it seems that both the causative agent and the time of duration of the cirrhotic process are relevent to the magnitude of this risk. According to present knowledge, alpha1-antitrypsin deficiency, alcoholism, naturally occurring carcinogens, drugs, and the hepatitis B virus seem to carry the greatest risk of cancer developing in a cirrhotic patient. Cirrhosis, however, is not an essential prerequisite, and some or possibly all of these agents can also induce cancer without cirrhosis. Bile duct carcinoma commonly follows infestation with liver flukes. Cirrhosis is usually absent but duct epithelial hyperplasia is present prior to the development of cancer. Many cellular changes have been observed in patients and among populations considered to be at risk from liver cancer. Of these, liver cell dysplasia is the most striking and studies of its prevalence, natural history, and association with cirrhosis suggest that it is a precancerous change.
Cancer Res 1976 Jul
PMID:Precursor lesions for liver cancer in humans. 77 94

Alkylation of liver DNA was studied following administration to Sprague-Dawley rats of doses of dimethylnitrosamine (DMN) varying from 0.25 to 20 mg/kg body weight. Measurements were made of the amounts of O6-methylguanine and 7-methylguanine present in liver DNA at 4 and 24 hours after treatment with the carcinogen. There was a linear relationship between 7-methylguanine levels and dose of the nitrosamine at both of these times. In contrast, the corresponding levels of O6-methylguanine were not directly proportional to dosage but were less than expected, particularly at low doses below 2.5 mg/kg. This discrepancy was significant at 4 hours, but was even more marked at 24 hours. Only doses above 4 mg/kg at the 4-hour time point gave rise to a 0.11 ratio of alkylation of guanine at the O6-position to that at the 7-position. This ratio was that expected for the initial interaction of the alkylating species derived from DMN with DNA. Evidence was obtained to support the hypothesis that these results were due to an enzymatic removal of O6-methylguanine from liver DNA, which occurred much more efficiently at lower initial levels of alkylation. Repeated daily injections of DMN up to 11 days alos gave rise to O6-methylguanine levels that were not proportional to dosage but were relatively greater at higher dose levels. The significance of these findings in the induction of liver cancer by feeding or repeated injection of DMN was explored.
J Natl Cancer Inst 1977 Mar
PMID:Alkylation of rat liver DNA by dimethylnitrosamine: effect of dosage on O6-methylguanine levels. 83 63

A new hypothesis leading to a new model of liver carcinogenesis is described; it is based on the acquisition by carcinogen-altered hepatocytes during initiation of a new functional handle--resistance to the cytotoxicity of a carcinogen--and on the ability of such cells to proliferate in an environment that prevents proliferation of normal hepatocytes. The creation of such a differential environment now enables a quantitative analysis for initiation, the beginning synchronization of the putative premalignant hepatocytes for about 15 cell cycles, the study of the pattern of growth of such resistant cells to form nodules that have some resemblance to the organizational pattern of fetal liver, the analysis of the appearance of distinctive positive and negative markers for these cells, and the further investigation of the development of liver cancer from such cells. The remarkable similarity in overall pattern betweeen the development of cancer in the skin and in the liver with chemicals and the possible role of both somatic mutation and neodifferentiation in carcinogenesis are briefly discussed.
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PMID:Newer insights into the pathogenesis of liver cancer. 92 Jul 80

40 patients with primary or metastatic liver malignancies have been treated with hepatic dearterialization, 19 of them in combination with regional infusion with 5-fluoroacil. The survival was longer than expected from untreated materials. This was especially shown to be valid for patients with primary liver cancer and liver metastases from cancer coli-recti, in which the prolongation of survival was associated with an acceptable quality of life. The long term results were correlated with the "aggressiveness" in therapeutic approach. Only studies of prospective randomized series can settle whether the results depend on the specific measures against the liver tumours or on the general treatment.
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PMID:Results of liver dearterialization combined with regional infusion of 5-fluorouracil for liver cancer. 93 36


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