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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the risk of development of second primary cancers, with particular reference to subsequent hepatocellular carcinoma (HCC), in 592 patients diagnosed as non-Hodgkin's lymphoma (NHL), at Osaka Medical Center for Cancer and Cardiovascular Diseases. During 1978-1994, 2,163 person-years of observation were accrued, and 27 of the patients developed a second primary cancer, yielding an observed-to-expected ratio (O/E) of 1.53 [95% confidence interval (CI) = 1.01-2.23]. Significant excess risk was noted for primary liver cancer (PLC; O/E = 4.36, 95% CI = 1.99-8.28; O = 9) and non-lymphocytic leukemia (O/E = 26.17, 95% CI = 5.26-76.46; O = 3). The excess risk of PLC was relatively constant within the first 10 years after the NHL diagnosis. Patients who received chemotherapy as the NHL treatment had a significantly increased risk of PLC (O/E = 5.91, 95% CI = 2.70-11.23; O = 9). Their clinical reports indicated that all nine patients with PLC were diagnosed as HCC, and eight of them had clinical and/or histologic evidence of cirrhosis at the time of HCC diagnosis. None of the nine patients had a history of blood transfusion between the first NHL treatment and the diagnosis of HCC. These findings suggested that Japanese NHL patients might have an increased risk of developing HCC, and they indicated the importance of medical surveillance for liver malignancies, as well as subsequent leukemias. Possible explanations for the excess risk of subsequent HCC are discussed.
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PMID:Second primary cancers following non-Hodgkin's lymphoma in Japan: increased risk of hepatocellular carcinoma. 926 30

Oncogenesis is a multifactorial process in which environmental, genetic and infectious factors are variably involved. A possible role of specific viruses has been suggested in at least 15% of human cancers. Hepatitis C virus (HCV), which is both hepato- and lymphotropic, is responsible for various liver disorders, i.e. chronic hepatitis, cirrhosis and hepatocelluar carcinoma, as well as for a constellation of extrahepatic immune-mediated manifestations, among which is mixed cryoglobulinaemia. This is a systemic disorder secondary to a chronic, benign B-lymphocyte proliferation, which in some subjects may evolve to a malignant non-Hodgkin's lymphoma (NHL). Interestingly, recent studies reported the appearance of malignant B-cell neoplasias in patients with type C chronic hepatitis; moreover, in a significant number (from 22% to 50%) of 'idiopathic' NHLs, the presence of HCV infection has been demonstrated. The presence of a geographical etherogeneity in the prevalence of HCV-positive NHL suggests that other co-factors, i.e. genetic and environmental, could be involved in the lymphomagenesis. HCV may exert its oncogenic potential in two different directions, leading to liver cancer or B-cell lymphoma.
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PMID:Viruses and cancers: possible role of hepatitis C virus. 935 39

Using data from a case-control study in the United States (the Selected Cancers Study), we examined the relationship between non-Hodgkin's lymphoma (NHL) and family history of different cancers. Cases were 1,511 men aged 31 to 59 years and diagnosed pathologically with non-Hodgkin's lymphoma during 1984-88. Controls were men, frequency-matched to cases by age range and cancer registry (n = 1,910). All study subjects with acquired immunodeficiency syndrome were excluded from analyses. Our results showed that the risk of NHL is associated with a history of lymphoma (odds ratio [OR] = 3.0, 95 percent confidence interval [CI] = 1.7-5.2) and hematologic cancer (OR = 2.0, CI = 1.2-3.4) in first-degree relatives after adjustment for age, ethnic background, and educational level. Further analyses were performed for the subgroups defined by age at diagnosis (younger than 45 years cf 45 years or older). The association of NHL with a family history of lymphoma and hematologic cancer was found primarily among men aged 45 and older (OR = 4.1, CI = 1.9-8.8 for lymphoma and OR = 2.3, CI = 1.3-4.0 for hematologic cancer). The association among men aged 45 and older did not vary by whether or not there were any familial patients diagnosed at the age of 45 or older. No significant associations could be found for a family history of lung cancer, breast cancer, prostate cancer, colon cancer, skin cancer, liver cancer, stomach cancer, brain cancer, thyroid cancer, or myeloma. This study suggests that the familial risk of NHL is influenced primarily by hematolymphoproliferative malignancies rather than other cancers. The familial effects of hematolymphoproliferative malignancies may be stronger for men aged 45 to 59, compared with those aged 31 to 44.
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PMID:Non-Hodgkin's lymphoma and family history of malignant tumors in a case-control study (United States). 948 66

A study was undertaken to estimate the magnitude of association between self-reported infectious mononucleosis (IM) and 6 types of cancer, including Hodgkin's disease, non-Hodgkin's lymphoma, nasopharyngeal cancer, nasal cancer, primary liver cancer, and sarcoma. Cases were male, aged 15-39 y in 1968, who lived in 8 cancer registry areas. Controls were men selected by random-digit telephone dialing. Cases included 1511 persons with non-Hodgkin's lymphoma, 343 with Hodgkin's disease, 386 with sarcoma and 168, 113 and 70 with primary liver, nasopharyngeal and nasal cancers, respectively. There were 1910 controls. For the 6 cancers combined, the overall odds ratio for IM occurring < 5 and > or = 5 y of the reference date were 5.40 [95% (Confidence Interval (CI) = 1.61, 18.09] and 1.08 (0.84, 1.40), respectively. Analogous values were 4.59 (1.25, 16.85) and 1.07 (0.78, 1.48) for non-Hodgkin's lymphoma and 7.49 (1.52, 36.92) and 1.35 (0.87, 2.09) for Hodgkin's disease. There was the suggestion of a protective association with IM occurring > or = 5 y before cancer onset for the 4 non-lymphomatous cancers. Strongly positive associations between self-reported IM and 6 types of cancer were observed for IM occurring < 5 y before the onset of cancer. There was a suggestion, which is noted with extreme caution, that IM earlier in life might have had a protective association with the 4 non-lymphomatous cancers.
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PMID:Self-reported infectious mononucleosis and 6 cancers: a population-based, case-control study. 979 Jan 25

Little is known about the cancer risk following sarcoidosis. In a retrospective cohort study, we tested the hypothesis of an increased risk for malignant lymphomas, lung cancer as well as cancer in other organs frequently involved in sarcoidosis. Four hundred seventy-four patients from an incidence study 1966-1980 and 8,541 patients identified in the Swedish Inpatient Register (IPR) 1964-1994 were linked to the Cancer Register, the Register of Causes of Death, and the Register of Total Population. Relative risks were estimated using standardized incidence ratios (SIR). The overall relative risks for cancer were similar and elevated in both cohorts (IPR presented), SIR = 1.3; 95% confidence interval (CI) 1.2 to 1.4. For lung cancer and non-Hodgkin's lymphoma, the relative risk was doubled during the first decade of follow-up. Thereafter, the risk for lung cancer was significantly decreased whereas the risk for non-Hodgkin's lymphoma equaled unity. Throughout follow-up, elevated risks were found for melanoma (SIR = 1.6; 95% CI 1.0 to 2.3) and nonmelanoma skin cancer (SIR = 2.8; 95% CI 2.0 to 3.8). An increased risk was also found for liver cancer (SIR = 1.4; 95% CI 0.8 to 2.2). Thus, sarcoidosis appears to be associated with a significantly increased risk for cancer in affected organs. Chronic inflammation is a putative mediator of this risk.
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PMID:Increased risk for cancer following sarcoidosis. 1055 38

The German Thorotrast study comprises 2,326 patients and 1,890 controls. Forty-eight Thorotrast patients and 239 controls are still alive and are invited for a follow-up examination every 2 years. In the deceased patients, the following neoplastic diseases with excess rates were registered (Thorotrast/controls): liver cancer (454/3); cancer of the bile ducts, including gallbladder (42/7); myeloid leukemia (40/7); myelodysplastic syndrome (30/4); plasmacytoma (10/2); non-Hodgkin's lymphoma (15/5); bone sarcoma (4/1); malignant peritoneal or pleural mesothelioma (9/0). Dose calculations are based on results of whole-body counting, X-ray films, and data obtained from the hospital records on the volume of Thorotrast injected. For liver cancer, the cumulative risk estimate was calculated to be 40 per 10(4) person Sv (radiation weighting factor = 20). These figures are close to the results of the Danish study and are comparable to the results of the Life Span Study of A-bomb survivors after 40 years at risk with 18 to 48 liver cancers per 10(4) person Sv. For hematopoietic malignancies, the cumulative risk was calculated to be about 7 per 10(4) person Sv (radiation weighting factor = 20). This risk estimate is lower by a factor of 10 compared to the results of the Life Span Study.
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PMID:The german thorotrast study: recent results and assessment of risks. 1056 40

Trichloroethylene is an organic chemical that has been used in dry cleaning, for metal degreasing, and as a solvent for oils and resins. It has been shown to cause liver and kidney cancer in experimental animals. This article reviews over 80 published papers and letters on the cancer epidemiology of people exposed to trichloroethylene. Evidence of excess cancer incidence among occupational cohorts with the most rigorous exposure assessment is found for kidney cancer (relative risk [RR] = 1.7, 95% confidence interval [CI] 1.1-2.7), liver cancer (RR = 1.9, 95% CI(1.0-3.4), and non-Hodgkin's lymphoma (RR = 1.5, 95% CI 0.9-2.3) as well as for cervical cancer, Hodgkin's disease, and multiple myeloma. However, since few studies isolate trichloroethylene exposure, results are likely confounded by exposure to other solvents and other risk factors. Although we believe that solvent exposure causes cancer in humans and that trichloroethylene likely is one of the active agents, we recommend further study to better specify the specific agents that confer this risk and to estimate the magnitude of that risk.
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PMID:Trichloroethylene and cancer: epidemiologic evidence. 1200 39

In South Africa, with changes in environmental factors, varyingly, there have been measures of westernization of diet, with slight rises in intakes of energy and fat, with more of animal, but less of plant foods, being eaten, and with a fall in dietary fibre intake. Smoking practice has increased, particularly in males, likewise alcohol consumption. Physical activity has fallen, especially in urban dwellers. Changes in cancer incidence rates, as reported in the South African Cancer Registry for the periods 1986 and 1993-1995 have been investigated. Additionally, changes in percentages of cancers in hospitals in Johannesburg during 1953-1955 and in Durban during 1994-1996, have been looked into. The high occurrences of oesophageal and cervix cancers have fallen slightly, although more so in respect of liver cancer. But there have been rises, widely varying, in the cases of cancers of the lung, prostate and breast. While some of these changes would be expected from the changes in environmental factors, many cancer occurrence situations remain problematical, e.g. the continuing low occurrence of colorectal cancer. Recently, the rapidly rising epidemic of HIV/AIDS has slightly increased the occurrence of certain cancers, particularly Kaposi's sarcoma and non-Hodgkin's lymphoma. Regarding prevention, chances of cancer control in Africans, through lessening personal risk factors, are very remote, which unfortunately also prevails in large measure in western populations, regarding their reluctance to make the recommended beneficial changes.
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PMID:With recent changes in environmental factors among Africans in South Africa, how have cancer occurrences been affected? 1239 27

Geographic patterns of cancer mortality can often provide clues for public health professionals to identify high-risk areas where limited resources can be directed to conduct cancer epidemiological studies or improve health services related to cancer prevention and treatment. From spatial cluster analyses of mortality cases from 16 specific cancers in Texas over the period from 1990 to 1997, geographic patterns of cancer mortality clusters in Texas were identified. The results suggest that Texas citizens would benefit if cancer epidemiology studies and cancer prevention and treatment practices in Texas would target counties in Southeast Texas for mortality related to lung and bronchial cancer, female breast cancer, colon cancer, and non-Hodgkin's lymphoma; target counties in East (particularly Northeast) Texas for mortality from lung and bronchial cancer, pancreatic cancer, cancer of the brain and other nervous systems, and liver cancer; examine colon cancer mortality in Kaufman County; pay particular attention to mortality from liver cancer in San Antonio and the counties south of San Antonio; direct extra efforts to prostate cancer in the Dallas-Fort Worth area; and investigate the unusually high mortality rate of cervical cancer in Crockett County.
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PMID:Geographic patterns of cancer mortality clusters in Texas, 1990 to 1997. 1296 49

Diabetics may have a higher risk of cancer, notably liver and pancreatic cancers. Evidence about other cancer types remains sparse. The authors examined potential associations between diabetes and several types of cancer in a large multicancer case-control project carried out in Montreal, Canada, in the 1980s. This report, based on 3,107 male cancer cases and 509 population controls, uses information on diabetes and several covariates collected by interview. Adjusted odds ratios (ORs) and 95% confidence intervals (CI) were estimated for the associations between diabetes and each of 12 cancer types. Risks of pancreatic and liver cancers were increased among diabetics: adjusted ORs were 2.1 (95% CI: 1.0, 4.3) for pancreatic and 3.1 (95% CI: 1.1, 8.8) for liver cancer. The increased risk of pancreatic cancer was completely restricted to those with recent onset of diabetes; this was likely a manifestation of reverse causality. Conversely, the increased risk of liver cancer was independent of the interval between diabetes and cancer diagnoses. No associations were observed with melanoma, non-Hodgkin's lymphoma, cancers of the esophagus, stomach, colon, rectum, lung, prostate, bladder and kidney. In conclusion, diabetes was associated with an increased risk of liver cancer among men, but with no other cancer type including pancreatic cancer.
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PMID:Diabetes mellitus and cancer risk in a population-based case-control study among men from Montreal, Canada. 1628 45


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