UMLS:C0345904 - FACTA Search

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

A 10% increased risk of developing a second cancer was observed among approximately 36,000 persons reported to the Danish Cancer Registry with a cancer of the respiratory system during 1943-80. This estimate is markedly influenced by a striking tendency by physicians not to report or the Cancer Registry not to accept a report of a second lung cancer following a primary lung cancer (14 observed vs. 99 expected). A significant 30% excess of all second cancer was seen after laryngeal cancer (368 vs. 282), whereas the 22% excess following cancer of the nasal cavities and paranasal sinuses did not quite reach the level of statistical significance (95% CI = 0.9-1.6). For cancers of the lung and larynx, second cancers arose mainly in the buccal cavity, bladder, kidney (after lung cancer only) and lung (after laryngeal cancer only). These second cancers may be due to common carcinogenic factors, most likely tobacco. Elevated risks of second cancers of the breast, cervix uteri, and other female genital organs were found consistently. Radiotherapy may have contributed to the increased risk of breast cancer, but the excess risk of cancer of the female genital organs other than the cervix was unexpected. Although not significant, the risk of esophageal cancer following cancer of the larynx was below expectation (1 vs. 4.1), which was surprising because alcohol consumption and smoking are thought to be common risk factors for these 2 sites. Significant excesses of pancreatic cancer were observed following cancers of the lung, larynx, and nasal cavities, which might be due to more careful medical surveillance of these patients or to common risk factors such as cigarette smoking. Finally, the risk of a patient developing liver cancer after lung cancer was significantly elevated (22 vs. 11.6). This increase is unlikely to be due to misdiagnosed metastases from the lung, inasmuch as the risk was generally elevated throughout the observation period.
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PMID:Second cancer following cancer of the respiratory system in Denmark, 1943-80. 408 5

Risk of cancer mortality from 1973 to 1985 in persons born in the Indian subcontinent who migrated to England and Wales was analysed by ethnicity, and compared with cancer mortality in the England and Wales native population, using data from England and Wales death certificates. There were substantial highly significant raised risks in Indian ethnic migrants for cancers of the mouth and pharynx, gall bladder, and liver in each sex, larynx and thyroid in males, and oesophagus in females. There were also substantial raised risks in these migrants of each sex for non-Hodgkin's lymphoma and myeloma. For the mouth and pharynx, and liver in each sex, and gall bladder in females, there were also raised risks of lesser magnitude in British ethnic migrants. For colon and rectal cancer and cutaneous melanoma in each sex, ovarian cancer in women and bladder cancer in men, there were appreciable significantly reduced risks in the Indian ethnic migrants not shared by those of British ethnicity. Appreciable raised risks in British ethnic migrants not shared by those of Indian ethnicity occurred for nasopharyngeal cancer in males, soft tissue malignancy in both sexes and non-melanoma skin cancer in males. In migrants of both ethnicities there were appreciable significantly raised risks in each sex for leukaemia and decreased risks in each sex for gastric cancer, for lung cancer except in females of British ethnicity and in males for testicular cancer. The results suggest the need for public health measures to combat the high risks of oral and pharyngeal cancers and liver cancer in the Indian ethnic immigrant population of England and Wales, by prevention of betel quid chewing and hepatitis transmission respectively. The data also imply that early exposures or early acquired behaviours in India, or exposures during migration, may increase the risk of leukaemia and reduce the risks of gastric and testicular cancers in the migrants irrespective of their ethnicity. Aetiological studies would be worthwhile to investigate the reasons for the sizeable decreased risk of colon and rectal cancer and increased risk of gall bladder cancer in each sex and the increased risk of thyroid and laryngeal cancer in males and oesophageal cancer in females of Indian ethnicity but not of British ethnicity who have migrated from the Indian subcontinent.
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PMID:Cancer mortality in Indian and British ethnic immigrants from the Indian subcontinent to England and Wales. 757 89

This study presents the risk of various cancers in relation to ginseng intake based on the data from a case-control study conducted in the Korea Cancer Center Hospital. Ginseng intakers had a decreased risk [odds ratio = 0.50, 95% confidence interval (CI) = 0.44-0.58] for cancer compared with nonintakers. On the type of ginseng, the odds ratios for cancer were 0.37 (95% CI = 0.29-0.46) for fresh ginseng extract intakers, 0.57 (95% CI = 0.48-0.68) for white ginseng extract intakers, 0.30 (95% CI = 0.22-0.41) for white ginseng powder intakers, and 0.20 (95% CI = 0.08-0.50) for red ginseng intakers. Intakers of fresh ginseng slice, fresh ginseng juice, and white ginseng tea, however, showed no decreasing risk. There was a decrease in risk with the rising frequency and duration of ginseng intake, showing a dose-response relationship. On the site of cancer, the odds ratios were 0.47 for cancer of the lip, oral cavity, and pharynx; 0.20 for esophageal cancer; 0.36 for stomach cancer; 0.42 for colorectal cancer; 0.48 for liver cancer; 0.22 for pancreatic cancer; 0.18 for laryngeal cancer; 0.55 for lung cancer; and 0.15 for ovarian cancer. In cancers of the female breast, uterine cervix, urinary bladder, and thyroid gland, however, there was no association with ginseng intake. In cancers of the lung, lip, oral cavity and pharynx, and liver, smokers with ginseng intake showed decreased odds ratios compared with smokers without ginseng intake. These findings support the view that ginseng intakers had a decreased risk for most cancers compared with nonintakers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Preventive effect of ginseng intake against various human cancers: a case-control study on 1987 pairs. 765 37

Data are presented on the frequency of malignant tumours registered at the population-based cancer registry in the southern prefecture of Butare, Rwanda, from May 1991 until 2 months before the outbreak of civil war in April 1994. Beginning in 1992, subjects were also interviewed about socio-demographic and life-style factors that have been associated with cancer risk in the West. The distribution of cancer in Rwanda is similar to that in other countries in sub-Saharan Africa. The most frequent cancers are those with possible infectious aetiologies: liver cancer (12%), cervical cancer (12%) and stomach cancer (9%). In addition, cancers known to be associated with HIV infection are relatively frequent (Kaposi's sarcoma [6%] and non-Hodgkin's lymphoma [3%]). Chronic infection, including infection with HIV, high parity and multiple sexual partners are important determinants of cancer incidence in this population. Tobacco consumption is low in Rwanda and there are few tobacco-related tumours, such as lung and laryngeal cancer. Other tumours believed to be associated with aspects of Western life-style, such as colorectal and breast cancer, are also relatively infrequent.
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PMID:Cancer in Rwanda. 860 71

We have been investigating the mathematical nature of intercancer linkage that underlies the mutual regulation of cancer risks between any 2 tumors in their variations in time and space. Applications of both sequential regression test and topological manipulation of age-adjusted incidence rate (AAIR) data set enabled us to prepare the oncogene (Onc) activation profile and the tumor suppressor gene (TSG) inactivation profile for each tumor. The purpose of this study was to investigate the relation between the changes of 2 cancer gene profiles and the sex discrimination of cancer risk in 7 human neoplasias. Results obtained are as follows: i) The sex discrimination of cancer risk could better be defined by the use of log-transformed AAIR data rather than of untransformed AAIR data. ii) The sex discrimination of cancer risk, as calculated with the AAIR data of 47 population units of the world, is as follows: a) breast cancer (Br), M:F=1:120.2; b) thyroid cancer (Thy), M:F=1:2. 64; c) colon cancer (Co), M:F=1.18:1; d) liver cancer (Li), M:F=2. 63:1; e) lung cancer (Lu), M:F=3.66:1; f) esophageal cancer (Eso), M:F=3.68:1; g) laryngeal cancer (Lar), M:F=7.26:1. iii) Female-dominant cancers were associated with inversion (Br) or defectiveness (Thy) of male oncogene profile, whereas male-dominant cancers were associated with inversion (Lar) or defectiveness (Li, Lu and Eso) of female Onc profiles. Sex-indifferent cancer, Co, was distinguished from other tumors by the emergence of defectiveness in the TSG profiles of both sexes. TSG defectiveness was also detectable in female (Br, Thy) and bisexual (Lu) tumors. iv) The Onc vs TSG interaction, as assessed in terms of r value of the reciprocal regression analysis, was increasing in its positivity rate from the top of the female-dominant family (Br) through the sex-indifferent tumor (Co) to the bottom of the male-dominant family (Lar). In conclusion, the emergence of sex discrimination of cancer risk was positively correlated to the extent of integrity of oncogene activation in the dominant gender relative to the recessive gender. Findings with 6 sex-discriminant tumors are discussed in their relevancy to tumorigenesis from the point of view of endocrinological epidemiology.
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PMID:Relation between the changes of oncogene versus tumor suppressor gene interaction and the transition of cancer risk from female dominance through no sex discrimination to male dominance, as investigated by the reciprocal regression analysis of 5 human neoplasias. 968 28

Our earlier reports indicated that the changes of age-adjusted incidence rates (AAIRs) of any 2 tumors in time and space, as investigated by the sequential regression analysis, showed a good fitness to the equilibrium model under the control of the law of mass action. The purpose of this study is to investigate the problem of whether or not the changes of AAIRs of individual tumors in time and space show a similar fitness to the equilibrium model of the law of mass action. The cancer risk data set of: a) 20 neoplasias in scope; b) 6 cancer registration areas in space; and c) 5 sequential investigations from early 1960's to mid 1980's in time, were subjected to the sequential regression analysis - a modification of the least square method. Results obtained are as follows: a) out of 20 tumors tested, all tumors other than 5 tumor types showed a good fitness (P<0.05) to the equilibrium model of the law of mass action in their risk changes in space. The 5 tumor types that failed to fit to the equilibrium model were male gall-bladder cancer, male breast cancer, male thyroid cancer, female liver cancer and female laryngeal cancer. They were all classified as the members of low-risk gender in the cancer family with sex discrimination of cancer risk. b) All tumors other than male thyroid cancer of Birmingham-England showed a good fitness to the equilibrium model of the law of mass action in their risk changes in time. c) It is argued that the good fitness to the equilibrium model of the law of mass action and the poor fitness to the equilibrium model can be taken each as indication of the predominant expression of oncogene activation and the emergence of intervention of tumor suppressor gene inactivation to the full expression of oncogene activation in the mathematical structure of the cancer risk data set. The significance of the above findings as the supporting evidence of the steroid criminal hypothesis of carcinogenesis as well as the pertinence of the least square method to the mathematical analysis of cancer risk are discussed in the light of historical development of science from early 19th century to late 20th century.
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PMID:Statistical analysis of the age-adjusted incidence rates of human neoplasias: changes in time and space from early 1960's to mid 1980's with special reference to the steroid criminal hypothesis of carcinogenesis. 1008 20

The present study is an extension of our recent study in which we attempted statistical analysis of the data assembly of age-adjusted incidence rates (AAIRs) of a tumor without topological data manipulation for each of 20 individual tumors in scope, for each of 6 cancer registration areas in space, and for a period of early 1960's to mid 1980's in time. This time, a data assembly of log AAIR changes in time and space first passed through the process of topological data manipulation, and then underwent the sequential regression analysis so that we could assess the fitness of log AAIR changes either in space or in time to the equilibrium model of the law of mass action from the viewpoint of the interaction between oncogene activation and tumor suppressor gene inactivation. For the sake of comparison, the fitness of the cancer risk data to the equilibrium model was assessed in the framework of 3 sets of coordinates: a) the original (x org, y org) coordinates in which most of the log AAIR data assemblies in their data variations were classified as the oncogene activation type in the field of centripetal force (r seq=-1.000). b) The rect (X rect, Y rect) coordinates in which the log AAIR data assemblies were very often classified as the tumor suppressor gene inactivation type in the field of centrifugal force (r seq=+1.000). c) The para (X para, Y para) coordinates in which the log AAIR data assemblies were mostly classified as the intermediate type as regards the fitness to the equilibrium model. The rect-coordinates and the para-coordinates, 2 variants of angular rotation of the original coordinates, were so designed as to allow their X-axes to run each at a right angle and parallel to the regression line of the original pair data block. The results obtained were as follows: a) poor fitness of the log AAIR changes in space to the equilibrium model in the rect-coordinates was found in male breast cancer, male thyroid cancer, female esophageal cancer, female laryngeal cancer and female lung cancer. The summation of the present study and the last study from our laboratory led to the conclusion that the members of low-risk gender in the tumor family with sex discrimination of cancer risk were inclined to show either failed expression of oncogene activation or failed expression of tumor suppressor gene inactivation or both. b) There was a subtle difference of the fitness of log AAIR data to the equilibrium model between the log AAIR changes in time and those in space in that the log AAIR changes in time within the framework of the rect-coordinates, which usually represented the field of centrifugal force or site of tumor suppressor gene inactivation expression, showed an increase in the number of oncogene activation type data sets as compared with the log AAIR changes in space. c) Upon further insight into the AAIR changes in time, consistent association of prominent cancer risk increase in time with the transition of tumor suppressor gene inactivation expression (r seq=+1.000) from the rect-coordinates to the para-coordinates was detected in skin cancer of both sexes, testicular tumor, liver cancer of both sexes and thyroid cancer of both sexes, all of which were related to the prevalence of environmental hormones as regards the recent boost of their cancer risks in the Western countries. In summary, the log AAIR, a cancer risk parameter, in its changes in time and space was found to provide useful information in assessing the interaction between the oncogene-tumor suppressor gene complex and the hormonal milieu of the host in the genesis of both environmental hormone-dependent and -independent human neoplasias. The significance of our statistical maneuver (the sequential regression analysis) is discussed in the light of the development of mathematics in early 19th century.
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PMID:Topological transition of the parametric expression site of tumor suppressor inactivation as a marker evidence of environmental hormone-oriented cancer risk increase. 1040 82

Occupational exposure to vinyl chloride (VC) is causally related to liver angiosarcoma, whereas there is inconsistent epidemiologic evidence for other neoplasms. Two pooled analyses of worker cohorts from 56 plants in North America and Europe provide the most comprehensive and updated data on cancer risk among workers exposed to VC. These included over 22,000 workers, with a total of 640,000 person-years of observation, followed-up for up to 50 years. Overall, a total of 1,778 cancer deaths were observed versus 1,829.46 expected, corresponding to a standardized mortality ratio (SMR) of 0.97 (95% confidence interval (CI)=0.93-1.02). Excluding 71 confirmed angiosarcomas, there were 60 deaths from liver cancers versus 44.35 expected (SMR=1.35, 95% CI=1.03-1.74). Lung and laryngeal cancer mortality were significantly lower than expected (SMR=0.88 and 0.59, respectively). The SMRs for soft tissue sarcoma, brain, lymphoid and haematopoietic system cancers were not materially different from unity. Thus, the aggregate data from over 20,000 VC workers in North America and Europe exclude any excess mortality from lung, laryngeal, soft tissue sarcoma, brain, lymphoid and haematopoietic neoplasms. There appears to be a slight excess of liver cancer other than angiosarcoma, which is difficult to interpret and is likely due to residual misclassification of angiosarcomas.
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PMID:Occupational exposure to vinyl chloride and cancer risk: a review of the epidemiologic literature. 1451 8

This study investigated the spatial distributions of mortality rates of six cancers: mesothelioma, lung cancer, intestinal cancer, nasopharyngeal and laryngeal cancer, liver cancer, and stomach cancer in Dayao using Geographic Information Systems. Relationships between the mortality rates of the six cancers and land use patterns were investigated by Pearson Correlation Coefficients. The results indicated that the mortality rates of nasopharyngeal and laryngeal cancer, lung cancer, intestinal cancer, and mesothelioma were significantly associated with outcropped asbestos. Both the proportions of farmland and urban area were positively related to the mortality rates of nasopharyngeal and laryngeal cancer, lung cancer, intestinal cancer, and mesothelioma, and significant negative correlations were found between the proportion of forestland and nasopharyngeal and laryngeal cancer and intestinal cancer. It can be concluded that naturally occurring asbestos may significantly elevate the mortality rates of nasopharyngeal and laryngeal cancer, intestinal cancer, lung cancer, and mesothelioma. Moreover, higher proportions of farmland, urban area, and lower proportions of forested land may elevate the mortality rate of the four cancers.
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PMID:Impacts of land use on spatial distribution of mortality rates of cancers caused by naturally occurring asbestos. 2276 Apr 39

Fifty two patients with metastatic lung tumors were treated surgically in our hospital. Second pulmonary resections were performed in 6 patients. They consist of 1 male and 5 females, their age ranged from 59 to 80 years old( average 66 years old). Tumors originate from laryngeal cancer, colorectal cancer in 2 cases respectively, lung cancer and hepatic cancer in 1 case respectively. Three-year and 5-year survival was seen in 75% and 75% of patients, respectively.
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PMID:[Re-operation for recurrent pulmonary metastases]. 2391 99

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