Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cells derived from 9 human tumors were tested in vitro using 5 doses ranging from 1 to 5000 units of recombinant human erythropoietin (rhEpo) per ml to assess a proliferation response to this hormone. The following tumors were used: 2 melanomas, 1 hepatoma, 3 renal cell carcinomas, 1 adenocarcinoma of the lung, and 2 mammary carcinomas (with and without sex steroid hormone receptors). Compared to untreated cells, none of the cell lines exposed to rhEpo revealed differences in proliferation extending beyond the limits of methodological fluctuation. rhEpo thus does not have any effect on the growth of human tumors in vitro under the experimental conditions applied.
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PMID:Effect of recombinant human erythropoietin on the growth of human tumor cell lines in vitro. Micro-titertec-tetrazolium assay. 158 90

The CA 50 levels in serum samples from 440 patients were estimated using a dissociated enhanced lanthanide immunofluorimetric assay. The distribution was similar to CA 50-RIA assays. Raised levels (greater than 14 U/ml) were present in 95% pancreatic cancer, 68% hepatoma, 54% advanced colorectal cancer, 58% advanced breast cancer and 48% lung cancer. High values were observed in adenocarcinoma of the lung, and were related to tumour mass in small cell lung cancer. CA 50 is independent of CEA. The marker is of considerable potential in pancreatic cancer where the majority of patients express the Can 50 Ag.
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PMID:An evaluation of serum CA 50 levels in cancer using a time-resolved fluoroimmunoassay. 317 5

Mortality, major causes of moribundity, and spontaneous tumors in CD-1 mice were studied in 891 males and 890 females, which were used as controls in 11 different 2-year chronic and oncogenicity studies during the past 5 years. Average mortality of males and females at 83 weeks of age was 32.6% and 28.6%, respectively, and at 109 weeks of age was 66.4% and 63.3%, respectively. Mortality was significantly lowered in males and females born after 1980 in accordance with an abruptly decreased occurrence of systemic amyloidosis in these animals. The major cause of death or moribundity included systemic arteritis, systemic amyloidosis, auricular thrombosis, glomerulosclerosis, lymphoma, and pulmonary adenocarcinoma in both sexes. Dysuria and hepatocellular carcinoma in males and mammary adenocarcinoma in females were also critical lesions. The major tumors occurring at more than 3% incidence were systemic lymphoma, adenoma/adenocarcinoma of the lung, adenoma/carcinoma of the liver and adenoma/adenocarcinoma of the Harderian gland for males, and systemic lymphoma, adenoma/adenocarcinoma of the lung, adenoma/carcinoma of the liver, leiomyoma/leiomyosarcoma of the uterus, adenoma/adenocarcinoma of the pituitary (anterior), adenoma/adenocarcinoma of the mammary gland and adenoma/adenocarcinoma of the Harderian gland for females. Intralaboratory heterogeneities in the incidence were recorded as follows: systemic lymphoma in 1 of 11 control groups (1/11) and adenoma/adenocarcinoma in 1/11 for males, and systemic lymphoma in 3/11, adenoma/adenocarcinoma of the lung in 2/11, adenoma/adenocarcinoma of the liver in 1/11, and adenoma/adenocarcinoma in 1/11 for females.
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PMID:Mortality, major cause of moribundity, and spontaneous tumors in CD-1 mice. 319 56

The carcinogenicity of N-nitrosomethyl-(2-hydroxyethyl)amine (NMHEA), N-nitrosomethyl-(3-hydroxypropyl)amine (NMHPA), and the p-toluenesulfonate (tosylate) ester of NMHEA (NMHEATs) was tested in male and female F344 rats. The chemicals (25.6 mumol per application) were administered by twice-weekly gavage in corn oil (0.2 ml) for the lifetime of the animals. NMHEA was found to be an effective carcinogen under those conditions. The median survival time for the females was 9 mo after treatment was initiated, while for the males it was 12 mo. The principal cause of death of the females was hepatocellular carcinoma (14 of 20), while only 6 of 20 male rats exhibited that tumor. A few of the male rats had squamous cell carcinomas of the nasal epithelium (4 of 20), tumors which were not observed in the females. NMHPA was a much weaker carcinogen. Many of these rats survived for 2 yr and most had many age-related cancers. Nevertheless, 10 of the NMHPA-treated males and 2 females had adenocarcinoma of the lung, which was absent in the controls and also induced a significant number of neoplastic nodules in the livers of rats of both sexes. NMHEATs was also a weak carcinogen. However, besides many age-related tumors, it induced some hepatocellular carcinomas as well as hemangiosarcomas of the liver. NMHEATs was at least partially hydrolyzed to NMHEA, which was detected in the blood plasma of treated rats. A hypothesis has been advanced that NMHEA is activated to a proximate carcinogen by sulfate conjugation of the hydroxyl group; the present data do not contradict this hypothesis. The relatively lower carcinogenic potency of NMHPA, the different tumor spectrum induced by this chemical, and particularly the differences in chemical behavior suggest that its mode of activation is not the same as that for NMHEA.
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PMID:Carcinogenicity of hydroxyalkylnitrosamines in F344 rats: contrasting behavior of beta- and gamma-hydroxylated nitrosamines. 334 26

A 75 year old man presented with metastatic carcinoma of the brain. At autopsy a primary scar adenocarcinoma of the lung was found. By light microscopy the cytoplasm of the tumor cells was seen to contain hyalin masses with tinctorial properties identical to those of the Mallory bodies seen in human alcoholic liver disease and in hepatocellular carcinoma. The hyalin stained positively with anti-Mallory body antibody by the peroxidase antiperoxidase technique, and had the characteristic filamentous and granular amorphous appearance of alcoholic hyalin by electron microscopy. Our observation is of interest in light of recent information relating Mallory bodies to prekeratin, and vitamin A deficiency to lung cancer.
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PMID:Mallory bodies in scar adenocarcinoma of the lung. 617 20

Twenty-one (100%) Haitians and 42 (21.5%) of 192 native black Americans autopsied in a 33-month period at Jackson Memorial Hospital, Miami, were included in this review. All autopsied materials were examined. Among the Haitians autopsied, infectious diseases accounted for 11 (52%) of 21 deaths. Toxoplasma encephalitis was the leading cause of death (five cases). Other infectious causes of death included disseminated cryptococcosis (one), disseminated cytomegalovirus diseases (one), Pneumocystis carinii pneumonia (one), chronic active hepatitis B (two), and bacterial pneumonia (one). Malignant neoplasms were also found to be causes of death and these included a single cases of each of the following: adenocarcinoma of the lung, multiple myeloma, diffuse histiocytic lymphoma, hepatoma, and Kaposi's sarcoma. Deaths of the remaining cases were due to hypertensive cardiovascular diseases (two), rheumatic heart disease (one), glomerulonephritis (one), and intimal fibroplasia of coronary arteries (one). Seven Haitian cases fulfilled the Centers for Disease Control case definition for the acquired immune deficiency syndrome (AIDS). For comparison, autopsies of black Americans were chosen from conditions that would most likely predispose them to opportunistic infections. Among the autopsies on black Americans there were no cases of opportunistic infections or Kaposi's sarcoma that were considered to be consistent with the AIDS.
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PMID:Unusual causes of death in Haitians residing in Miami. High prevalence of opportunistic infections. 634 27

Toxin T-514 is a dimeric anthracenone isolated from the Karwinskia humboldtiana (buckthorn) plant. Its potential anti-neoplastic effect was evaluated in vitro and the results obtained were compared with the effect of other known anti-cancer agents. Normal and malignant continuous cell lines were tested. After a 72-h exposure, neoplastic cells derived from hepatic, pulmonary and colonic tissues were more sensitive to toxin T-514 than normal cells from the corresponding organ. Hepatoma cells and colon adenocarcinoma CT50 values were < 10 micrograms/ml. Lung adenocarcinoma, undifferentiated bronchogenic cancer cells and small cell carcinoma CT50 values were < 20 micrograms/ml. All benign cell CT50 levels tested were > 113 micrograms/ml. This in vitro selective toxicity found with toxin T-514 was also seen with 5-fluororacil and mitomycin for colon adenocarcinoma and with epidoxorubicin for undifferentiated bronchogenic cancer cells.
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PMID:In vitro selective toxicity of toxin T-514 from Karwinskia humboldtiana (buckthorn) plant on various human tumor cell lines. 794 May 62

Six patients with multiple myeloma (MM) and a second non-hematological neoplasm (solid tumor) are documented in this study. Two patients had a previous history of adenocarcinoma of the colon prior to MM diagnosis; in three patients a second neoplasm (lung cancer, adenocarcinoma of the urinary bladder and adenocarcinoma of the colon) appeared at the time of MM diagnosis; one patient, a woman with a six-year history of MM, developed hepatoma. The two patients who had had a neoplasm of the colon ten years before and the patient with bladder carcinoma, responded to MM therapy. The patient with lung cancer and the patient with adenocarcinoma of the colon died; the last patient, with MM and liver cancer, is alive but with aggressive disease. In conclusion we have found that in MM patients a second neoplasm may develop or co-exist, in greater frequency than that of the general population.
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PMID:Patients with multiple myeloma and solid tumors: six case reports. 970 May 87

Carcinogenicity of pan masala, a dry powdered chewing mixture of areca nut, catechu, lime, spices and flavoring agents was evaluated by means of the long-term animal bio-assay 6- to 7-week old male and female S/RVCri mice were divided randomly into intermediate and lifetime exposure groups and fed normal diet without pan masala-(zero dose) or diet containing 2.5% and 5% pan masala. Animals in the intermediate-exposure group (n = 10/gender/dose group) were killed after 6, 12 or 18 months of treatment, while those in the lifetime-exposure group (n = 54/gender/dose group) were killed when moribund or at the termination of the experiment at 24 months. Several tissues were processed for histopathological examination. The body weight and survival rate of mice fed pan masala were lower than that of the controls. Histopathological observations of tissues from control animals did not reveal any neoplastic alterations. However, lifetime feeding of pan masala induced adenoma of the liver, stomach, prostate and sebaceous glands, also forestomach papilloma, liver hamartoma, hepatoma and hemangioma, carcinoma of the forestomach, adenocarcinoma of the lung and liver, and testicular lymphoma. Neoplastic lesions appeared mainly in the liver (n = 13), stomach (n = 3) and lung (n = 8). Lung adenocarcinoma, the most frequent malignant tumor type, was observed in 2/120 mice in the intermediate-exposure group and in 8/216 animals in the lifetime-exposure group. Statistical analysis of tumor-induction data revealed a significant dose-related increase in lung adenocarcinomas but not in liver and stomach neoplasms indicating that lung is the major target tissue for the carcinogenic action of pan masala.
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PMID:Long-term carcinogenicity of pan masala in Swiss mice. 1052 7

Familial risks for histopathology-specific cancers have not been determined. We used the nationwide Swedish Family-Cancer Database on 10.2 million individuals and 1 million tumors to calculate standardized incidence ratios (SIRs) for familial cancers of specific histology and morphology among 0- to 66-year-old offspring. We used histology codes for both offspring and parents, but because of the limited number of cases, the morphology-specific classification could be used only for offspring by all site-specific cancers in parents, resulting in inflated risk estimates. A number of novel findings emerged in the histopathology-specific analysis of familial risks, in addition to some known associations. Overall, specific histology showed an SIR of 2.07 for all cancers compared to an SIR of 2.00 for any histology. However, the small effect was due to breast and prostate cancers, which showed a negligible effect of specific histology. Familial risks of over 4.0 were found for serous papillary cystadenocarcinoma of the ovary, papillary thyroid cancer and low-grade astrocytoma. Familial risks of over 3.0 were found for signet-ring gastric cancer, various forms of ovarian cancer and squamous cell skin cancer. Also noteworthy were familial risks of hepatocellular carcinoma (2.48), pancreatic adenocarcinoma (1.92), large cell carcinoma and adenocarcinoma of the lung (2.29 and 2.18, respectively) and clear cell carcinoma of the kidney (2.73). Many of the findings were novel and could be revealed only by applying codes for specific histopathology. These data call for a closer description of familial aggregations and probing for the underlying genetic mechanisms.
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PMID:Familial risk of cancer by site and histopathology. 1245 61


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