Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0006826 (cancer)
 1,092,456 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cats represent an unusually valuable model for studying the role of the immune response to leukemia, lymphoma, and other mesodermal neoplasms. The agents that cause spontaneous feline leukemias, lymphomas, and fibrosarcomas, the feline leukemia and sarcoma viruses, are well characterized. A specific tumor cell membrane antigen, designated the feline oncornavirus-associated cell membrane antigen (FOCMA) has also been described. Feline leukemia and feline sarcoma viruses are antigenically indistinguishable, and FOCMA is common for both. Both laboratory-induced and spontaneous feline leukemias, lymphomas, and fibrosarcomas are available for study. A clear correlation has been shown between the resistance of cats to development of lethal tumors following inoculation of feline sarcoma virus and the presence of high humoral antibody titers to FOCMA. The geometric mean antibody titer to FOCMA for cats that resisted growth of fibrosarcomas was more than 20-fold higher than the mean for cats that succumbed to lethally progressing tumors. Cats with induced or spontaneous leukemia or lymphoma also have either no detectable FOCMA antibody or very low levels. Conversely, some cats resist development of leukemia or lymphoma following natural exposure to feline leukemia virus in leukemia cluster households, and these cats have high FOCMA antibody titers. These results support the concept of a natural immunosurveillance mechanism against leukemia or lymphoma development in an outbred mammalian species.
Cancer Res 1976 Feb
PMID:Immune response to leukemia virus and tumor-associated antigens in cats. 5 24

6 autopsy cases of primary leptomeningeal sarcomatosis are presented as a distinct nosological entity with a variable clinical picture and morphology in 5 males and 1 female. The clinical course from onset of symptoms till death ran for only a few weeks in most cases. 2 infants showed brain tumor symptoms and signs. 2 patients of advanced age presented a polyradiculoneuritic syndrome and 2 young adults had spinal cord compression symptoms and a mixed clinical form. In almost all cases, clinical symptoms and signs were for most of the course confined to one part of the neuraxis. The CSF was distinctly abnormal in all cases, showing elevated protein, depressed glucose and pleocytosis of variable extent. CSF sediment was investigated in 3 cases in all of which malignant tumor cells were found so a diagnosis of malignant meningeal tumor was made during life. Electron microscopy of CSF cells in 1 case confirmed the primitive character of the tumor cells. Complete autopsies revealed absence of any neoplasm outside of the CNS. Gross meningeal involvement was visible in all cases. Histologically, 3 tumor types were distinguished: polymorphic cell sarcoma, an undifferentiated form, and fibrosarcomatosis. Clinical data are analyzed in order to distinguish the condition from other neoplasms or infectious, especially tuberculous meningeal infiltrations. CSF cytology studies are considered the most useful step in clinical diagnosis. Neuropathological features are reviewed with stress on differentiation from malignant lymphomas of the CNS, diffusely spreading medulloblastoma, meningeal melanoblastosis and gliomatosis. The origin of meningeal sarcomatosis cells is briefly discussed. The use of the term "meningeal meningiomatosis" for this condition is deprecated.
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PMID:Primary leptomeningeal sarcomatosis. Clinicopathological report of six cases. 5 34

A striking chemotherapeutically curative effect on tumor was obtained by means of temporary interruption of regional blood flow combined with local hyperthermia. By analyzing various basic conditions required for this system using Ehrlich tumor implanted in the hind limbs of mice, the following were found to be essentially indispensable to obtain satisfactory chemotherapeutic effects: (a) a time interval of 1 to 3 min after systemic i.v. administration of drug to the mice, (b) use of a tourniquet on the tumor-bearing mouse limb to stop blood flow, and (c) warming at 37-41 degrees (d) for a period of at least 30 to 60 min. Among the chemotherapeutic drugs tested in the present study, Carbazilquinone (NSC 134679) was the most effective because it revealed the strongest antitumor effect despite its relative innocuousness to nontumorous adjacent normal tissues. Applying the present method, a large syngeneic mouse sarcoma transplanted to the limb 7 days before the experiment also completely regressed in 6 of 9 mice.
Cancer Res 1976 Jul
PMID:Temporary interruption of regional blood flow combined with local hyperthermia for cancer chemotherapy. 5 14

Twenty-three of 36 (64%) lung cancer patients, 19 of 36 (54%) melanoma patients and 18 of 27 (66%) sarcoma patients tested in the leukocyte migration in agarose assay against soluble extracts of histologically similar tumors showed significant inhibition of leukocyte migration. Reactivity to extracts of dissimilar tumors was low. Sera of only 1/13 (7%) lung cancer patients, 2/19 (10%) melanoma patients and 7/21 (33%) sarcoma patients were inhibited by extracts of histologically dissimilar tumors. Only 7-9% of cancer patients reacted to paired extracts of normal tissue from the tumor donors. An average of 13% of sera from normal controls reacted to tumor extracts. Stage of disease and mode of therapy appeared to have little effect on overall reactivity in this assay, although the number of patients within the various categories was small for purposes of statistical analysis. The leukocyte migration in agarose assay shows a sensitivity and specificity to tumor-associated antigens comparable to that of the older capillary tube method in general use and may facilitate performance of migration inhibition. This assay may not be useful as a prognostic test due to the lack ofcorrelation with stage of disease and treatment modality. However, its high specificity and economical use of tumor antigen suggest applications in tumor antigen purification. The use of soluble tumor antigen preparations may make it possible to purify these antigens further to increase specificity and reactivity.
Int J Cancer 1976 Aug 15
PMID:Detection of human tumor-associated antigens by the leukocyte migration in agarose assay. 6 Feb 86

When cells are infected by C-type viruses such as Moloney sarcoma/leukaemia virus, new antigens appear on the cell membrane. Mice and rats will respond immunologically to the antigen(s). It was uncertain whether the antigens were related to the viral structural proteins or to non-virion, tumour-specific surface antigens (TSSA) or both. In an 125I-antiglobulin binding assay, Moloney virus completely blocked the binding of mouse and rat sera to virus shedding target cells, thus suggesting that mice and rats recognise only viral proteins. Mice responded to type-specific and rats mainly to group-specific determinants on the virus. Individual Moloney viral proteins were prepared using the guanidine HCl method and were used to block the binding of the rat anti-Moloney immune serum to Moloney virus shedding target cells. By this method, it was demonstrated that the rat serum contains specificities for the viral proteins gp70 and p30, but it was not possible to detect any antibodies directed towards non-virion or TSSA-like molecules.
Int J Cancer 1976 Oct 15
PMID:Specificity of serum from rodents immune to Moloney C-type virus-induced tumours. 6 44

Tumors were induced by Kirsten sarcoma virus (KiSV) in an inbred guinea pig, strain 13. The tumor cells were established in culture and characterized. The KiSV-induced sarcoma cells were virus-free and nonproducing; however, they contained resuable sarcoma genome. A type B guinea pig retravirus was readily activated from the tumor cells after induction with 5-bromodeoxyuridine (BUDR). BUDR induction of guinea pig retravirus was further enhanced by treatment with dexamethasone, a synthetic glucocorticoid hormone.
J Natl Cancer Inst 1976 Jun
PMID:Characterization of virus-free guinea pig tumors induced by Kirsten sarcoma virus. 6 43

Three of 42 (7%) monkeys given aflatoxin B1 (AFB1) for longer than 2 years have developed primary malignant neoplasms of the liver. Liver biopsies performed at intervals during aflatoxin administration revealed that neoplasia was preceded by pathologic lesions of the liver, including toxic hepatitis, proliferation of pseudotubules, and hyperplastic nodules. Serum alpha-fetoprotein levels, monitored in one of the monkeys by radioimmunoassay, paralleled tumor growth and recurrence of the hepatocellular carcinoma. Normal serum alpha-fetoprotein levels were noted for a monkey with hemangioendothelial sarcoma. Our results implicate AFB1 as a liver carcinogen in monkeys and add additional support to the hypothesis that humans exposed to this substance may be at risk of developing liver cancer.
J Natl Cancer Inst 1976 Jul
PMID:Carcinogenicity of aflatoxin B1 in rhesus monkeys: two additional cases of primary liver cancer. 6 57

The chemotherapeutic action of Bleomycin, applied at a dosage which induced only a non-specific tumor inhibition on HRS-sarcoma, was potentiated by combination with inosine. This combination, without increasing toxicity, effected both a significant tumor inhibition and a significant curative action.
Cancer Lett 1975 Sep
PMID:Potentiation of the chemotherapeutic action of bleomycin by combination with inosine on HRS-sarcoma. 6 12

The genetics of late appearing MSV tumors showing a progressive growth pattern in AKR mice was investigated. The late MSV tumor response in F1 hybrids depended on the genetic background of the non-AKR parent. Within the 4-month observation period following virus injection, (CBA X AKR) F1, (DBA/2 X AKR)F1, and (NIH X AKR)F1 developed progressing MSV tumors, which exhibited latency and growth behavior comparable to that seen in AKR mice, (BALB X AKR)F1, (B6 X AKR)F1, and (B10br x akr)f1 mice did not show any late MSV tumors. In contrast to early regressing M-MSV tumors, whose development is independent of Fv-1 genotype, late MSV tumor progression is largely a function of this gene, since all late tumors which appeared in (B10BR x AKR) x AKR were observed in Fv-1n homozygous mice, H-2k halotype is a further factor in the occurrence of late MSV tumors, at least in (B6 x AKR) x AKR mice. In crosses of AKR with Fv-1 compatible mice, tumor appearance was strongly associated with inheritance of AKR-Mulv, and MSV recovered from late tumors of first back-cross animals appeared to be a new pseudotype with the endogenous AKR-MuLV. It is suggested that the host genetic control in both early and late MSV tumors is exerted mainly on the helper component of the leukemia-sarcoma complex.
Int J Cancer 1977 Apr 15
PMID:Genetics of murine sarcoma virus (MSV)--induced tumors in AKR mice: Evidence that late progressing and early regressing tumors are controlled by different gents. 6 12

Type C virus produced by dog thymus cells (A7573) that were infected with virus (HL-23V), isolated from cultured leukocytes of an acute myelogenous leukemia patient, transformed marmoset and horse cells in vitro and induced virus-producing fibromas in marmosets. The tumors and transformed foci were indistinguishable morphologically from those induced by simian sarcoma virus, type 1 (SSV-1/SSAV-1). HL-23V was indistinguishable from SSV-1/SSAV-1 by immunofluorescence and neutralization tests, and the nontransforming virus associated with HL-23V completely inhibited SSV-1 focus induction in interference tests. Cell cultures established from a marmoset fibroma produced transforming and nontransforming virus biologically and antigenically indistinguishable from HL-23V and SSV-1/SSAV-1.
J Natl Cancer Inst 1977 Apr
PMID:Oncogenicity in marmosets of HL-23V, a type C oncornavirus isolated from human leukemic cells, and comparison with simian sarcoma virus type 1 (SSV-1/SSAV-1). 6 19


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