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Query: UMLS:C0007097 (carcinoma)
 152,788 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five cases of hepatocellular carcinoma in whom diagnosis was made when the tumor was relatively small, are described. In 2 cases, serum alpha-fetoprotein (AFP) strted to rise sharply, which enabled early detection and surgical removal of the tumor. Serum AFP was below 100 ng per ml, but above the upper normal limit by radioimmunoassay, and was unfluctuating for a considerable period of time before it began to rise in 2 cases. It was negative throughout in 1 case, who lived more than 4 years after the tumor had reached a detectable size. In 4 of 5 cases, the tumor seemed to have evolved during a stage of chronic hepatitis or its transition to cirrhosis. In 1 case with chronic schistosomiasis and advanced mixed macro- and micronodular cirrhosis, a 1.5-cm tumor was detected by celiac angiography. These observations on time relationship of oncogenesis may be generalized to modify the cirrhotic liver. Necessity is emphasized for the early detection of this type of carcinoma to monitor serum AFP in chronic hepatitis patients, particularly in those with unfluctuating, mildly abnormal levels of AFP.
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PMID:Clinical observations during a relatively early stage of hepatocellular carcinoma, with special reference to serum alpha-fetoprotein levels. 5 Feb 51

A study on the experimentally induced yolk sac tumor in the rat was made in special regard to the characteristics and origin of tumor cells. Pregnant rats which fetuses were removed on the 12th day of gestation, developed tumors derived from the fetal membranes left outside the uterus, which were composed of differentiated teratomas and yolk sac tumors. Serial observation of the oncogenesis revealed that an early lesion of the yolk sac tumor appeared in a nodule found as early as 3 weeks after the fetectomy and production of alpha-phetoprotein (AFP) was observed histochemically in the tumor cells 5 weeks after the fetectomy. A cultured cell line established after cloning from the transplantable yolk sac tumor which had been induced similarly and converted into ascitic form was also investigated. Light and electron microscopic studies on both induced tumors and the cultured cells indicated a similarity of AFP producing tumor cells with parietal yolk sac cells and of PAS-positive hyaline-like substance with the Reichert membrane. It is reasonable to conclude that the yolk sac tumor observed is regarded as a parietal yolk sac carcinoma described by Pierce. Histogenesis of the tumor is also discussed.
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PMID:[Experimental yolk sac tumors in the rat (author's transl)]. 8 66

BALB/c and (C57BL times DBAf)F1 mice were treated with 7,12-dimethylbenz[a]anthracene and urethan, respectively, to induce mammary dysplasias. Nine transplantable outgrowth lines of dysplastic tissue were established by transplantation of the primary lesions into the cleared mammary fat pads of syngeneic mice; 8 of the 9 lesions were ductal in origin. The growth and tumorigenic potentials of these 9 lines were followed over 6-9 transplant generations. Most outgrowth lines exhibited a rapid decline in growth potential and/or a progression to papillomatosis and subsequent carcinoma by transplant generation 7. The ductal outgrowth lines and mammary tumors established from urethan-induced dysplasias in hybrid mice were ovary-dependent for tumorigenesis and tumor growth. The transplantation experiments confirmed the hypothesis that ductal dysplasias have high tumorigenic potentials and can be classified as "high-risk" lesions, similar to murine mammary tumor virus-induced hyperplastic alveolar nodules.
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PMID:Serial transplantation of chemical carcinogen-induced mouse mammary ductal dysplasias. 10 3

Because there is strong evidence for the involvement of Epstein-Barr virus in the etiology of Burkitt's lymphoma and nasopharyngeal carcinoma, we have discussed the relationship of Epstein-Barr virus to these two diseases in the context of geographic distribution, pathology, epidemiology, genetics, immunovirology, and biochemistry. We have also discussed the relationship of Epstein-Barr virus to other diseases, both malignant and non-malignant. Although the etiologic relationship of herpes simplex virus type 2 to squamous carcinoma of the uterine cervix is not on as firm ground, we feel that some good evidence does exist. We have also discussed two oncogenic simian viruses, Herpesvirus saimiri and Herpesvirus ateles. These have a great number of similarities to EBV, and thus may provide models for the study of viral-induced oncogenesis in man. Agents similar to Epstein-Barr virus have been isolated from old world monkeys. These may possibly be of greater importance than either Herpesvirus saimiri or Herpesvirus ateles in the investigation of human virally-induced cancers.
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PMID:Herpesviruses and cancer in man and subhuman primates. 18 59

Five brothers of from 6 to 18 years of age experienced immunological or neoplastic disorders during an 8-year interval. 2 boys succumbed to glioblastoma multiforme, another to metastatic carcinoma, and the 2 surviving brothers had a histiocytic lymphoma and idiopathic thrombocytopenia purpura, respectively. The mother of the boys was healthy, but her twin sister died in utero of birth defects. We suggest that an intrinsic cellular defect inherited from their mother rendered the boys vulnerable to oncogenesis.
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PMID:Immunological disorders and malignancies in five young brothers. 19 48

The etiology of cancer resembles that of many other diseases in that multiple factors may be required. Because of this, the role or viruses in the etiology of human cancers is especially difficult to assess. When animal tumor systems were used as models, the roles of various predisposing characteristics in virus oncogenesis were elucidated. Extrapolation of these findings to the human diseases suggests the importance of genetics, age, hormones, immune competence, and stress in determining susceptibility to tumor development in individuals infected with an oncogenic virus. The importance of cofactors in induction of those human tumors most strongly associated with virus infection, including Burkitt's lymphoma, nasopharyngeal carcinoma, cerviccal carcinoma, acute myelogenous leukemia, and breast cancer, is reviewed. Understanding of the role of these cofactors in virus carcinogenesis may lead to disease prevention through elimination of one or more of the cofactors.
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PMID:The viral etiology of cancer: a realistic approach. 19 10

This paper describes two different experiments of nature: 1) the persistence of unusual virus strains of Epstein-Barr virus (EBV) (which proved oncogenic in vitro) and cytomegalovirus (CMV) in lymphoid cells following congenital or early acquired infection; 2) the occurence of multiple cases of Burkitt's lymphoma and nasopharyngeal carcinoma in one family. All the members of this family were EBV viral capsid antigen (VCA) and nuclear antigen (EBNA) antibody positive. The two patients with nasopharyngeal carcinoma had high titers of EBV-VCA, EA, and EBNA antibodies. The only member of this family having EBV early antigen (EA antibodies in addition to the patients with tumors was the mother. Borderline IgA deficiency was documented in 3 members of this family. These findings illustrate the importance of host factors (intracellular resistance to transformation and secondarily, immunological surveillance) in the outcome of the host-virus challenge whether cancer or infectious disease is the outcome. Extensive studies of these cases may provide the best insight into the mysteries of viral oncogenesis.
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PMID:Viral attributes and host factors in carcinogenesis: herpesviruses. 20 Sep 83

The avian carcinoma virus MC29 (MC29V) contains a sequence of approximately 1,500 nucleotides which may represent a gene responsible for tumorigenesis by MC29V. We present evidence that MC29V has acquired this nucleotide sequence from the DNA of its host. The host sequence which has been incorporated by MC29V is transcribed into RNA in uninfected chicken cells and thus probably encodes a cellular gene. We have prepared radioactive DNA complementary to the putative MC29V transforming gene (cDNA(mc) (29)) and have found that sequences homologous to cDNA(mc) (29) are present in the genomes of several uninfected vertebrate species. The DNA of chicken, the natural host for MC29V, contains at least 90% of the sequences represented by cDNA(mc) (29). DNAs from other animals show significant but decreasing amounts of complementarity to cDNA(mc) (29) in accordance with their evolutionary divergence from chickens; the thermal stabilities of duplexes formed between cDNA(mc) (29) and avian DNAs also reflect phylogenetic divergence. Sequences complementary to cDNA(mc) (29) are transcribed into approximately 10 copies per cell of polyadenylated RNA in uninfected chicken fibroblasts. Thus, the vertebrate homolog of cDNA(mc) (29) may be a gene which has been conserved throughout vertebrate evolution and which served as a progenitor for the putative transforming gene of MC29V. Recent experiments suggest that the putative transforming gene of avian erythroblastosis virus, like that of MC29V, may have arisen by incorporation of a host gene (Stehelin et al., personal communication). These findings for avian erythroblastosis virus and MC29V closely parallel previous results, suggesting a host origin for src (D. H. Spector, B. Baker, H. E. Varmus, and J. M. Bishop, Cell 13:381-386, 1978; D. H. Spector, K. Smith, T. Padgett, P. McCombe, D. Roulland-Dussoix, C. Moscovici, H. E. Varmus, and J. M. Bishop, Cell 13:371-379, 1978; D. H. Spector, H. E. Varmus, and J. M. Bishop, Proc. Natl. Acad. Sci. U.S.A. 75:4102-4106, 1978; D. Stehelin, H. E. Varmus, J. M. Bishop, and P. K. Vogt, Nature [London] 260:170-173, 1976), the gene responsible for tumorigenesis by avian sarcoma virus. Avian sarcoma virus, avian erythroblastosis virus, and MC29V, however, induce distinctly different spectra of tumors within their host. The putative transforming genes of these viruses share no detectable homology, although sequences homologous to all three types of putative transforming genes occur and are highly conserved in the genomes of several vertebrate species. These data suggest that evolution of oncogenic retroviruses has frequently involved a mechanism whereby incorporation and perhaps modification of different host genes provides each virus with the ability to induce its characteristic tumors.
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PMID:DNA and RNA from uninfected vertebrate cells contain nucleotide sequences related to the putative transforming gene of avian myelocytomatosis virus. 22 69

One thousand common "epithelial" tumours of the ovary were encountered in a 25-yr study period at the King George V Memorial Hospital. These tumours were classified according to the World Health Organisation (W.H.O.) Histological Classification of Ovarian Tumours. In this report a detailed histological assessment of the 298 malignant "epithelial" tumours is presented, including criteria for histological grading and typing. Evidence for the multifocal tumorigenesis of serous tumours and the pathological correlates of endometrioid carcinoma are stressed.
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PMID:The pathological assessment of ovarian neoplasms. III: The malignant "epithelial" tumours. 23 Apr 44

A significant aspect of primary hepatic carcinoma in man is the high positive correlation of hepatocellular carcinoma with infection with hepatitis B virus (HBV)1. Analysis of the relationship between HBV infection and oncogenesis is difficult because natural infection with HBV is limited to man and experimental infection has been achieved only in chimpanzees and gibbons. Furthermore, because HBV has not been successfully propagated in cell culture, basic study of virus-cell interaction of the aetiological agent of one of the most widespread infections of man has been impossible. Recently, however, a cell line (PLC/PRF/5) derived from a human hepatoma biopsy was described which produces the HRV surface antigen (HBsAg) and so provides a tool for the experimental investigation of HBV in viro. We now report the derivation and characterisation of two additional cell lines primary liver carcinomas. In contrast to the PLC/PRF/5 cell line, these cell lines retain the capacity to synthesise many human plasma proteins, including both albumin and alpha-fetoprotein (AFP). One of these lines also produces BHsAg. We also present evidence that HBsAg synthesis and secretion in this cell line are correlated with the growth state of the culture. This finding is in contrast to the continuous HBsAg production found in the PLC/PRF/5 cell line.
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PMID:Controlled synthesis of HBsAg in a differentiated human liver carcinoma-derived cell line. 23 37


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