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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary cultures of human umbilical vein endothelial cells (HEC) developed extensive cytopathic changes and necrosis after high multiplicity infection with wild-type SV40 virus. Using the calcium co-precipitation technique, stable transformation was obtained with purified preparations of intact circular SV40 DNA and restriction endonuclease-derived linear DNA fragments containing the entire early gene region. Smooth muscle cells, isolated from the same blood vessels, showed neither cytopathic effects nor transformation after similar treatment with SV40 virus or DNA. The HEC cultures transformed by SV40 (SVHEC) expressed SV40-specific T (tumor) and Tr (transplantation) antigens, but not V (viral capsid) antigen. No evidence of infectious virus production was found upon co-cultivation with the CV-1 line of monkey kidney cells. Transformation resulted in markedly increased growth potential, loss of anchorage dependence and topoinhibition of growth, and a reduced serum requirement. Prolonged subcultivation was accompanied by chromosomal abnormalities and eventual "crisis". Transformed cells did not exhibit endothelial-specific organelles (Weibel-Palade bodies) or factor VIII antigen, but angiotensin-converting enzyme occasionally was detectable in SVHEC cultures. SV40-transformed human vascular endothelium, a nonfibroblast diploid cell type, may be useful in studies of oncogenesis and control of the differentiated state.
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PMID:Transformation of cultured human vascular endothelium by SV40 DNA. 18 41

The effects of neonatal and perinatal thymectomy on mammary tumorigenesis in (C57BL X I)F1fC3H hybrid female mice were determined. When hybrid females were neonatally thymectomized by controlled suction, a procedure that removes thymic lobes completely, a large proportion of animals developed stigmas of a fulminant wasting disease and died before tumors developed. However, when hybrid females were subjected to neonatal thymectomy by continuous suction, a procedure that resulted in retention of thymic remnants, they survived and manifested a significant prolongation of latent period before tumorigenesis. When complete removal of the thymus was carried out in the perinatal period, the effect on mammary tumorigenesis was critically dependent on the age at surgery. The procedure was without effect when performed at 1, 3, and 8 weeks of age. However, when it was performed at 9-12 days of age, there was a delay or a decrease in the appearance of mammary tumors. The extent of T-cell depletion and/or its timing in relationship to the introduction of murine mammary tumor virus appeared to play a critical role in determining the effect on eventual tumor development.
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PMID:Inhibition of mammary tumors by incomplete T-cell depletion. 19 Apr 16

It is unequivocal that prolactin is an influential hormone in murine mammary tumorigenesis. The Berenblum hypothesis (7), a well-known theoretical model of tumorigenesis that depicts this oncogenic process as a two-step mechanism, i.e., initiation and promotion, is a conceptual scheme in which the action of prolactin in mammary tumorigenesis may be understood. According to this conceptual model, prolactin would participate in both the initiation and promotion steps of mammary tumorigenesis, In the initiation phase, variations in prolactin secretion appear to influence the metabolism of the mammary epithelium, so that the epithelium would be either more receptive to or refractory to an initiating agent (e.g., chemical carcinogen, physical carcinogens, oncogenic viruses, ets.) i.e., a permissive action. In the promotion phase, prolactin may act as either a promoter or an antipromoter of the "transformed" mammary epithelium. In promotion, the hormone may either directly or indirectly (via the ovary) stimulate mitotic activity of the "transformed" epithelium. In antipromotion the hormone, in the presence of requisite hormones (e.g., glucocorticoids), may synergistically induce differentiation (e.g., lactation) in the "transformed" epithelium. A tumor would result in the former (promotion) but not in the latter (antipromotion) case. Whether or not prolactin is significantly influential in human breast tumorigenesis remains to be determined. This is an extremely important area of research which is justifiably receiving increased attention. For if prolactin can be shown to influence human breast epithelium in a manner similar to its effect on rodent mammary tissue, then prophylactic and/of chemotherapeutic control of human breast tumorigenesis may be feasible by appropriate drug-mediated prolactin suppression.
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PMID:Prolactin and murine mammary tumorigenesis: a review. 19 Nov 83

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

All known tumor types have been reported in the neonate. A numerical listing and discussion are beyond the scope of this review. Wells and Fraumeni give some insight into common congenital malignant neoplasms. Table 2 lists the percentage of neonatal deaths caused by type-specific cancers. Retinoblastoma is probably the most common malignant tumor in the neonate. About seven per cent of these tumors have been apparent at birth. This tumor is not discussed in either article because it is not lethal until muypes in neonatal and pediatric patients. Some congenital malformations in the in the neonate are recognized as being frankly benign (cysts), potentially malignant (teratomas), and frankly malignant (neuroblastoma). A high percentage of teratomas are benign in the newborn period. Leukemia in the newborn appears to be more aggressive yet neuroblastoma has a better prognosis. More studies are needed to help us define why the neonate does better with some tumors and worse with others. Surface cell markers on neonatal leukemia, B and T cell function studies, and other immunologic surveillance studies are needed. Study of neonatal oncology may add to our knowledge of carcinogenesis and oncogenesis in the future.
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PMID:Neonatal oncology. 19 75

Mammary tumorigenesis in genetic crosses between the high mammary tumor incidence GR and the low incidence C57BL mouse strains is highly correlated with murine mammary tumor virus expression in milk. Although the F1 and first backcross females had a mammary tumor incidence which was consistent with a single dominant gene segregation, the tumor incidence in the critical second backcross segregants disproved the single gene hypothesis. Genetic factors were clearly involved in regulation of virus expression which in turn correlated with both tumor incidence and tumor latency; these complex phenotypes are however best explained as threshold or quasicontinuous characters. As predicted from this model, the age specific incidence of mammary tumors showed a broad peak at 14-19 mo of age with no evidence of an early or late phase. Hematopoietic tumors showed no correlation with virus expression or mammary tumorigenesis suggesting different etiologies for these tumors.
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PMID:Mammary tumors and mammary tumor virus expression in hybrid mice of strains C57BL and GR. 20 Jun 97

Using electrophysiological techniques we have examined the apical membrane ionic permeabilities of primary cell cultures of the mouse mammary gland in the midpregnant, preneoplastic, and neoplastic states. Membrane Na+ permeability changed with tumorigenesis, whereas K+ and Cl- permeabilities were unaltered. With tracer flux techniques the unidirectional efflux rate constant of 22Na was found to be greater in tumor cells than it is in normal cells. This increase in 22Na efflux was eliminated by the addition of ouabain. The results are interpreted as an increase in Na+ permeability and in Na+-K+-ATPase activity with the neoplastic transformation. The presence or absence of the virus in midpregnant cells does not seem to affect Na+ permeability.
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PMID:Alteration of sodium transport in mouse mammary epithelium associated with neoplastic transformation. 20 64

Mammary tumorigenesis and mammary tumor transplantation immunogenicity have been studied and compared in three sublines of the C3H strain: in standard mammary tumor virus (MTV-S)-infected C3H/He mice; in MTV-S-infected C3H/Ki mice; and in MTV-S-free C3Hf/He mice. The age at the appearance of the first tumor, the growth rate of the tumors in their first transplant generation, and the immunogenicity of each tumor in syngeneic female recipients have been determined for the first tumor to appear in each of 25 breeding females from each of the three sublines. Two statistically significant trends were evident among the tumor characteristics compared in the three sublines: (a) an early appearance of tumors was related to the presence of the MTV-S. The genetically dissimilar sublines, C3H/He and C3H/Ki, both infected with the MTV-S, developed mammary tumors at an average age of about 10 months, 11 months before MTV-S-free C3Hf/He mice; (b) the tumor characteristics of immunogenicity and growth stimulation were related to host genetic factors. The genetically similar sublines, C3H/He and C3Hf/He, developed similar proportions of immunogenic and growth-stimulating mammary tumors; the genetically divergent C3H/Ki subline developed tumors that were not immunogenic and tended to be strongly growth stimulating.
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PMID:Mammary tumor virus oncogenesis and tumor immunogenicity in three sublines of the C3H mouse. 20 67

Data on 148 cases of liver tumor in women have been registered. Analysis of these data shows that 1) the average age is 30.3 years; 2) 85% of the patients had a history of oral contraceptive use; 3) pain was the most usual symptom followed by incidental discovery during an operation; 4) 19 were hepatomas, 56 were adenomas, 67 were focal nodular hyperplasia, and 6 were unclassified; and 5) 67% of the benign tumors were in the right lobe, there were 15 cases of multiple focal nodulat hyperplasia and 11 cases of multiple adenomas, and several of the adenomas were only partially encapsulated. The histopathologic differentiation of focal nodular hyperplasia from adenomas can be obtained by detection of the presence of bile duct epithelium in focal nodular hyperplasia; this is always absent in adenoma. Of the 19 patients with hepatomas, 12 have died (7 had metastasis, 3 deaths were related to the operative status), 2 are near death, and 5 are alive following resection. Treatment in most cases was resection or lobectomy, but biopsy only was performed in 22 cases of benign tumor. Follow-up of these cases should add to the knowledge about the necessity extent of surgery. The possible relationship of oral contraceptive use to liver oncogenesis is as yet undefined, but the incidence of tumors is very low considering the numbers of women who are current users of steroid contraceptives. Benign tumors have been reported to involute after discontinuation of steroidal medication. This therapeutic dilemma may be resolved when the patients in this series who underwent biopsy only have been followed for a longer interval.
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PMID:Liver oncogenesis and steroids. 21 80

Adult mice were immunized with varying doses of inactivated Moloney murine leukemia virus (M-MuLV). Eight weeks after immunization, mice were challenged with a dose of Moloney murine sarcoma virus (M-MuSV) that could induce tumors in approximately 50% of normal animals. Mice immunized with high doses of M-MuLV (10(10) particles) had significantly decreased tumor incidences, whereas mice immunized with low doses of M-MuLV (10(2) particles) had significnatly increased tumor incidences compared to those in nonimmunized controls. The stimulatory effect could be abrogated by the irradiation of mice with 450 rads 24 hours prior to M-MuSV challenge, whereas the inhibitory effect was resistant to this irradiation procedure. The results suggested that immunization with virus can either stimulate or inhibit virus-induced tumorigenesis, depending on the dose of virus used for immunization.
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PMID:Stimulatory effect of immunization on tumor induction by Moloney murine sarcoma virus. 21 13


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