Viral oncogenes

Bishop, J. Michael

doi:10.1016/s0092-8674(85)80098-2

Cited by 668 publications

(259 citation statements)

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“…These oncogenes arise because of mutations that deregulate expression of the proto-oncogene or affect the structure of the encoded protein (Bishop, 1985;Weinberg, 1985). Once created, oncogenes are thought to confer a growth advantage, thus facilitating clonal expansion of the mutant cell.…”

Section: Discussionmentioning

confidence: 99%

N-myc amplification causes down-modulation of MHC class I antigen expression in neuroblastoma

Bernards

Dessain

Weinberg

1986

Cell

262

151

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Section: Discussionmentioning

confidence: 99%

N-myc amplification causes down-modulation of MHC class I antigen expression in neuroblastoma

Bernards

Dessain

Weinberg

1986

Cell

262

151

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“…The more recently developed concept of infection with oncogenic viruses or of activation of proto-oncogenes (7,8) as the causative events in cancer has been explained by action of oncogene products on adult cells causing transformation to malignant phenotype (dedifferentiation). This explanation is supported by the observation that transfection or activation of oncogenes can cause proliferative changes in apparently mature cells in tissue culture.…”

Section: Embryonal Theory Of Cancermentioning

confidence: 99%

Cellular origin of cancer: dedifferentiation or stem cell maturation arrest?

Sell

1993

Environ Health Perspect

189

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Given the fundamental principle that cancer must arise from a cell that has the potential to divide, two major nonexclusive hypotheses of the cellular origin of cancer are that malignancy arises a) from stem cells due to maturation arrest or b) from dedifferentiation of mature cells that retain the ability to proliferate. The role of stem cells in carcinogenesis is clearly demonstrated in teratocarcinomas. The malignant stem cells of teratocarcinomas are derived from normal multipotent stem cells and have the potential to differentiate into normal benign mature tissue. A widely studied model supporting dedifferentiation has been the putative origin of hepatocarcinomas from "premalignant" foci and nodules induced in the rat liver by chemicals. However, the dedifferentiation concept for hepatocarcinogenesis is challenged by more recent interpretations indicating that hepatocellular carcinoma arises from maturation arrest caused by abherrant differentiation of determined stem cells. Either hypothesis is supported by the cellular changes that occur in the rodent liver after different hepatocarcinogenic regimens. The formation of foci and nodules from altered hepatocytes supports dedifferentiation; the proliferation of small oval cells with the potential to differentiate into either biliary ducts or hepatocytes supports arrested maturation of determined stem cells. It is now postulated that foci and nodular change reflect adaptive changes to the toxic effects of carcinogens and not "preneoplastic" stages to cancer. The stem cell model predicts that genotoxic chemicals induce mutations in the determined stem cell which may be expressed in its progeny. Proliferation of initiated cells is induced by promoting events which also allow additional mutations to occur.

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“…Morphological transformation of primary cells is a multistep phenomenon (reviewed in Bishop, 1985;Stanbridge, 1990). In this report, the multistep nature of transformation was examined using two primary human cell types derived from gingival tissue.…”

Section: Introductionmentioning

confidence: 99%

Characterization of primary human fibroblasts transformed by human papilloma virus type 16 and herpes simplex virus type 2 DNA sequences

Dhanwada

Veerisetty

Zhu

et al. 1992

Journal of General Virology

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Human papilloma virus type 16 (HPV-16) and herpes simplex virus type 2 (HSV-2) are human viruses implicated in the development of cancer, in particular cervical cancer. The ability of HSV-2 and HPV-16 to transform early passage human cells was examined in this report. For these studies, gingival fibroblasts were utilized. One gingival cell strain was derived from a normal individual (N-16). The second cell strain was derived from hyperplastic gingival tissue of an epileptic individual (R-30) treated with phenytoin, an antiseizure drug. A common side effect of phenytoin is the induction of gingival overgrowth. R-30 cells contained a stable chromosomal translocation between chromo-

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Viral oncogenes

Cited by 668 publications

References 0 publications

N-myc amplification causes down-modulation of MHC class I antigen expression in neuroblastoma

N-myc amplification causes down-modulation of MHC class I antigen expression in neuroblastoma

Cellular origin of cancer: dedifferentiation or stem cell maturation arrest?

Characterization of primary human fibroblasts transformed by human papilloma virus type 16 and herpes simplex virus type 2 DNA sequences

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