Suppression of tumorigenicity

Hp, Klinger

doi:10.1159/000131688

Cited by 66 publications

(19 citation statements)

References 3 publications

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“…Chromosome analysis reveals that the tumorigenic segregants have lost several chromosomes originally present in the nontumorigenic hybrid cells. These results have now been confirmed by extensive studies of rodent and human intraspecies hybrids (Miller & Miller, 1983;Sager, 1985;Stanbridge, 1987) together with rodent x human interspecies hybrids (Klinger, 1982). The simplest interpretation of these observations is that non-malignant cells contain one or more tumour suppressor genes that are capable of repressing aspects of the malignant phenotype, and which are presumably inactive in, or absent from, malignant cells.…”

Section: Tumour Suppressor Genesmentioning

confidence: 86%

“…However the rapidity with which human chromosomes are lost still provides a serious obstacle since reexpression of malignancy is usually associated with the loss of multiple chromosomes. It is therefore not surprising that both of these approaches have usually failed to identify specific suppressor chromosomes although there are a few notable exceptions to this (Klinger, 1982;Evans et al, 1982;Stoler & Bouck, 1985).…”

Section: Tumour Suppressor Genesmentioning

confidence: 99%

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Recessive mechanisms of malignancy

Green

1988

Br J Cancer

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It is increasingly recognised that recessive mutations play an important role in the pathogenesis of many forms of malignancy. Some of the affected loci may prove to be recessively-activated proto-oncogenes, but others are now known to be tumorigenic solely by virtue of their loss or inactivation and therefore form a distinct and novel family of tumour genes. Preliminary evidence suggests that such genes are likely to be functionally heterogeneous and to encode molecules involved in the inhibition of cellular proliferation and/or the induction of differentiation. Their further study is likely to illuminate fundamental mechanisms of normal cellular growth and differentiation as well as having important implications for the pathogenesis and management of cancer.

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Section: Tumour Suppressor Genesmentioning

confidence: 86%

Section: Tumour Suppressor Genesmentioning

confidence: 99%

Recessive mechanisms of malignancy

Green

1988

Br J Cancer

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“…Several lines of evidence associate the inactivation of a diploid pair of suppressor alleles with the development of retinoblastoma (1,2), and evidence is accumulating that similar events are involved in the genesis of other hereditary tumors (3)(4)(5). In vitro cell fusions both within and across species involving human tumor lines not derived from hereditary cancers also indicate that malignancy is recessive (6)(7)(8)(9)(10)(11)(12). This recessiveness implies that during the process of carcinogenesis there has been a loss of some function that maintains normal constraints on growth.…”

mentioning

confidence: 99%

Identification of a single chromosome in the normal human genome essential for suppression of hamster cell transformation.

Stoler¹,

Bouck²

1985

Proc. Natl. Acad. Sci. U.S.A.

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“…Another line of evidence, suggesting that human cells are more resistant to tumorigenesis than are rodent cells, comes from the stable nontumorigenicity of human cell hybrids produced by fusion between normal and tumor-derived (i.e., HeLa) cells of human origin (16,17). Human cell hybrids of this type are much more stable than the analogous intraspecies cell hybrids of rodent origin.…”

mentioning

confidence: 99%

Resistance of human cells to tumorigenesis induced by cloned transforming genes.

Sager¹,

Tanaka²,

Lau³

et al. 1983

Proc. Natl. Acad. Sci. U.S.A.

130

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The transformation of human cells was examined by transfection of cloned oncogenic DNAs derived from the tumor virus simian virus 40 and from the human bladder carcinoma cell line EJ into diploid fibroblasts derived from foreskin Modern cancer research has been caught for some years on the horns of a dilemma: the concept of neoplastic transformation in a single step based largely on the studies of tumor viruses in animal systems and the vast evidence, both clinical and experimental, of neoplasia as a multistage process. A synthesis of these opposing views has begun as a consequence of the availability of a new set of analytical reagents called oncogenes, which are cloned fragments of DNA with transforming activity.Oncogenes have been recognized by two kinds of experiments: identification by mutational analysis of transforming sequences in the genomes of avian and rodent retroviruses and identification of transforming sequences (in some instances related to retroviral transforming genes) in DNAs of tumor origin by their ability to induce oncogenic transformation of NIH/3T3 mouse cells (1). These experiments have been interpreted as support for the single-step origin of tumorigenicity, but the recipients being tested were either preneoplastic cells (e.g., NIH/ 3T3) that had already undergone unspecified genomic changes or animals infected with multifunctional viruses (i.e., containing long terminal repeats as well as transforming genes). Recently, transfection experiments using early passage rodent cells instead of established cell lines have implicated multiple oncogenes in animal cell culture models of neoplasia (2-4). These results herald a growing recognition among virologists that oncogenesis is a multistage process. The problem now is to identify the multiple stages in terms of specific genes and specific functions. As yet, neither the number nor the nature of essential functions required for tumorigenic transformation of rodent cells is known.Superimposed on this hiatus in our knowledge is the question of the appropriateness of rodent cells as model systems in

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Suppression of tumorigenicity

Cited by 66 publications

References 3 publications

Recessive mechanisms of malignancy

Recessive mechanisms of malignancy

Identification of a single chromosome in the normal human genome essential for suppression of hamster cell transformation.

Resistance of human cells to tumorigenesis induced by cloned transforming genes.

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