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

Stoler, Andrea; Bouck, Noël

doi:10.1073/pnas.82.2.570

Cited by 69 publications

(44 citation statements)

References 47 publications

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“…Thrombospondin has a number of regulatory elements in its complex promoter region, including AP-1, AP-2, Spl, SRE, and many others. It has already been reported that thrombospondin gene expression is dependent on the expression of an unknown tumor suppressor gene, which is presumably located on human chromosome 1 (30). Inactivation of this chromosome 1-related gene following transformation resulted in the inactivation of thrombospondin and the loss of angiogenesis-suppressing activity (9,27).…”

Section: Resultsmentioning

confidence: 99%

Loss of thrombospondin transcriptional activity in nickel-transformed cells.

Salnikow¹,

Cosentino²,

Klein³

et al. 1994

Mol. Cell. Biol.

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Nickel and its compounds are among the few well-documented human carcinogens, and only recently have the molecular mechanisms of Ni carcinogenesis been addressed (6). Ni ions have a much higher affinity for proteins than for DNA, and thus Ni compounds have been found to selectively damage protein-rich heterochromatic chromosomal regions (3-6). In Chinese hamster (CH) cells the longest contiguous region of heterochromatin is found on the X chromosome. This is thought to explain the disproportionately high incidence of transformation among male Chinese hamster embryo (CHE) cells compared with female cells, since over half of the male Ni-transformed cells had a complete deletion of the long arm of the X chromosome as their primary chromosomal aberration (3). The striking deletion of protein-rich heterochromatin may simply model other protein-DNA interactions occurring in genetically active promoter regions. CHE cells are used in cell transformation studies because, unlike mouse cells, they can be transformed by nickel compounds with a low spontaneous background. Human cells are not generally transformed by chemical carcinogens, and other mammalian cell types (e.g., mouse cells) exhibit such high transformation backgrounds that it is difficult to attribute the transformation to the carcinogen treatment.

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Section: Resultsmentioning

confidence: 99%

Loss of thrombospondin transcriptional activity in nickel-transformed cells.

Salnikow¹,

Cosentino²,

Klein³

et al. 1994

Mol. Cell. Biol.

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“…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%

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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“…Screening of genetic databases revealed the possible location on chromosome 1 of a locus with a malignant transformation suppression activity (Stoler and Bouck, 1985). Because of syntheny with mouse chromosome 4, the locus identi®ed by Stodler and Bouck is likely to map on 1p, distal to 1p22.1 (Zabel et al, 1985).…”

mentioning

confidence: 99%

The human growth factor-inducible immediate early gene, CYR61, maps to chromosome 1p

et al. 1997

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Complementary DNA encoding the human CYR61 protein was isolated from human embryonic tissues and mapped to chromosome 1p22-p31. We show that CYR61 encodes a 381 amino acid protein rich in cysteine and proline residues that is strongly conserved with the mouse homologue. Sequence analysis reveals the presence of several distinct protein domains which confer a mosaic structure to this protein and makes human CYR61 a member of a recently described growth regulator family that includes several proto-oncogene products. From our results we hypothesize that this new immediate early gene may play a role in cell commitment during embryogenesis and more generally in the control of cell proliferation.

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

Cited by 69 publications

References 47 publications

Loss of thrombospondin transcriptional activity in nickel-transformed cells.

Loss of thrombospondin transcriptional activity in nickel-transformed cells.

Recessive mechanisms of malignancy

The human growth factor-inducible immediate early gene, CYR61, maps to chromosome 1p

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