Literature DB >> 3463446

Suppression of tumorigenicity in somatic cell hybrids. IV. Chromosomes of normal human cells associated with suppression of tumorigenicity in hybrids with D98AH2 carcinoma cells.

H P Klinger, M Kaelbling.   

Abstract

An analysis for cosegregation of chromosomes and tumorigenicity in 52 hybrids of human diploid X D98AH2 human carcinoma-derived cells reveals the consistent presence of four copies of chromosome 11 in all nontumorigenic hybrids (two from each of the parental cells) and a consistent loss of one or two copies of the 11 in all tumor cells derived from tumorigenic hybrids that grow in nude mice. In our earlier study, assays with restriction fragment length polymorphic (RFLP) markers for the cell parent origin of the chromosomes 11 in the hybrids indicated that at least one of the Nos. 11 lost in the tumor cells is from the diploid. Thus both Nos. 11 of the diploid seem to be required for complete and stable suppression of the tumorigenic phenotype. The results of the present study suggest that chromosome 2 may also carry suppressor information, but this causes only partial suppression of the tumorigenic phenotype in the absence of both Nos. 11. On the other hand, when the hybrids contain full complements of the 2 and the 11, suppression is very stable. All other chromosomes except for Nos. 1, 16, 17, 19, and 21 are clearly discordant with suppression. The latter chromosomes are not discordant often enough to allow their exclusion as possible carriers of suppressor information, particularly in the absence of RFLP evaluations. It is clear, however, that if they do carry such information it is not adequate for maintaining a stably suppressed phenotype in the absence of both Nos. 11 of the diploid.

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Year:  1986        PMID: 3463446     DOI: 10.1159/000132283

Source DB:  PubMed          Journal:  Cytogenet Cell Genet        ISSN: 0301-0171


  7 in total

1.  Levels of fos, ets2, and myb proto-oncogene RNAs correlate with segregation of chromosome 11 of normal cells and with suppression of tumorigenicity in human cell hybrids.

Authors:  B M O'Hara; H P Klinger; T Curran; Y D Zhang; D G Blair
Journal:  Mol Cell Biol       Date:  1987-08       Impact factor: 4.272

2.  Alterations of chromosome 11q13 in cervical carcinoma cell lines.

Authors:  N C Popescu; D B Zimonjic
Journal:  Am J Hum Genet       Date:  1996-02       Impact factor: 11.025

3.  Nonrandom duplication of the chromosome bearing a mutated Ha-ras-1 allele in mouse skin tumors.

Authors:  A B Bianchi; C M Aldaz; C J Conti
Journal:  Proc Natl Acad Sci U S A       Date:  1990-09       Impact factor: 11.205

4.  Molecular nature of genetic changes resulting in loss of heterozygosity of chromosome 11 in Wilms' tumours.

Authors:  M Mannens; R M Slater; C Heyting; J Bliek; J de Kraker; N Coad; P de Pagter-Holthuizen; P L Pearson
Journal:  Hum Genet       Date:  1988-12       Impact factor: 4.132

5.  Induction of anchorage-independent growth of human embryonic fibroblasts with a deletion in the short arm of chromosome 11 by human papillomavirus type 16 DNA.

Authors:  H L Smits; E Raadsheer; I Rood; S Mehendale; R M Slater; J van der Noordaa; J ter Schegget
Journal:  J Virol       Date:  1988-12       Impact factor: 5.103

6.  HeLa D98/aH-2 studied by chromosome painting and conventional cytogenetical techniques.

Authors:  D Ruess; L Z Ye; C Grond-Ginsbach
Journal:  Chromosoma       Date:  1993-07       Impact factor: 4.316

7.  Construction of mouse A9 clones containing a single human chromosome (X/autosome translocation) via micro-cell fusion.

Authors:  M Koi; H Morita; M Shimizu; M Oshimura
Journal:  Jpn J Cancer Res       Date:  1989-02
  7 in total

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