Display options
Cite
Doneda L, Custode P, Morghen Cde G, et al. Localization of viral transforming sequences within marker chromosomes associated with tumor formation and progression in a murine fibrosarcoma. Cytotechnology. 1987;1(1):47-55doi: 10.1007/BF00351122.
Doneda, L., Custode, P., Morghen, C. d. e. . G., & Larizza, L. (1987). Localization of viral transforming sequences within marker chromosomes associated with tumor formation and progression in a murine fibrosarcoma. Cytotechnology, 1(1), 47-55. https://doi.org/10.1007/BF00351122
Doneda, L, et al. "Localization of viral transforming sequences within marker chromosomes associated with tumor formation and progression in a murine fibrosarcoma." Cytotechnology vol. 1,1 (1987): 47-55. doi: https://doi.org/10.1007/BF00351122
Doneda L, Custode P, Morghen Cde G, Larizza L. Localization of viral transforming sequences within marker chromosomes associated with tumor formation and progression in a murine fibrosarcoma. Cytotechnology. 1987 Oct;1(1):47-55. doi: 10.1007/BF00351122. PMID: 22358440.
Copy Download .nbib Format: NLM
Share it on

Cytotechnology. 1987 Oct;1(1):47-55. doi: 10.1007/BF00351122.

Localization of viral transforming sequences within marker chromosomes associated with tumor formation and progression in a murine fibrosarcoma.

Cytotechnology

L Doneda, P Custode, C de G Morghen, L Larizza

Affiliations

  1. Dipartimento di Biologia e Genetica per le Scienze Mediche, Università degli Studi di Milano, Via Viotti 5, I-20133, Milano, Italy.

PMID: 22358440 DOI: 10.1007/BF00351122

Abstract

The low-metastatic RSV-transformed fibrosarcoma line B77-3T3 and its metastatic variant AA12, selected in vitro, have been analysed by blot and in situ hybridization with v-src and murine c-myc specific probes in order to detect molecular rearrangements underlying the transition from the low-metastatic to the high-metastatic phenotype. Previous cytogenetic analysis had evidenced that a marker chromosome of the parental tumor line (chromosome A) is replaced in the metastatic counterpart by a new marker chromosome (chromosome B), possibly arisen by duplication of a chromosome A segment, included between two C-positive regions (L. Doneda et al., 1985). In situ hybridization on chromosome spreads of the two related lines with a (3)H-labelled v-src probe showed that src sequences are located within the marker chromosomes A and B, and the percentage of grains over the AA12 marker chromosome is always double that found on the B77-3T3 marker. These signals were considered to identify v-src sequences as they were found to be slightly amplified in the metastatic variant DNA by blot hybridization with the v-src probe. As regards the intrachromosomal location of the signals, most grains were clustered near the heterochromatic bands, suggesting a possible role for heterochromatic sites in tumor formation and evolution. No involvement of the A and B marker chromosomes was shown by in situ hybridization experiments with a c-myc probe. However the dosage of c-myc sequences was also found to be slightly increased in the metastatic variant DNA.

References

  1. Nucleic Acids Res. 1976 Sep;3(9):2303-8 - PubMed
  2. Int J Cancer. 1982 Dec 15;30(6):751-7 - PubMed
  3. Nature. 1980 Sep 18;287(5779):198-203 - PubMed
  4. Int J Cancer. 1983 Apr 15;31(4):455-61 - PubMed
  5. Chromosoma. 1981;83(3):431-9 - PubMed
  6. Cell. 1981 Jan;23(1):29-39 - PubMed
  7. Mol Cell Biol. 1986 May;6(5):1787-95 - PubMed
  8. Cancer Genet Cytogenet. 1985 Feb 15;15(3-4):283-91 - PubMed
  9. Cancer Genet Cytogenet. 1981 Apr;3(3):261-72 - PubMed
  10. J Mol Biol. 1977 Jun 15;113(1):237-51 - PubMed
  11. Nature. 1985 May 23-29;315(6017):345-7 - PubMed
  12. Nature. 1983 Jun 2-8;303(5916):401-6 - PubMed
  13. Exp Cell Res. 1972 Jan;70(1):253-6 - PubMed
  14. Nature. 1982 Mar 18;296(5854):219-25 - PubMed

Publication Types