Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 107 (1984), S. 172-177 
    ISSN: 1432-1335
    Keywords: Two rat tumor cell lines ; Karyotype/G-banding ; DMs/HSR ; Metastasis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The rat tumor cell lines BSp73AS (AS, nonmetastasizing with pronounced adherent capacities) and BSp73ASML (ASML, highly metastasizing with reduced adherent capacities) were cytogenetically investigated. The ASML cell line.is reportedly derived from the AS cell line. Both lines exhibited abnormal numerical and structural chromosomal characteristics. The metastasizing ASML cells showed a higher chromosome number (modal number: 62–63) than the nonmetastasizing AS cells (modal number: 48). The AS karyotype was characterized by the presence of a large metacentric marker chromosome resulting from a Robertsonian translocation (Rb 6.7). This chromosome is as such absent in ASML cells but perhaps it may be present in these cells with a major part of chromosome 7 being deleted. The most interesting feature of the ASML karyo-type was the presence of double minutes (DMs) and a homogeneously staining region (HSR) at the telomeric end of chromosome 6. These were peculiar to the ASML cells, being absent in the AS cells. DMs and HSR are reported to be correlated with the resistance to various drugs and with the acquired virulence of tumor cells through gene amplification. Therefore, we assume that in the metastasizing ASML cell line the DMs and HSR were established through genetic selection and that they are probably related to the acquired metastasizing capacity of these cells.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...