Loss of heterozygosity on chromosome 9 in human breast cancer: Association with clinical variables and genetic changes at other chromosome regions

Primary breast tumors were tested for loss of heterozygosity (LOH), on chromosome 9p with microsatellite markers restricted to a 28 cM region including the MTSI gene. LOH was found with at least I marker in 38% of the 201 cases analyzed. A high frequency of deletions was detected at the 9p23-p21 reg...

Full description

Bibliographic Details
Main Authors: Sigurður Ingvarsson 1956-, Guðný Eiriksdóttir 1950-, Ásgeir Sigurðsson 1969-, Jón Gunnlaugur Jónasson 1956-, Bjarni A. Agnarsson 1952-, Helgi Sigurðsson 1952-, Júlíus Guðmundsson 1968-, Jón Þór Bergþórsson 1966-, Rósa Björk Barkardóttir 1958-, Valgarður Egilsson 1940-
Other Authors: Háskóli Íslands
Format: Article in Journal/Newspaper
Language:English
Published: 1995
Subjects:
Online Access:http://hdl.handle.net/1946/20738
Description
Summary:Primary breast tumors were tested for loss of heterozygosity (LOH), on chromosome 9p with microsatellite markers restricted to a 28 cM region including the MTSI gene. LOH was found with at least I marker in 38% of the 201 cases analyzed. A high frequency of deletions was detected at the 9p23-p21 region, indicating a tumor suppressor gene(s) important for breast cancer tumorigenesis. Tumors with and without LOH on 9p were compared with respect to clinico-pathological factors using chi(2) analysis. Tumors with 9p LOH were significantly associated with high S-phase status and aneuploidy, but not with type, node status, estrogen and progesterone receptor content or age of the patients at diagnosis. Survival analysis showed that LOH at 9p did not significantly affect the survival rate of breast cancer patients. Our results indicate that the aberrations on 9p detected in this study are not of independent prognostic value. A significant association was found between LOH at 9p and LOH at chromosomal arms 3p and 6q, which is an additional contribution toward understanding the genetic events in breast tumor pathogenesis. This work was financially supported by the Nordic Cancer Union, the Icelandic Cancer Society, the University of Iceland Research fund, the Memorial Fund og Bergthora Magnusdottir and Jakob B. Bjarnason, the Science Fund of Iceland, the Science Fund of the University Hospital of Iceland and the Nordic Council of Ministers.