Mapping of a New Target Region of Allelic Loss to a 2-cM Interval at 22q 13.1 in Primary Breast Cancer

  • Iida Aritoshi
    Department of Molecular Biology, Institute of Gerontology (ROUKEN), Nippon Medical School
  • Kurose Keisuke
    Department of Molecular Biology, Institute of Gerontology (ROUKEN), Nippon Medical School
  • Isobe Rie
    Department of Molecular Biology, Institute of Gerontology (ROUKEN), Nippon Medical School
  • Akiyama Futoshi
    Department of Pathology, Cancer Institute
  • Sakamoto Goi
    Department of Pathology, Cancer Institute
  • Yoshimoto Masataka
    Department of Surgery, Cancer Institute
  • Kasumi Fujio
    Department of Surgery, Cancer Institute
  • Nakamura Yusuke
    Laboratory of Molecular Medicine, Institute of Medical Science, The University of Tokyo
  • Emi Mitsuru
    Department of Molecular Biology, Institute of Gerontology (ROUKEN), Nippon Medical School

Search this article

Description

Allelic losses on chromosome arm 22q are frequently observed in human meningiomas and in carcinomas of the colon, ovary, and breast. Among 140 primary breast cancers we examined for loss of heterozygosity (LOH) at 16 polymorphic loci on the long arm of chromosome 22,56 (40%) showed LOH for at least one locus. Eleven of these tumors had retained heterozygosity for markers proximal to the NF2 locus but showed LOH for markers distal to NF2. Deletion mapping indicated a new common region of deletion, 2-cM in extent, at q13.1 between Interleukin 2 receptor β (IL2RB) and D22S279. Our results raise the possibility that one or more tumor suppressor genes associated with breast cancer may exist at 22q13.1. Comparison of these results with clinicohistological data indicated that allelic losses on 22q tend to occur more frequently in tumors of malignant histological types. Genes Chromosomes Cancer 21 : 108-112,1998.

Journal

Details 詳細情報について

  • CRID
    1570854176876805120
  • NII Article ID
    110001071178
  • NII Book ID
    AN1047681X
  • ISSN
    13409662
  • Text Lang
    en
  • Data Source
    • CiNii Articles

Report a problem

Back to top