ArticleJapanese journal of cancer research : Gann1997
Mapping of a breast cancer tumor suppressor gene locus to a 4-cM interval on chromosome 18q21.
Article in Japanese journal of cancer research : Gann, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 38 citations in OpenAlex.
- Cyclin E Overexpression in Human Mammary Epithelial Cells Promotes Epithelial Cancer-Specific Copy Number Alterations.iScience · 2019Article
- Article
- The role of estrogen in the initiation of breast cancer.The Journal of steroid biochemistry and molecular biology · 2006Review
- Association of allelic losses at 3p25.1, 13q12, or 17p13.3 with poor prognosis in breast cancers with lymph node metastasis.Japanese journal of cancer research : Gann · 2001Article
- Mapping of target regions of allelic loss in primary breast cancers to 1-cM intervals on genomic contigs at 6q21 and 6q25.3.Japanese journal of cancer research : Gann · 2000Article
- Transforming growth factor-beta and breast cancer: Transforming growth factor-beta/SMAD signaling defects and cancer.Breast cancer research : BCR · 2000Review
- Allelic loss on chromosome 9q is associated with lymph node metastasis of primary breast cancer.Japanese journal of cancer research : Gann · 1998Article
- Frequent allelic loss at 7p14-15 associated with aggressive histologic types of breast cancer.Japanese journal of cancer research : Gann · 1998Article
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8 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
DPC4 and DCC, putative tumor suppressor genes implicated in the genesis of several types of human cancer, lie on the long arm of human chromosome 18. We examined 200 primary breast cancers for allelic losses on chromosome 18, using 15 microsatellite markers distributed along the long arm. Allelic loss was detected most frequently (29-30%) at loci mapped to 18q21. Deletion mapping of the 34 tumors showing partial or interstitial deletions identified a commonly deleted region within the 4-cM interval flanked by D18S474 and D18S487 at 18q21.1-q21.3. Although this interval included the DPC4 and DCC genes, we excluded DPC4 from candidacy when polymerase chain reaction-single-strand conformation polymorphism analysis of each exon failed to detect abnormalities in any of the 54 breast cancers that exhibited loss of heterozygosity involving 18q. Allelic loss on 18q was found more frequently in tumors of the solid tubular histological type (24 of 55, 44%) than in other types (24 of 113, 21%) (P = 0.0049). The results suggest that a tumor suppressor gene located within the 4-cM region at 18q21, either DCC or another gene not yet identified, may play a role in the development of some sporadic breast cancers, particularly those of the solid tubular type.
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