DNA samples from tumors and paired normal tissues from 48 patients with prostate cancer (stage B, I 6 cases; stage C, I 4 cases; stage D, I 8 cases) were examined with 26 polymorphic markers spanning chromosome 10. Allelic losses were observed in I7 of the 46 cases (37%) that were informative with a
Loss of alleles at loci on human chromosome 11 during genesis of Wilms' tumour
โ Scribed by Koufos, A.; Hansen, M. F.; Lampkin, B. C.; Workman, M. L.; Copeland, N. G.; Jenkins, N. A.; Cavenee, W. K.
- Book ID
- 109735433
- Publisher
- Nature Publishing Group
- Year
- 1984
- Tongue
- English
- Weight
- 403 KB
- Volume
- 309
- Category
- Article
- ISSN
- 0028-0836
- DOI
- 10.1038/309170a0
No coin nor oath required. For personal study only.
๐ SIMILAR VOLUMES
Breast-carcinoma development presumably results from multiple mutational events in tumor-associated genes. Certain results indicate that some tumor-suppressor genes may combine their pathogenetic potential to synergistically promote tumor growth. In an effort to identify such mechanisms in breast tu
We recently isolated the KAI1 gene, a metastasis suppressor gene for prostate cancer, from human chromosome region 11p13-cen-containing rat prostate cancer cells. The present study was performed to further locate the region of the KAI1 gene on the short arm of chromosome 11, and to examine whether l
## Forty -six cases of sporadic melanoma have been investigated for loss of heterozygosity at 4 loci: D I IS29 ( I lq23), YNZ22 (I 7p I 3.3), 7P53 (I 7p I 3. I ); and NM23 ( 17q22). Each of the loci is thought to be important in the pathogenesis of other turnours. Mutations were found infrequently
Spontaneously immortalized fibroblast cell lines derived from embryonic tissues of C3D2F 1 mice were analyzed for loss of heterozygosity (LOH) at multiple chromosomal loci to identify candidate suppressor loci for immortalization. Among 47 simple sequence repeat (SSR) loci selected for screening, th
To obtain a comprehensive overview of chromosomal alterations that may underlie human papillomavirus (HPV)mediated immortalization, 4 foreskin keratinocyte cell lines generated by transfection with either HPV 16 (cell lines FK16A and FK16B) or HPV 18 (FK18A and FK18B) were subjected to chromosomal a