✦ LIBER ✦

Association of allelic losses on human chromosomal arms 11q and 16q in sporadic breast cancer

✍ Scribed by Rita K. Schmutzler; Rolf Fimmers; Erhard Bierhoff; Barbara Lohmar; Anke Homann; Paul Speiser; Ernst Kubista; Klaus Jaeger; Dieter Krebs; Robert Zeillinger; Otmar D. Wiestler; Andreas Von Deimling

Publisher: John Wiley and Sons
Year: 1996
Tongue: French
Weight: 517 KB
Volume: 69
Category: Article
ISSN: 0020-7136
DOI: 10.1002/(sici)1097-0215(19960822)69:4<307::aid-ijc12>3.0.co;2-2

No coin nor oath required. For personal study only.

✦ Synopsis

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 tumors, a series of 77 (group I) paired blood tumor samples from patients with sporadic mammary carcinomas was analyzed for loss of heterozygosity with I 5 polymorphic markers on the chromosomal arms 7q, I I q, I3q, I6q, I7p and I7q. A significant association was observed for the combination of allelic losses on chromosomes I I q and 16q. In order to confirm these findings, we studied a second independent series of 189 breast-tumor patients (group 2) with comparable histopathological tumor stages. Group 2 was examined for the same genetic alterations using the identical set of polymorphic markers. The data from this group confirmed the detected association of loss of heterozygosity on chromosomes I I q and 16q and indicate the cooperation of putative tumor-suppressor genes on the chromosomal arms I I q and 16q in a sub-set of breast carcinomas. The regions involved harbor the candidate genes ATM (mutated in ataxiatelangiectasia) on chromosome I I q23 and UVO (uvomorulin, cadherin E) and BBCl (breast basic conserved I ) on chromosome I6q22-q24.

📜 SIMILAR VOLUMES

Loss of heterozygosity on chromosome arm

Loss of heterozygosity on chromosome arm 16q in breast cancer metastases

✍ Keltouma Driouch; Françoise Dorion-Bonnet; Marianne Briffod; Marie-Hélène Champè 📂 Article 📅 1997 🏛 John Wiley and Sons 🌐 English ⚖ 111 KB 👁 2 views

One of the main genetic abnormalities associated with breast carcinogenesis is the loss of genetic material from chromosome arm 16q. Different groups have identified two regions (16q22.1 and 16q24-ter) that are frequently deleted in primary tumors, suggesting the presence of tumor suppressor genes i

Allele loss in Wilms tumors of chromosom

Allele loss in Wilms tumors of chromosome arms 11q, 16q, and 22q correlates with clinicopathological parameters

✍ Barbara Klamt; Michael Schulze; Claudia Thäte; Jaroslav Mares; Peter Goetz; Roma 📂 Article 📅 1998 🏛 John Wiley and Sons 🌐 English ⚖ 101 KB 👁 1 views

An extended analysis for loss of heterozygosity (LOH) on eight chromosomes was conducted in a series of 82 Wilms tumors. Observed rates of allele loss were: 9.5% (1p), 5% (4q), 6% (6p), 3% (7p), 9.8% (11q), 28% (11p15), 13.4% (16q), 8.8% (18p), and 13.8% (22q). Known regions of frequent allele loss

Loss of heterozygosity at loci from chro

Loss of heterozygosity at loci from chromosome arm 22Q in human sporadic breast carcinomas

✍ Florence Allione; François Eisinger; Patricia Parc; Tetsuro Noguchi; Hagay Sobol 📂 Article 📅 1998 🏛 John Wiley and Sons 🌐 French ⚖ 196 KB 👁 2 views

Forty-four breast carcinomas were studied for loss of heterozygosity (LOH) at 25 microsatellite markers distributed almost evenly along chromosome arm 22q. LOH at at least one marker were observed in 66% tumors, while 6 regions of consistent LOH were identified. The size of each region ranged betwee

Allelic loss on chromosomes 8p, 22q and

Allelic loss on chromosomes 8p, 22q and 18q (DCC) in human prostate cancer

✍ Malcolm C. Crundwell; Shaheen Chughtai; Margaret Knowles; Lindsay Takle; Mike Lu 📂 Article 📅 1996 🏛 John Wiley and Sons 🌐 French ⚖ 706 KB

Previous studies have suggested the involvement of tumour-suppressor genes on chromosomes 8p, 22q and 18q (DCC) in prostate cancer. The aim of this study was to further characterize these regions. We investigated 20 polymorphic regions on the 3 chromosome arms in 43 cancers and 10 cases of benign pr

Functional loss of E-cadherin and cadher

Functional loss of E-cadherin and cadherin-11 alleles on chromosome 16q22 in colonic cancer

✍ Braungart, Evelyn; Schumacher, Christoph; Hartmann, Elke; Nekarda, Hjalmar; Beck 📂 Article 📅 1999 🏛 John Wiley and Sons 🌐 English ⚖ 226 KB 👁 1 views

Proteins of the cadherin family regulate cellular adhesion and motility and are believed to act as tumour suppressors. Previous studies have identified frequent mutation and allelic inactivation of the E-cadherin (cadherin-1) locus in diffuse gastric cancer. At least two other cadherin genes, P-cadh

Recurrent allelic deletions of chromosom

Recurrent allelic deletions of chromosome arms 15q and 16q in human small cell lung carcinomas

✍ Sasha E. Stanton; Sang Won Shin; Bruce E. Johnson; Matthew Meyerson 📂 Article 📅 2000 🏛 John Wiley and Sons 🌐 English ⚖ 102 KB 👁 2 views

The genetic lesions that lead to the development of small cell lung carcinoma (SCLC) remain incompletely defined. To identify recurrent allelic deletions in specific chromosomal regions that could serve as markers for tumor suppressor gene (TSG) inactivation in SCLC, we performed a comprehensive all