𝔖 Bobbio Scriptorium
✦   LIBER   ✦

Allelic losses on chromosome band 11q13 in aldosterone-producing adrenal tumors

✍ Scribed by Aritoshi Iida; Yusuke Nakamura; Takashi Imai; Kirsten Blake; Terry Tunny; Shelley Klemm; Michael Stowasser; Richard Gordon; Nicholas Hayward


Publisher
John Wiley and Sons
Year
1995
Tongue
English
Weight
516 KB
Volume
12
Category
Article
ISSN
1045-2257

No coin nor oath required. For personal study only.

✦ Synopsis


We examined loss of heterozygosity (LOH) in I 4 aldosterone-producing adrenal tumors, with six linearly ordered restriction fragment length polymorphism (RFLP) markers that map within a 12-cM region containing the MEN/ locus on I I q 13. Among I I tumors that were informative for at least one marker, five showed LOH at one or more loci, and two distinct regions of deletion were identified. The proximal region overlapped with the location of the MEN/ locus previously predicted by linkage analyses in MENl families and the commonly deleted region in hyperparathyroid tumors. This suggests that one of the genes associated with development of aldosterone-producing adrenal tumors may coincide with the MEN/ locus, and that a second Rene, distal to the MEN/ locus, may also play a role in the development of this type of tumor. Genes Chrornosorn Cancer -. I

12:73-75 (199.5).


πŸ“œ SIMILAR VOLUMES


Allelic loss on chromosome bands 13q11-q
✍ Guang Li; Nan Hu; Alisa M. Goldstein; Ze-Zhong Tang; Mark J. Roth; Quan-Hong Wan πŸ“‚ Article πŸ“… 2001 πŸ› John Wiley and Sons 🌐 English βš– 203 KB

## Abstract Allelic loss on chromosome 13 occurs frequently in esophageal squamous cell carcinoma. However, studies of the two known tumor suppressor genes located on 13q, __RB1__ and __BRCA2__, have shown few mutations, suggesting that other genes are likely to be involved in the development of th

Allelic loss on chromosomes 2q21 and 19p
✍ Karmen Stankov; Alessandro Pastore; Luca Toschi; James McKay; Fabienne Lesueur; πŸ“‚ Article πŸ“… 2004 πŸ› John Wiley and Sons 🌐 French βš– 173 KB

## Abstract HΓΌrthle thyroid tumors are characterized by frequent numerical chromosomal aberrations, including aneuploidy or polyploidy, losses and gains of some chromosomal regions and DNA fragmentation. In recent years, great attention has been paid to the combined analysis of morphologic and gene

Allele loss in Wilms tumors of chromosom
✍ Barbara Klamt; Michael Schulze; Claudia ThΓ€te; Jaroslav Mares; Peter Goetz; Roma πŸ“‚ Article πŸ“… 1998 πŸ› John Wiley and Sons 🌐 English βš– 101 KB πŸ‘ 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

Deletion mapping of endocrine tumors loc
✍ Rita Chakrabarti; Eri S. Srivatsan; Thomas F. Wood; Patricia J. Eubanks; Sam A. πŸ“‚ Article πŸ“… 1998 πŸ› John Wiley and Sons 🌐 English βš– 133 KB

Multiple endocrine neoplasia type 1 syndrome (MEN1, MIM 131100), an autosomal dominant disease, is characterized by parathyroid hyperplasia, pancreatic endocrine tumors, and pituitary adenomas. These tumors also occur sporadically. Both the familial (MEN1) and the sporadic tumors reveal loss of hete

Association of allelic losses on human c
✍ Rita K. Schmutzler; Rolf Fimmers; Erhard Bierhoff; Barbara Lohmar; Anke Homann; πŸ“‚ Article πŸ“… 1996 πŸ› John Wiley and Sons 🌐 French βš– 517 KB

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

Three non-overlapping regions of chromos
✍ Jennifer A. Byrne; Lisa A. Simms; Melissa H. Little; Elizabeth M. Algar; Peter J πŸ“‚ Article πŸ“… 1993 πŸ› John Wiley and Sons 🌐 English βš– 713 KB

Tumor and constitutional chromosome arm I I p genotypes were compared in 6 hepatoblastoma (HB) patients and 2 adrenal adenoma (AA) patients, with one HB patient and both AA patients displaying clinical features associated with the Beckwith-Wiedemann syndrome (BWS). Using up t o 14 chromosome I I pol