Little is known about the genetic mechanisms behind the genesis of anaplastic thyroid carcinoma. This is among the most virulent of all human malignancies, and it is believed to result most often from transformation of differentiated thyroid carcinomas of the papillary type. So far, TP53 and beta-ca
Chromosome 22q a frequent site of allele loss in head and neck carcinoma
β Scribed by Regina C. Poli-Frederico; Nadia A. Bergamo; Patricia P. Reis; Luiz P. Kowalski; Maria Zielenska; Jeremy A. Squire; Silvia R. Rogatto
- Publisher
- John Wiley and Sons
- Year
- 2000
- Tongue
- English
- Weight
- 228 KB
- Volume
- 22
- Category
- Article
- ISSN
- 1043-3074
No coin nor oath required. For personal study only.
π SIMILAR VOLUMES
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
Background. Loss of heterozygosity (LOH) correlates with inactivated tumor suppressor genes. The aim of this study was to see if LOH on chromosomes 2q, 3p, 5q, 9p, and 17p correlated with survival in early squamous cell carcinoma of the head and neck (SCCHN). Methods. A case control study was perfo
Cigarette smoking is the major known risk factor for head and neck cancer. Tobacco promotes oxidative stress and enhances tissue levels of 8-hydroxyguanine (8-OH-G) in smokers. The presence of 8-OH-G does not impede replication but leads to an accumulation of G 3 T transversions. Recently, the gene
Several lines of evidence suggest that the progression of head-and-neck squamous-cell carcinoma (HNSCC) involves inactivation of at least one and possibly several tumorsuppressor genes on the long arm of chromosome 13. The fact that neither Rb1 nor BRCA2 appears to be inactivated in the majority of
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