The 9p21-23 chromosome region harbors a number of known and putative tumor-suppressor genes (TSGs). The best characterized gene in this area is p16 INK4A (CDKN2A). Alterations of its product have been observed in various malignancies, including non-small-cell lung carcinomas (NSCLCs). We earlier inv
Chromosome alterations in 21 non-small cell lung carcinomas
β Scribed by Ikuo Miura; Jill M. Siegfried; James Resau; Steven M. Keller; Jian-Yuan Zhou; Dr. Joseph R. Testa
- Publisher
- John Wiley and Sons
- Year
- 1990
- Tongue
- English
- Weight
- 886 KB
- Volume
- 2
- Category
- Article
- ISSN
- 1045-2257
No coin nor oath required. For personal study only.
β¦ Synopsis
1. R.)
Cytogenetic analysis was performed on I 6 primary tumors, 2 effusions, and 3 cell lines from 2 I patients with non-small cell lung cancer (NSCLC). In 20 patients specimens were obtained prior t o initiating cytotoxic therapy. Extensive clonal chromosome alterations were found in all cases. The most frequent numerical changes were polysomy 7 and polysomy 20 (each seen in I2 specimens). In addition, tumor cells from another six cases exhibited partial trisomy 7, with the shortest region of overlap (SRO) at 7p I I-p I 3. Rearrangements of chromosomes I , 3,6,8, I I, 15, 17, and I9 were each observed in nine or more tumors.
Breakpoints were clustered at several chromosomal sites, including I p I 3, 3p I 3, I5p I I-q I I, I7p I I, and 19q I 3. Recurrent loss involving I p. 3p, 6q, I I p, I5p, I7p, and 19q were each seen in at least eight cases. The SRO of 3p losses was at band 3~21. Double minute chromosomes were found in three tumors. Overall, our findings indicate that even though karyotypes in newly diagnosed NSCLC are very complex, recurrent cytogenetic changes can be identified. The high incidence of loss of I7p (I 4 of 2 I specimens) appears t o be compatible with reports implicating the TP53 gene (at band I7p I 3) as a frequent site for genetic alteration in lung cancer. Moreover, the recurrence of loss of 3p (I 2 cases) and I I p ( I0 cases) is also consistent with recent molecular evidence. The existence of other "hot spots" for cytogenetic change, particularly those involving specific regions on chromosomes 7, 15, and 19, warrants further molecular investigation of these sites in NSCLC.
π SIMILAR VOLUMES
The status of the P16 gene was investigated by Southern blot, polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP), and DNA sequencing analyses in 30 primary resected non-small cell lung carcinomas (NSCLCs) with metastatic involvement of thoracic lymph nodes and 33 NSCLCs w
Several somatic genetic alterations have been described in non-small-cell lung carcinomas (NSCLC). Recurrent chromosomal deletions have suggested the presence of tumor-suppressor genes specifically involved in lung carcinogenesis. For one of these, 2 non-overlapping regions have been proposed on the
Evidence for the existence of neuroendocrine (NE) differentiation in non-small cell lung carcinomas (NSCLCs) is at present based on histochemical, ultrastructural, and immunohistochemical data. The aim of this study was to investigate the extent of NE differentiation in NSCLCs as revealed by mRNA an
## Abstract The cyclinβdependent kinase inhibitor known as __p16__ (__CDK41, CDKN2, INK4A, MTS1__) has been proposed as a tumor suppressor gene on chromosome segment 9p21. We have evaluated __CDKN2__ alterations in 34 nonβsmall cell lung cancers (NSCLCs) with matched normal tissue controls and in 9
## Human gene MAGE-I codes for an antigen that is recognized on melanoma cells by autologous cytolytic T lymphocytes (CTL). This antigen is potentially useful as a target for cancer immunotherapy because gene MAGE-I is not expressed in any normal tissues except the testis. We tested 46 surgical sa