Diana M. Pitterle, Young-Chul Kim, Youjia Cao, Ashish Gautam, Baohui Zhao, Amy Beck and Gerold Bepler Pages 281 - 288 ( 8 )
Cancer biology as seen from chromosome 11 involves a plethora of mechanisms for chromosomal changes. The high frequency of repeated elements, the presence of active retrotransposons, the appearance of fragile sites, and the presence (and amplification) of drug resistance genes are all expected to destabilize the integrity of this chromosome. Thus, it is not unexpected that chromosome 11 is often mutated in a variety of tumors. Here, we review genes relevant to lung carcinogenesis and progression. Numerous loci and genes will be omitted since their role appears to be restricted to organ sites other than lung (i.e., the KAI gene at 11p11.2 which is involved in metastatic prostate cancer; the EXT2 gene at 11p11.2, which is one of the genes responsible for hereditary multiple exostoses; the WT1 gene at 11p13, which is frequently mutated in nephroblastoma; the TSG101 gene at 11p15.1-2, which may play a role in breast cancer; the ST5 (HTS1) gene at 11p15.3-4, which may be responsible for suppression of HeL a cell somatic cell hybrids). These genes may represent tissue-specific alterations that push certain types of cells into uncontrolled growth. In contrast, chromosome 11 also has genes for basic metabolic processes that are integral to the proliferation of cells (i.e., RRM1) and these are expected to be involved in a broad range of tumors. This review specifically focuses on HRAS, RRM1, MEN1, PPP2R1B, and ATM. Studies of the chromosomal abnormalities that underly cancer has produced a greater understanding of the normal patterns of gene regulation in healthy cells. Imprinting is one example of this, and the future promises to reveal much more.
Lung Cancer, Chromosome 11, EXT2 gene, Nephroblastoma, Carcinogenesis, PPP2R1B, DUTT1, NCAM-related protein, LOH
Roswell Park Cancer Institute, Buffalo, NY 14263