DNA mismatch repair genes hMLH1, hMSH2, and hMSH6 are not inactivated in bronchioloalveolar carcinomas of the lung
MC Aubry, KC Halling, JL Myers… - … Journal of the …, 2001 - Wiley Online Library
MC Aubry, KC Halling, JL Myers, HD Tazelaar, P Yang, SN Thibodeau
Cancer: Interdisciplinary International Journal of the American …, 2001•Wiley Online LibraryBACKGROUND Defective DNA mismatch repair (MMR) appears to be rare in nonsmall cell
carcinomas of the lung. Defective DNA MMR results from genetic or epigenetic alterations
that inactivate the DNA MMR genes hMLH1 or hMSH2, and rarely hMSH6. The loss of
normal DNA MMR is thought to promote tumorigenesis by accelerating the accumulation of
mutations in oncogenes and tumor suppressor genes. Inactivation of hMLH1, hMSH2, and
hMSH6 is observed as a loss of expression of these proteins by immunohistochemistry …
carcinomas of the lung. Defective DNA MMR results from genetic or epigenetic alterations
that inactivate the DNA MMR genes hMLH1 or hMSH2, and rarely hMSH6. The loss of
normal DNA MMR is thought to promote tumorigenesis by accelerating the accumulation of
mutations in oncogenes and tumor suppressor genes. Inactivation of hMLH1, hMSH2, and
hMSH6 is observed as a loss of expression of these proteins by immunohistochemistry …
BACKGROUND
Defective DNA mismatch repair (MMR) appears to be rare in nonsmall cell carcinomas of the lung. Defective DNA MMR results from genetic or epigenetic alterations that inactivate the DNA MMR genes hMLH1 or hMSH2, and rarely hMSH6. The loss of normal DNA MMR is thought to promote tumorigenesis by accelerating the accumulation of mutations in oncogenes and tumor suppressor genes. Inactivation of hMLH1, hMSH2, and hMSH6 is observed as a loss of expression of these proteins by immunohistochemistry. Bronchioloalveolar carcinoma is a subtype of adenocarcinoma with distinctive clinical and pathologic features.
MATERIALS AND METHODS.
An immunohistochemical study was performed on paraffin embedded sections of 33 bronchioloalveolar carcinomas (20 nonmucinous and 13 mucinous) for hmlh1, hmsh2, and hmsh6 proteins.
RESULTS
All the tumors showed normal expression of hmlh1, hmsh2, and hmsh6.
CONCLUSIONS
These findings suggest that defective DNA MMR due to inactivation of hMLH1, hMSH2, or hMSH6 does not play a significant role in the pathogenesis of bronchioloalveolar carcinomas. Cancer 2001;92:2898–901. © 2001 American Cancer Society.
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