DNA mismatch repair genes hMLH1, hMSH2, and hMSH6 are not inactivated in bronchioloalveolar carcinomas of the lung

Marie Christine Aubry, Kevin C. Halling, Jeffrey L. Myers, Henry D. Tazelaar, Ping Yang, Stephen N. Thibodeau

Research output: Contribution to journalArticle

17 Scopus citations

Abstract

BACKGROUND. Defective DNA mismatch repair (MMR) appears to be rare in non-small 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 hMLHJ, 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.

Original languageEnglish (US)
Pages (from-to)2898-2901
Number of pages4
JournalCancer
Volume92
Issue number11
DOIs
StatePublished - Dec 1 2001

Keywords

  • Bronchioloalveolar carcinoma
  • Hereditary nonpolyposis colorectal carcinomas
  • Immunohistochemistry
  • Microsatellite instability
  • Mismatch repair genes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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