alexa Assessment of DNA Repair Mechanisms to Determine the Susceptibility of Non-small Cell Lung Cancer to Alkylating Agents
ISSN: 1948-5956

Journal of Cancer Science & Therapy
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Research Article

Assessment of DNA Repair Mechanisms to Determine the Susceptibility of Non-small Cell Lung Cancer to Alkylating Agents

Ivette F. Emery1,2*, Chiara Battelli1,2, Li Cai3 and Daniel M. Hayes1

1Maine Center for Cancer Medicine, Scarborough, ME 04074

2Maine Medical Center, Portland, ME 04102

3LabCorp, Center for Molecular Biology & Pathology, Research Triangle Park, NC

*Corresponding Author:
Dr. Ivette F. Emery, PhD
Maine Medical Center Cancer Institute
100 Campus Drive, Suite 102, Scarborough, ME 04074, USA
E-mail: [email protected]

Received date: February 28, 2011; Accepted date: May 15, 2011; Published date: May 15, 2011

Citation: Emery IF, Battelli C, Cai L, Hayes DM (2011) Assessment of DNA Repair Mechanisms to Determine the Susceptibility of Non-small Cell Lung Cancer to Alkylating Agents. J Cancer Sci Ther 3: 092-095. doi: 10.4172/1948-5956.1000067

Copyright: © 2011 Emery IF, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Background: The status of DNA repair systems impacts the sensitivity of tumors to chemotherapeutics. The anti-neoplastic activity of temozolomide, an alkylating agent, is affected by the enzyme O6-Methylguanine-DNA methyltransferase (MGMT), and by the mismatch repair system (MMR). Lack of MGMT makes a tumor susceptible to temozolomide provided MMR is functional. A non-functional MMR renders the tumor resistant to alkylating agents. We assayed MGMT and MMR in order to estimate the proportion of patients affected by NSCLC who may derive benefit from temozolomide, an alkylating agent not currently used in lung cancer. Method: MGMT and MMR were assayed by promoter methylation testing and by microsatellite instability testing, respectively, on 96 paraffin-embedded NSCLC samples. Methylation testing, which detects gene silencing, was conducted by methylation-specific PCR of the MGMT promoter. MSI testing, which detects a non-functional MMR, was conducted by multiplex PCR of six microsatellite regions. Results: Ninety three samples yielded interpretable results. Eighty of those (83%) had no defects detected in either MGMT or MMR. Nine samples (10%) had methylation of the MGMT promoter and four samples (4%) had microsatellite instability. The defects were not overlapping. Conclusions: Our results indicate that approximately 10% of NSCLC may be susceptible to alkylating agents, and that in the remaining population, only 4% will be resistant to these agents. Our understanding of the molecular characteristics of NSCLC suggests that alkylating agents, such as temozolomide, alone or in combination with MGMT inhibitors, may be viable option to treat selected NSCLC patients.


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