Data from Response Genetics' tests against cancer to be presented at ASCO 2012

Response Genetics, Inc. (NASDAQ:RGDX), a company focused on the development and sale of molecular diagnostic tests for cancer, announced today four presentations to be held during the 2012 American Society of Clinical Oncology (ASCO) Annual Meeting in Chicago, IL from June 1 to June 5, 2012. Study results are based on the company's proprietary technology and approach.

"Data to be presented at ASCO 2012 will highlight the clinical utility of Response Genetics' tests in the fight against cancer," said Stephanie H. Astrow, Ph.D., MBA, vice president for R&D. "Through rapid and accurate assessment of genetic biomarkers, we're helping doctors personalize cancer care by providing them valuable insights into potential cancer recurrence and tumor response to drugs such as pemetrexed and crizotinib."

All studies presented used technology developed by Response Genetics to isolate nucleic acids from formalin-fixed, paraffin-embedded (FFPE) archived tissue for quantitative RT-PCR analysis of gene expression and other genetic analyses. Following is a summary of presentations:

Poster Discussion Sections

Monday June 4, 11:30 a.m. to 12:30 p.m., E450a

Abstract No. 4563: Generation of a prognostic cancer stem-like gene expression signature in men undergoing radical prostatectomy for localized prostate cancer. Fairey, AS, Yang, D, et al.

Genes typically expressed by cancer stem-like cells were analyzed to determine their potential as predictive biomarkers of prostate cancer recurrence after radical resection. In this study, twelve candidate genes were evaluated in 241 tumor samples, with results identifying a novel three-gene expression signature (Axin2, NANOG, CTNNB1) with potential predictive benefit.

General Poster Sections

Saturday June 2, 1:15 p.m. to 5:15 p.m., S Hall A2

Abstract No: 7066: Prospective study of tumor suppressor gene (TSG) methylation as a prognostic biomarker in surgically resected non-small cell lung cancer (NSCLC). Azzoli, CG, Drilon, A, et al.

To further explore the findings that promoter methylation of the certain tumor suppressor genes was associated with early recurrence in NSCLC, a prospective study was designed to analyze the methylation status of ten gene promoters (p16, CDH13, RASSF1A, APC, MGMT, WIF-1, METH-2, GSTP1, SOCS3, DAPK) and correlate status with clinical features, pathologic stage, disease-free survival (DFS) and overall survival (OS). Results showed no significant associations between promoter methylation and DFS, or OS.

Saturday June 2, 1:15 p.m. to 5:15 p.m., S Hall A2

Abstract No. 7582: Thymidylate synthase (TS) gene expression in patients with ALK positive (+) non-small cell lung cancer (NSCLC): Implications for therapy. Gandara, DR, Huang, E, et al.

Thymidylate synthase (TS) and anaplastic lymphoma kinase (ALK) gene expression was analyzed in the Response Genetics (RGI) tissue database to determine the potential association between ALK+ tumors and the chemotherapy agent pemetrexed - TS is a candidate predictive biomarker for pemetrexed activity and published results suggest increased sensitivity of ALK+ NSCLC to pemetrexed. Findings demonstrate low TS expression in ALK+ tumors, providing a possible mechanism of action of pemetrexed sensitivity in ALK+ NSCLC.

Saturday June 2, 1:15 p.m. to 5:15 p.m., S Hall A2

Abstract No. 7594: Update on the large-scale screening of ALK fusion oncogene transcripts in archival NSCLC tumor specimens using multiplexed RT-PCR assays. Li, T, Huang, E, et al.

More than 4,700 NSCLC specimens in the RGI database were tested for the presence of ALK fusion transcripts using single and multiplexed RT-PCR assays. Results not only provided information on fusion transcript positivity, but the specific genetic variants present in each tumor. In addition, information on expression of chemotherapy-related biomarkers (TS, ERCCI, and RRM1) was available for a subset of tumors. Together, these results underscore the utility of an RT-PCR-based assay as a companion diagnostic test for drugs targeting EML4-ALK fusion gene products.