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Genomic Health Nets Second Validation Study Publication for Oncotype DX Colon Cancer Test

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The Journal of Clinical Oncology has published data from the second validation study involving Genomic Health's Oncotype DX colon cancer recurrence test.

Researchers from Genomic Health and several universities used the company's 12-gene expression RT-PCR-based diagnostic test to analyze more than 690 tissue samples collected from patients who were initially enrolled in the trial, CALGB 9581, to gauge if the test could assess which of them were at greater risk of colon cancer recurrence. That original study, which randomized more than 1,700 patients with stage II colon cancer to either receive treatment with the monoclonal antibody edrecolomab or be observed for progression, failed to find a survival difference between the two arms. Edrecolomab has not shown to benefit colon cancer patients in late stage trials compared to conventional chemotherapeutics.

The retrospective analysis found that the test's recurrence score, as well as patients' mismatch repair deficiency, were significantly linked to their risk of colon cancer recurrence. The test recurrence score was the strongest predictor of disease recurrence independent of other factors, such as T-stage, mismatch repair status, number of nodes examined, tumor grade, and lymphovascular invasion.

Among patients with stage T3 disease (or colon cancer that hasn't spread to nearby organs), with intact mismatch repair ability, those the multi-gene expression test found to be at high risk had an average five-year recurrence risk of 21 percent and those the test deemed low risk had an average recurrence risk of 13 percent.

Based on these findings, the researchers concluded that the Oncotype DX colon cancer recurrence test predicted recurrences in Stage II colon cancer patients in the CALGB 9581 trial. "This is consistent with the importance of stromal response and cell cycle gene expression in colon tumor recurrence," researchers led by Alan Venook of the University of California, San Francisco, concluded in the JCO paper. The test recurrence score "appears to be most discerning for patients with T3, mismatch repair-intact tumors, although markers such as grade and lymphovascular invasion did not add value in this subset of patients."

This latest validation study follows positive data from the QUASAR trial, the first validation study involving Genomic Health's Oncotype DX colon cancer test. The QUASAR study, also published in JCO in 2011, found that the 12-gene recurrence score could gauge recurrence risk in colon cancer patients with stage II disease after surgery. In that study, the researchers found that T4 stage (when the tumor has grown through the bowel wall) and patients' mismatch repair status were also independent prognostic factors of cancer recurrence (PGx Reporter 11/9/2011).

The CALGB 9581 validation study shows the ability of the Oncotype DX colon test to gauge recurrence risk in low- to intermediate-risk stage II colon cancer patients, said Genomic Health. "Since Oncotype DX provides the biological understanding necessary to accurately distinguish patients with a lower risk of recurrence from those with high-risk disease, we expect that this publication will accelerate our momentum toward gaining greater acceptance among treating physicians and reimbursement by payors," Genomic Health Chief Medical Officer Steve Shak said in a statement announcing the publication of the study.

In the JCO paper, the study authors also noted that the genes comprising the test's recurrence score point to the pathways that are critical to cancer recurrence and may offer drug development opportunities. "It is plausible that directing inhibitors toward elements of the pathways identified in the recurrence score could lead to the development of novel adjuvant therapies for colon cancer," the researchers wrote. For example, among the 12 genes included in the test algorithm are stromal response genes – fibroblast activation protein, inhibin A, and biglycan – which are implicated in biological mechanisms that cause a wound healing response and spurs the growth of tumor cells.