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Testing for KRAS Mutation in Colon and Lung Cancers


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http://www.marketwatch.com/story/exiqon ... dist=msr_2

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VEDBAEK, Denmark, May 11, 2009 (GlobeNewswire via COMTEX) -- Exiqon Diagnostics announced today that it now offers KRAS Mutation Analysis through its CLIA laboratory in California. Cancer treating physicians now have access to this critical test for their advanced stage colorectal and non-small cell lung cancer patients who are candidates for anti-EGFR therapy. In the United States, there are approximately 150,000 new colorectal cancer cases and over 200,000 lung cancer cases diagnosed each year.(1) Many of these patients may present with advanced disease. In those cases, confirmed KRAS mutation status is important information for physicians to have when deciding on a treatment regimen that may contain EGFR-targeted therapies. Published clinical studies demonstrate that KRAS gene mutations are associated with poor prognosis and lack of response to EGFR inhibitor therapies.

Recent studies strongly correlate the presence of KRAS mutations in colorectal cancer patients with lack of response to cetuximab and panitumumab, shorter progression-free survival (PFS) and shorter overall survival. Studies performed in NSCLC have shown that mutations in the KRAS gene are strongly predictive of resistance to tyrosine kinase inhibitors such as gefitinib and eroltinib.

KRAS mutation testing is recommended by the National Comprehensive Cancer Network (NCCN) before starting EGFR-targeted therapy in both metastatic colorectal cancer and advanced non-small cell lung cancer patients.(2,3) The American Society of Clinical Oncology (ASCO) favors routine KRAS mutation testing for patients diagnosed with metastatic colorectal cancer before initiating anti-EGFR therapies.

"The ability to determine patient response to a particular therapy before it is administered is critical to prioritizing from an ever increasing list of potential treatment options," said Doug Harrington, M.D., Medical Director, Exiqon Diagnostics. "KRAS Mutation Analysis is an important new diagnostic that is now available to help physicians stratify their advanced stage colorectal or non-small cell cancer patients as appropriate candidates for treatment with EGFR inhibitors. Those patients who have the mutation would most likely not respond to anti-EGFR drugs and should not be treated with those ineffective and expensive agents."

KRAS Mutation Analysis is a welcome addition to the growing molecular diagnostics test menu available at Exiqon Diagnostics. Additional targeted molecular profiling assays are currently in development and will be launched later this year to help physicians more effectively guide treatment decisions. KRAS testing is just one of the many molecular biomarkers that will be available to help physicians personalize therapeutic treatment plans.

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(Market Watch, Globe News via COMTEX, May 11, 2009)

Disclaimer:

The information contained in these articles may or may not be in agreement with my own opinions. They are not being posted with the intention of being medical advice of any kind.

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Mutations in the gene KRAS, which encodes a signaling protein activated by EGFR, are found in 15 to 30 percent of certain cancers. The presence of a mutated KRAS gene in a biopsy sample is associated with primary resistance to drugs. The change of a single base in DNA that encodes the mutant EGFR protein has been shown to cause drug resistance.

The American Society of Clinical Oncology (ASCO) advised oncologists not to prescribe oncology drugs Vectibix and Erbitux to certain colon cancer patients. Research revealed that patients with KRAS gene mutations will not respond to anti-EGFR therapy. Tests for the KRAS mutation involve analyzing a sample of tissue from a patient's tumor.

In studies, Erbitux and Vectibix reduced by 30% the risk that colon cancer worsened. Subsequent analyses found patients with the normal KRAS gene did much better than those with mutations. The whole concept of proper genetic markers is not to put patients in the position of having to receive toxic cancer drugs if they're not going to do any good.

The situation with Erbitux and Vectibix is that all the EGFR mutation or amplification studies can tell us is whether or not the cells are potentially susceptible to this mechanism of attack. They don’t tell you if Erbitux or Vectibix is worse or better than some other drug which may target this.

The cell is a system, an integrated, interacting network of genes, proteins and other cellular constituents that produce functions. You need to analyze the systems’ response to drug treatments, not just one target or pathway.

No genetic profile can discriminate differing levels of anti-tumor activity occurring among different targeted therapy drugs. Nor can it identify situations in which it is advantageous to combine a targeted drug with other types of conventional cancer drugs.

EGFR-targeted drugs are poorly-predicted by measuring the ostansible target, but can be well-predicted by measuring the effect of the drug on the function of live cells. You still need to measure the net effect of all processes, not just the individual molecular targets.

I would not want to be denied treatment with EGFR antibody therapy because of KRAS gene testing. KRAS gene testing for EGFR is not a clear predictor of a lack of benefit from EGFR antagonist antibodies in colon and lung cancer.

Source: Cell Function Analysis

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