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January 27, 2009 • Volume 6 / Number 2 About the Bulletin  |  Bulletin Archive/Search
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Featured Article

Study Forecasts Savings for Marker-based Colorectal Cancer Treatment

ATCG's with silhouettes of people of varying heights. Genetic testing to identify patients who will–and who won't–benefit from treatment is becoming the standard of care for some diseases.

Using the anti-EGFR therapy cetuximab (Erbitux) to treat patients with metastatic colorectal cancer who have the normal form of the KRAS gene—and not the mutant form—would save more than $600 million annually, according to study results presented January 14 at the Gastrointestinal Cancers Symposium in San Francisco.

Some health services researchers warned that the findings from a single study should be interpreted with caution, arguing that they may not adequately account for various factors that could limit the extent of the savings.

Calling it a “macroeconomic statement,” Dr. Nicole Mittmann, executive director of the Health Outcomes and PharmacoEconomics Research Centre at Sunnybrook Health Sciences Centre in Toronto and co-chair of the Working Group on Economic Analysis at the National Cancer Institute of Canada Clinical Trials Group, said the study provides a good first “global estimate” of potential savings from more targeted use of cetuximab and other anti-EGFR inhibitors in patients with metastatic colorectal cancer.

The study relied on an economic model that included the estimated incidence of metastatic colorectal cancer for 2008, the average cost of a commercial test for KRAS status, and—relying on data from the CRYSTAL trial—the average number of cetuximab doses each patient receives and the number of patients expected to have KRAS mutations. After subtracting the cost of testing all patients from the projected savings of giving the drug only to patients with normal KRAS, the final savings came to an estimated $604 million.

That might be a conservative figure, stressed the study’s lead author, Dr. Veena Shankaran from the Robert H. Lurie Comprehensive Cancer Center, during a press briefing, because it does not include savings associated with recurrent disease or with managing the toxicities related to treatment in patients with mutated KRAS.

Following the results from retrospective analyses of several large clinical studies, which showed that cetuximab has a clinical benefit only in patients who have normal KRAS, testing metastatic colorectal cancer patients for KRAS status is slowly becoming the standard of care, Dr. Jennifer Obel of NorthShore University HealthSystem said during the briefing.

On the same day the study’s findings were presented, the American Society of Clinical Oncology released its first-ever “provisional clinical opinion,” which advises that all patients with metastatic colorectal cancer undergo KRAS gene mutation testing to determine whether they are eligible for anti-EGFR therapy with cetuximab or a similar agent, panitumumab (Vectibix).

Last November, the National Comprehensive Cancer Network added a similar recommendation to its guidelines on the treatment of colon and rectal cancers. (Free registration is required to view the links.)

Given the expense of new cancer therapies, Dr. Mittmann said, “The challenge has become, can you afford them? Treating only patients with genetic characteristics associated with improved clinical benefits may improve the affordability of these targeted agents.”

Most insurers are now routinely paying for KRAS testing, Dr. Obel noted, even though the FDA has yet to act on requests from the companies that manufacture cetuximab and panitumumab, ImClone (which was recently acquired by Eli Lilly) and Amgen respectively, to revise the drug labels so that they reflect the data on KRAS status and clinical benefit.

The FDA’s Oncologic Drugs Advisory Committee heard presentations on the companies’ labeling change applications last month, but the committee was not asked to make a labeling recommendation.

Also from the GI Cancers Symposium

Specific mutations in the EGF gene in people with gastroesophageal reflux disease (GERD) are associated with higher esophageal cancer risk compared with GERD patients who don't have the mutations, researchers from the University of Toronto and Harvard University reported at the 2009 Gastrointestinal Cancers Symposium in San Francisco. The mutation did not have the same effect in patients who did not suffer from GERD. GERD is a known risk factor for esophageal cancer, but, according to the researchers who led the case-control study, this is the first time specific genetic mutations have been identified that may predict which people with GERD are at elevated risk of developing the malignancy. Patients with the EGF mutations who suffered from GERD more frequently or for at least 15 years were at the highest cancer risk.

Results from a phase II study presented by German researchers at the same meeting suggested an important new treatment option for patients with malignant neuroendocrine tumors of the midgut (or lower part of the small intestine), a rare cancer with few effective treatments. In the multi-institutional study, patients treated with the drug octreotide LAR (Sandostatin LAR) had a median time to tumor progression of 14.3 months, compared with 6 months in patients who received a placebo. At 6 months, 64 percent of patients treated with the drug had stable disease, versus 37.2 percent of patients in the placebo arm. Overall survival data are not yet available. During a press briefing, Dr. Jennifer Obel from NorthShore University Health System in Illinois called the study results "practice changing."

—Carmen Phillips

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