Gene Status, Key In Reaping Erbitux’s Benefits: Study
by Jyoti Pal Published on June 3, 2008 - 0 comments
Testing for the gene mutation would help determine in advance whether a colondefine cancerdefine patient will benefit from treatment with ImClone Systems' drug Erbitux, a new research from Eurpoe claims.
Colondefine cancers triggered from the normal form of gene, the KRAS, respond best to an important class of cancerdefine drugs, known as EGFR inhibitors (Imclone’s Erbitux and Amgen’s Vectibix), than tumors with a common mutation of the gene, the facts presented at the 44th Annual Meeting of the American Society of Clinical Oncology held in Chicago on Sunday, confirmed.
Researchers examined tissue samples of a little less than 600 patients undergoing initial treatment for advanced colorectal cancer. While, all patients were administered a drug combination called Folfiri, some also got Erbitux.
While, 59 percent of the patients with normal KRAS gene responded to Erbitux combination treatment and their tumors shrank by more than half, 43 percent of those who took chemotherapy alone posted no major benefits.
Moreover, amongst all patients with normal KRAS, those treated with Erbitux posted a 32 percent reduction in the risk of tumor progression and recurrence, compared with the 15 percent reduced risk, which was for all patients, during the risk study.
"KRAS testing should be routinely conducted in all colorectal cancer patients immediately after diagnosis," urged study’s lead author Dr. Eric Van Cutsem, professor at the University Hospital Gasthuisberg in Leuven, Belgium. "If you focus on the KRAS patients, you see a much bigger benefit, which is clinically very important," he claimed.
The testing for gene mutation costs between $500 and $1,000, while Erbitux costs between $8,000 and $10,000 a month.
Erbitux is a monoclonal antibody naturally produced by the immune systemdefine in response to infection. As the normal standard KRAS gene transmits signals for cell division and is associated with uncontrolled division of tumor cells, the Erbitux treatment attacks the cancer cells by latching onto them and blocking their replication.
"These findings are very important for patients and also for clinicians, as we have shown that, using this KRAS test, we can predict which patients will benefit and which will not benefit from Erbitux," said Cutsem.
"We have shown that the activity of Erbitux is confined to the patients with the KRAS tumor so, if we know in advance that a patient has the mutation, we know that we don't have to treat them with Erbitux," he concluded.
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