Although we know that KRAS tumor mutations limit benefit from Erbitux, about six out of ten colorectal cancer patients have normal or wild type KRAS. Yet Erbitux doesn’t work for many of them either.

There may be a simple way to predict early in treatment whether Erbitux is going to help to not.

Significantly more patients whose blood levels of magnesium dropped more than 50 percent after their first treatment with irinotecan and Erbitux had their tumors shrink. It also took longer before their cancer got worse, and they lived longer. Read the rest of this entry »

Dr. Lenz

Recent data suggest that some KRAS mutations act like normal or wild-type KRAS. Maybe for those mutations, Erbitux could be used for treatment.

A recent publication in the Journal of the American Medical Association by Dr. Sabine Tejpar using an international collaboration showed that some mutations act like wild-type KRAS and that these patients actually may benefit from Erbitux therapy.

Maybe we were wrong thinking that all KRAS mutations are the same. Haven’t we learned from our mistakes before? Read the rest of this entry »

There is some evidence that patients having a specific type of KRAS gene mutation may respond better to Erbitux® (cetuximab) chemotherapy than others who have KRAS-gene mutations.

Previous studies have shown that people with KRAS-mutated tumors did not respond to Erbitux®, and practice guidelines now recommend testing all tumor cells for the mutation before starting Erbitux therapy in patients with recurrent, advanced colorectal cancer.

The study, reported in the Oct. 27 Journal of the American Medical Association (JAMA), examined both the data and tissue samples of 579 patients in several studies who received Erbitux® between 2001 and 2008 for chemotherapy-refractory cancer. Those patients with “codon-13” mutations had longer overall and progression-free survival by several months than those with other KRAS mutated tumor cells. Laboratory tests of tumor cell responses also showed that codon-13-mutated cells responded to cetuximab when other KRAS-mutated cells did not.

The study authors concluded that “Evaluation of cetuximab therapy in these tumors in prospective randomized trials may be warranted.”

What it means for patients:

Current evidence has shown the codon-13 type of KRAS mutation to be relatively rare, and more research on therapy response is necessary. It is probably too soon to change recommendations for therapy for those having the codon-13 mutation.

Source: Journal of the American Medical Association, Oct. 27, 2010

Disclosure:  The Colorectal Cancer Coalition has received funding from Eli Lilly & Company, Bristol-Myers Squibb and ImClone Systems, the companies that manufacture and market Erbitux, in the form of unrestricted educational grants.  The Coalition has ultimate authority over website content.

Does adding Erbitux to chemotherapy help people whose colorectal cancer has spread beyond the colon or rectum to distant body sites?

The answer is yes, according to a pooled analysis of two large randomized clinical trials comparing chemotherapy alone to chemotherapy plus Erbitux® (cetuximab).  However, benefits depend on whether or not patient tumors have mutations of two genes, KRAS and BRAF.

Previous studies have shown that only patients with normal or wild type KRAS get any benefit from EGFR inhibitors Erbitux or Vectibix™ (panitumumab) so a combined analysis of the CRYSTAL and OPUS studies looked only a outcomes in KRAS wild type tumors.  In addition, the research team studied the effect of mutations to BRAF.

They found that adding Erbitux to initial chemotherapy improved overall survival time, time until cancers got worse (progression-free survival), the percent of tumors that shrank with treatment (overall response rate) for tumors with wild-type KRAS.  The best outcomes were in patients who had both wild-type KRAS and wild-type BRAF. Read the rest of this entry »

Adding Erbitux® (cetuximab) to standard chemotherapy for stage III colon cancer didn’t improve patient outcomes and added more side effects.

All of the patients in the NO147 trial had cancer that had spread to their lymph nodes and had surgery before beginning chemotherapy. They had normal or wild-type KRAS genes in their tumors.They were randomly assigned to FOLFOX chemotherapy for 6 months or FOLFOX plus Erbitux. 

The trial was closed before the planned number of patients were enrolled because an analysis showed that there was no benefit to the additional Erbitux and continuing the trial would not help patients. Read the rest of this entry »