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Anne Law

Cancer cocktails not always the cure

by Anne Law | Dun & Bradstreet Editor

February 6, 2009 | 1 Comment »

Will combining two or more drugs to combat a specific cancer produce a more desirable outcome for patients? Two study results released this week have indicated differing answers.

Results of a late-stage clinical trial conducted on non-small cell lung cancer patients indicate that a combination of Genentech and OSI Pharmaceuticals’ Avastin and Tarceva drugs could delay the advancement of the disease.

Another study, however, conducted using Avastin combined with Eli Lilly/ImClone’s Erbitux to combat colon cancer indicated the opposite – that using the two drugs together could worsen the patients’ condition, despite earlier indications that the combination might be helpful.

The moral of the story is that despite the progress that’s been made in cancer treatment, especially using new biotech treatments (on top of traditional chemotherapy treatments), doctors and patients shouldn’t be too hasty in mixing and matching drugs when those combinations, or ‘cocktails,’ haven’t been fully tested and approved. The success of one cocktail does not indicate another’s effectiveness.

Combination therapies can be a profitable avenue for drug companies in areas outside of cancer treatment, but they can also backfire, like Schering-Plough and Merck’s failed attempt to combine Claritin and Singulair. Merck and Schering-Plough have also faced some scrutiny over the effectiveness of Vytorin, a combination of the companies’ Zocor and Zetia medications that has been on the market since 2004.

Overall, drug cocktails require the same level of testing for efficacy and side effects as single medications. This is especially true for biotechnology drugs, which are rapidly moving beyond the realms of traditional success in cancer treatment but which also need to be used with caution, as we do not yet know their historical implications.

Instead of “blindly” mixing and matching drugs to individual cancer patients, what would be more beneficial is to sort out what’s the best profile in terms of which patients benefit from this drug or any other drug. Can they be combined? What’s the proper way to work with these new drugs?

If a drug works extremely well for a certain percentage of cancer patients, identify which ones. If one drug or another is working for some people (not average populations) then obviously there are others out there who would also benefit.

What’s good for the group (population) may not be good for the individual, affirms that in the tactic of using “fresh” biopsied cells to predict which cancer treatments will work best for the individual patient, these “smart” drugs have to get inside the cells in order to “target” anything.

If the “targeted” drug either won’t “get in” in the first place or if it gets pumped out/extruded or if it gets immediately metabolized inside the cell, it just isn’t going to work. Each of these new “targeted” drugs are not for everybody. Even when the disease is the same type, different patients’ tumors respond differently to the same agent.

Upgrading clinical therapy by using drug sensitivity assays measuring “cell death” of three dimensional microclusters of live “fresh” tumor cells, can improve the situation by allowing more drugs to be considered. The more drug types there are in the selective arsenal, the more likely the system is to prove beneficial.

Drug sensitivity tests support the idea that a marginal benefit in terms of overall survival is observed in cancer patients with normal prognoses, but there are marked survival benefits for cancer patients with poor prognoses.

Every cancer patient should have his/her own unique chemotherapy based on consultation of pathogenic profiles and drug sensitivity testing data. Having some foreknowledge of a given agent’s expected result before its administration would benefit the individual patient.

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