gpawelski Posted August 30, 2011 Share Posted August 30, 2011 The U.S. Food and Drug Administration (FDA) approved crizotinib (Xalkori), a drug that shrinks tumors in lung-cancer patients with a rare genetic abnormality, the latest molecularly targeted therapy to win a rapid approval from the agency. Patients with this cancer would be identified by a genetic test made by Abbott Laboratories that was also approved, and then take the pills twice a day. As reported in Forbes, Xalkori will cost $9,600 per patient per month, meaning it could cost $80,000 or more for the average patient. But Xalkori is only effective in about 5% of patients whose tumors have a mutation in a gene called ALK. A biotech executive states the real cost of the drug is $9,600 plus 25 ALK tests, because that's how many patients will need to be screened for one to actually get Xalkori. Forbes stresses that given those costs, it’s easy to see how DNA sequencing in cancer might have a market in the future. That’s one of the big potential markets for companies like Illumina, Complete Genomics, and Life Technologies, which are sequencing whole human genomes at a cost of $5,000 or less. Those technologies could carry extra pathology costs, too. The question of whether to consider spending $3,000 or more for a cell-based functional profiling test is interesting, especially with the lastest press release from Pfizer about their new drug Xalkori (crizotinib). The drug will cost $9,600 per patient per month and the gene test for it will cost $1,500 per patient. There are lots of things which determine if drugs work, beyond the existence of a given target (like ALK for Xalkori). Does the drug even get into the cancer cell? Does it get pumped out of the cell? Does the cell have ways of escaping drug effects? Can cells repair damage caused by the drug? Do combinations of drugs work in ways which can't be predicted on the basis of static gene expression patterns? Tumor biology is a lot more complex than we'd like it to be. Cancer is more complex than its gene signature. Many common forms of cancer present as a host of mutated cells, each with a host of mutations. And they're genetically unstable, constantly changing. That's why so many cancers relapse after initially successful treatment. You kill off the tumor cells that can be killed off, but that may just give the ones that are left a free reign. The idea of searching for clinical responders by testing for a single gene mutation seems like a nice theoretical idea, but you may have to test for dozens of protein expressions that may be involved in determining sensitivity/resistance to a given drug. Because if you miss just one, that might be the one which continues cancer growth. And at $1,500 a pop, that's a lot of dough, on top of the inflated price of the single drug! The key to understanding the genome is understanding how cells work. The ultimate driver is "functional" pre-testing (is the cell being killed regardless of the mechanism) as opposed to "target" pre-testing (does the cell express a particular target that the drug is supposed to be attacking). While a "target" test tells you whether or not to give "one" drug, a "functional" pre-test can find other compounds and combinations and can recommend them, all from the one test. Source: Cell Function Analysis Quote Link to comment Share on other sites More sharing options...
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