HER2 Support Group Forums - View Single Post - circulating tumor cells as a surrogate for response to treatment

gdpawel · 08-30-2011, 01:54 PM

http://www.prnewswire.com/news-relea...128327503.html

Rich

Wonder if this is like the just FDA-approved Xalkori (crizotinib) for NSCLC. Patients with this cancer would be identified by a genetic test that will cost $1,500 per patient and then take the pills twice a day.

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 iin about 5% of patients whose tumors have the ALK gene mutation.

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. The question of whether to consider spending $3,000 or more for a cell-based functional profiling test is interesting.

There are lots of things which determine if drugs work, beyond the existence of a given target (like ALK for Xalkori or Her2 for Herceptin). 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.

08-30-2011, 01:54 PM	#2
gdpawel Senior Member Join Date: Aug 2006 Location: Pennsylvania Posts: 1,080	Biocept and Clarient Announce Collaboration on First Test for Circulating Tumor Cells http://www.prnewswire.com/news-relea...128327503.html Rich Wonder if this is like the just FDA-approved Xalkori (crizotinib) for NSCLC. Patients with this cancer would be identified by a genetic test that will cost $1,500 per patient and then take the pills twice a day. 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 iin about 5% of patients whose tumors have the ALK gene mutation. 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. The question of whether to consider spending $3,000 or more for a cell-based functional profiling test is interesting. There are lots of things which determine if drugs work, beyond the existence of a given target (like ALK for Xalkori or Her2 for Herceptin). 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.