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Me thinks you may be right about cancer stem cells being the root of the problem.
Stem cells have that infinite ability to renew themselves and produce the many different cell types that make up a human. Cancer's hallmark is its ability to grow infinitely, multiplying into various cells that make up a tumor. Is cancer the result of a normal stem cell turned bad or an ordinary cell that somehow acquires a stem cell's immortality and versatility?
The recent finding that Temodar (temozolomide) increased the number of cancer cells with stem-like characteristics sounds eerily similar to the increase in the number of metabolic activity of mitochondria of the surviving cells from taxane (Taxol) therapy, even in cases where the majority of the cells are being killed by taxanes. It may indeed give clinical response (tumor shrinkage), however, these are mostly short-lived and relapses after a reponse to taxanes are often dramatic.
In stem cell research, anti-cancer treatments often effectively shrink the size of tumors, but some might have the opposite effect, actually expanding the small population of cancer stem cells that then are capable of metastasizing. Using the CellSearch System technique that quantifies circulating tumor cells, scientists had shown that chemotherapy with Taxol causes a massive release of cells into the circulation, while at the same time reducing the size of the tumor, explaining that complete pathologic responses do not correlate well with improvements in survival.
Circulating tumor cells (CTCs) are cancer cells that have detached from solid tumors and entered the blood stream. This can begin the process of metastasis, the most life-threatening aspect of cancer. To metastasize, or spread cancer to other sites in the body, CTCs travel through the blood and can take root in another tissue or organ.
Even before the advent of the CellSearch technique, it had been observed in Cell Function Analysis that there was an increase in the number of metabolic activity of mitochondria of the surviving cells from Taxol therapy, even in cases where the majority of the cells were being killed by Taxol.
This new research hightens the faults of gene amplificaton/mutation studies. Genetic profiling assumes that all drugs within a class will produce precisely the same effect, even though from clinical experience, this is not the case. Nor can genetic profiling tell anything about drug combinations.
Are you sure that you’ve identified every single protein that might influence sensitivity or resistance to drugs? The "cell" is a system, an integrated, interacting network of genes, proteins and other cellular constituents that produce functions. You need to analyze the systems' response to drug treatments, not theoretical predispositions.
Cancer is a complex disease and needs to be attacked on many fronts. Cellular profiling holds the key to solving some of the problems confronting the critical task of matching individual patients with the treatments most likely to benefit them.
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