gpawelski Posted March 16, 2008 Share Posted March 16, 2008 The cancer research arena has reached a sorry state of affairs. The tiniest increase in the survival time or median time to progression of drug-treated cancer patients is touted as a cure. One example is the clinical reality for metastatic colorectal cancer. The FDA-approved combination regimen of irinotecan, bolus fluorouracil, and leucovorin (IFL) plus Avastin increases median overall survival by 4.7 months. This small increase comes with a host of side effects, which impinge upon the quality of life, as well as placing a burden on the patient, as well as the healthcare system. The clinical reality is that there is no cure for metastatic colorectal cancer. The much-vaunted blockbuster drug Avastin is simply an antibody supplement incorporated into an already complex chemotherapeutic drug regimen that may slow down the cancer process depending on the genetic constitution of that individual. The clinical reality for metastatic breast cancer is similar. The treatment with Herceptin followed by lapatinib and capecitabine only increase the median time to progression from 4.4 to 8.4 months. Furthermore, 70% of patients do not respond to Herceptin, and resistance develops in virtually all patients. The sobering fact remains, both advance diseases remain incurable, which contrasts with the glowing reports on Avastin and Herceptin emanating from the financial and tabloid media. What are the responses of government agencies and academic institutions to this clinical reality? Yes, progress is slow, it's a complex problem, but we are moving in the right direction. If billions of dollars are poured into DNA sequencing of primary tumors, then we hope to find the critical mutations that cause cancer and then make drugs so that each patient can have a unique treatment. The major problem with this is the primary tumor is so heterogeneous that each cell within it is likely to have a unique genomic signature at the level of mutations, as well as at the level of gross genomic imbalances and methylation signatures. And the cells that will be dangerous to the health of the patient and depart to other organs make up only a minute fraction of the tumor. They are also genomically different to the cells in the primary tumor. Which of the millions of mutations, methylation changes, and gemomic imbalances are in the cells that leave the primary tumor? This cannot be ascertained by bioinformatic and statistical methods. It involves isolating the cells that depart. Also, which of the genomic alterations that are in the departing cells will be instrumental in the process of subsequent metastatic growth? Most of the cells that lease home don't survive the journey in the blood or lymph systems, and many cancerous cells that eventually do lodge in a distant organ simply remain dormant. It would seem more prudent to invest in the development of diagnostic technologies for detecting cancer growths, as well as the properties of cells that are destined to metastasize. When the front-line treatment for solid tumors is still chemotherapy (cytotoxic or targeted) and radiation, and the best that blockbuster drugs can achieve is to prolong the inevitable by either a few months or not at all, then it's surely time to stop the delusion. Personalized cancer cures are not just around the corner and carte blanche DNA sequencing will produce just that - carte blanche. Is the future of cancer medicine one in which doctors become financial advisors, telling their patients whether they can or cannot afford expensive treatments of dubious survival value? The solution is to get back to using old fashion human brainpower to develop noninvasive screening technologies for detecting the earliest possible cancerous growths. Resources and intellectual horsepower need to flow into areas that have clinical impact. Source: George L. Gabor Miklos, Ph.D., Philip J. Baird, M.D., Ph.d., "Curing Cancer: Running on Vapor," May 1, 2007 edition of Genetic Engineering and Biotechnology News. Quote Link to comment Share on other sites More sharing options...
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