Managing HIV is now more practical where treatment is patient-specific, people get medicine based on sequencing of patients HIV drug targets. This way drug resistance in HIV can be easily managed. Is it possible to mange drug resistance in cancer also?
Maybe for some malignancies. The bright example is CML, but even there we have problems with drug resistance due to cancer cell biology and transformations.
Of course we can. Apart from the example mentioned by Ahed Khatib, there are more cases of this kind. The first targeted drug for cancer treatment, gleevec, is not for all but those patients with Ph+ CML. Tarceva and Iressa are found to be more effective in patient with special EGFR mutation. The trend to develop the targeted drugs would be success only if the right patients were involved. And we also need to learn more to distinguish the different background of each cancer and find out the best way to combat it.
I raised this question because this problem addressed in both case are different. In case of HIV drug is advised based on drug-target interaction. Based on sequence of target drug is advised because mutation in target is responsible for resistance in HIV (due to frequent mutation in HIV strains). I have not seen any study where similar approach has been adopted in case of cancer. As far as I know in case of cancer researchers are trying to under relation between expression of human gene and drug resistance. We are in process of creating database on cancer drug resistance from different angle see http://crdd.osdd.net/raghava/cancerdr/ , we are not sure how community will use this database.
Hi Gajendra,
Of course we have the similar cases in cancer treatment. As I mentioned above, the use of Tarceva and Iressa in lung cancer is a exact example. Usually, the patients would take a gene sequencing to see if the tumor would response to the drugs. Some mutations, like region deletions in exon 19 and point mutation L858R, predict high response to the drugs. In contrast, point mutation T790M means the cancer are very like to resistant to the treatment.
A recently approved drug Vemurafenib, for melanoma treatment, is specific to target the BRAF kinase with V600E mutation.Of course in this case, the patients need to sequence the tumor gene to determine if the drug would bring benefit to them.
hi Mr.Gajendra, we have this Zinc finger technology, ZiFT which creates knock out in viral genome, HPV genome. and this technology is currently tried for cancer therapy...
Hi Aiken
Thanks for response, you have given excellent example where drug become resistance due to mutation. Do you have any idea about database which provides comprehensive information about mutations responsible for drug resistance in cancer.
First of all we have to understand that cancer is not a single disease caused by a specific virus as HIV. It is rather a constellation of many diseases with similar outcome, caused by multiple overstepping and interlacing etiologies and events involving both the genetics and epigenetics at the cellular level. There are also grades and stages, genetic suscecptability, DNA repair, host's immune response and its dysregulation, environmental and micro-environmental issues that decide response to therapy. It is far more complex with lesser known than unknown.
Secondly, in lieu of above the common outcome that is called cancer, is an autonomous growth refractile to most bodily influences and has far reaching implications than just making and breaking the cells such as metabolic derangement and para-neoplastic syndrome etc.Invasion, metastasis and neo-angiogenesis complicate it further and so on.
Thirdly, there is an emerging stem cell hypothesis regarding cancer origin and its heterogeneity. Thus cancer is a constant evolution of new clones of cells against all odds with preferential growth and metabolic edge,invasbility, metastatic potential and not simply the evasion of immune response as may be true for most viral infections, including HIV.
Furthermore, there is no single drug or group of drugs or muti-modalities that could work even against a single cancer across geographic limits. For example the breast cancer approach so far has resulted in far more intricacies in management than what most workers believed a decade back. In fact it has been observed that in a particular patient, for a particular cancer, response may be quite different and beneficial effects far too variable from short term to long term. That is why the term survival index or rates came into being
Therefore, what most people aim at is molecular profiling, gene signatures, predictive and prognostic bio-markers and the resultant personalized therapy. Not to be confused further, from current available trends, we are still far away from determining drug resistance against cancer in general, although some headway in some specific cases might have been made.
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