Researchers have made an interesting find in the area of cancer research recently. Two different studies each independently provided a link between the FBW7 gene and a resistance to treatment with chemotherapy drugs that focus on tubulin to kill cancerous cells, such as Taxol. Tubulin is a protein which is integral in the network of filaments that maintains the cells infrastructure. Cells which are affected by anti-tubulin drugs cannot divide and eventually die without causing further spread of cancerous cell lines. However, many cells display a resistance to the affects of the anti-tubulin drugs. Which prompted some researchers to ask 'why?'.
One of the research projects that made the connection to FBW7 and this resistance was lead by Ingrid Wertz, this was prompted by the observation that some cells resist Taxol treatment. Wertz and her team noticed a trend that cells which had survived treatment had lower levels of MCL1, a protein associated with the cell's life cycle. Further observation revealed FBW7 was found to be destroying MCL1 in these cell, FBW7 was already known to be a cancer-fighting element in cells. Speculation was that defects in FBW7 may result in higher levels of MCL1 which allowed cells to resist treatment by anti-tubulin drugs. Sure enough, researchers soon found the link between these two proteins.
Another project, headed by Wenyi Wei was focused on researching a particular disease: T-cell acute lymphoblastic leukemia. With this disease, cells have a cocktail of proteins that should cause them to self-destruct but do not do so. Researchers looked into why this occurred and found that these cells lacked the FBW7 gene and without this, they did not break down MCL1 which was a necessary step in cell death. Wei connected this to drug resistance when T-ALL cells that were treated with drugs that targeted cell survivability-pathways were found to have lowered levels of MCL1 also. To try to fix this, Wei treated the cells with a drug that lowered MCL1 drugs and restored sensitivity to treatment.
While exciting in the prospect that oncologists now have insight into reasons why patients may be feeling less many experts in the field are quick to note that these results are only preliminary. They provide just a small glimpse at the bigger picture of cancer treatment. Research has shown only one implication of defects in the FBW7 gene, many other details may lie further downstream in the regulation of cell growth and death. But this is surely a good step for better, more effective cancer treatment.