[gdpawel]

One little-known effect of Paclitaxel is that in a subset of patients there will be up to a fivefold increase in the production of Interleukin - 8 (IL-8)- a cellular communication molecule that initiates the growth of new blood vessels to feed the growing cancer. In other words, if you fall into this subset of patients, treatment using Paclitaxel alone may not be effective at preventing recurrence.

IL-8 is under the control of an inflammatory regulating protein called nuclear factor-kappa Beta (NF-kB). When the activation of NF-kB is blocked, IL-8 dries up, much like a faucet that has been turned off. Thus, blocking NF-kB activation enhances the cancer killing ability of Paclitaxel. These results were seen with many types of cancer cells.

Inflammation is present before, and during the life of a cancer. In cancer, inflammation is a pathological process characterized by injury or destruction of tissues caused by a variety of cellular and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. However, inflammation is also essential for tissue repair and tissue rebuilding. Genomic testing allows to create a personalized map of your inflammatory tendencies based on your genomic predispositions.

It is this protein that is responsible for the abnormal rise in IL-8 during Paclitaxel administration. By measuring markers of cellular inflammation before, during, and after chemotherapy treatment, serves as a benchmark for your risk of cancer recurrence after chemotherapy treatment. Patients with high inflammatory markers during chemotherapy are at higher risk for recurrence, and thus need to more closely monitor and modulate their NF-kB expression after the chemotherapy ends.

Reference: Cell Function Analysis