From ScienceDaily.com is an article we can use to help with visulization ideas.
The latest generation of cancer chemotherapeutic drugs specifically targets mutant enzymes or "oncoproteins" that have run amok and now promote uncontrolled cell growth. Cancer cells, with their backs against the wall, have the tendency to fight back. A major goal of cancer research is to frustrate these acts of cellular desperation.
In a forthcoming issue of Cancer Cell, investigators at the Salk Institute for Biological Studies uncover one means cancer cells use to stay alive and in doing so suggest a strategy to overcome their tendency to fight back. The study, shows that resistance to the chemotherapeutic drug rapamycin is mediated by the survival factor NF-kB.
Rapamycin, like the pharmaceutical superstar Gleevec, which revolutionized the treatment of chronic myelogenous leukemia, is a so-called signal transduction inhibitor or STI, a small molecule that stifles inappropriate growth signals sent by mutant proteins in cancer cells.
The Hunter lab previously showed that mouse cells lacking tumor suppressors known as TSC genes are more susceptible to the lethal effects of chemotherapeutic agents than are normal cells. Why cells from these TSC null mice were so poorly equipped to survive was not entirely clear.
Now, the team found that human cells lacking TSC genes were vulnerable to chemotherapeutic attack because they couldn't activate a major line of defense mediated by the Nuclear Factor kappa B, known as NF-kB, which triggers both inflammatory and survival responses by inducing transcription of specific genes.
Not only did this explain why TSC null cells are vulnerable to insult, but it also provided biochemical evidence that there is crosstalk between two survival mechanisms. The findings show for the first time that the TSC complex can regulate the NF-kB signaling cascade.
The experiments also explained a paradox: TSC null cells treated with rapamycin actually survived cellular insult better than untreated cells-a highly inauspicious outcome if the goal is to kill cancer cells. By increasing NF-kB activity in the TSC null cells when they were exposed to chemotherapeutic drugs.
Rapamycin, an immunosuppressant used to block organ rejection after transplants, also inactivates proteins stimulating cell division and in clinical trials has been combined with other drugs to halt cancer cell growth.
But to cancer cells, rapamycin is both friend and foe. "Rapamycin is not as successful as initially expected in treating cancer," explains Ghosh. "Instead of killing cells, you end up triggering a survival response in them." This study, however, suggests that taking NF-kB out of the game would make rapamycin less "friendly."
A major problem of chemotherapy is that sooner or later cancer cells develop resistance, which requires higher and higher doses of chemotherapeutics. Rapamycin-mediated killing of cancer cells could be increased by inhibiting the function of NF-kB proteins.
So, how does all this apply to our work as hypnotherapists? Let's help our clients by visualizing the cancer cells just giving up! Talk to the proteins and let them just stop stimulating unwanted cell growth. Let those cancer cells just stop fighting back.