Research Shows that Promising Cancer Drug Works by Overactivating Cancer Gene

Researchers at the University of Michigan Comprehensive Cancer Center have been studying a drug called bortezomib, which has shown great promise as a melanoma cancer fighter, and have determined that it does not kill the cancer out right, but instead actually speeds up the action of the cancer promoting genes to the point where they become so active that they destroy themselves.

The researchers believe that this type of treatment might eventually prove to be effective for many other types of cancers as well.

Bortezomib, is a drug that the FDA has approved to fight advanced multiple myeloma, and in this laboratory study, they found that uses its ability to selectively restrain the melanoma tumor cells by causing the c-MYC oncogene, which is a gene that works with others to change a normal gene cancerous, to make too much of NOXA, which is a substance that promotes cell death.

The way the current cancer treatment work is by blocking certain of the oncogenes, genes that disrupt the normal cellular signals that tell the cells when it is time to multiply or when it is time to die. The premise for this type of treatment is that if they are able to disable the oncogenes, it is impossible for the cancer cells to rapidly reproduce and spread beyond control, But oncogenes not only make cancer cell divide and spread rapidly, they can also do the opposite and speed up the death of the cancer cells, a process called apoptosis.

Melanoma tumor cells are some of the toughest to treat. They are resistant to most of the existing cancer drugs and because of this, the prognosis for a patient with advanced melanoma has not shown any marked improvement for more than 30 years. Now, they have discovered that the melanoma cells themselves contain the one thing that can kill them, when it is triggered.

In the lab tests, the researchers studied not only how bortezomib acted on the cultured melanoma cell, but they tested other drugs as well.