When the drug Velcade® came on the market in 2003, it was seen as a godsend for patients with multiple myeloma, an intractable blood cancer that until then was uniformly fatal. Velcade was the first in a novel family of drugs called proteasome blockers, which make it hard for cancer cells to break down and recycle used, misfolded or excess proteins.
In the last decade, Velcade has been tested against a long list of other cancers, including melanomas, lymphomas, as well as prostate, lung and breast cancers. The results have been mixed, particularly for breast cancer.
But in the case of breast cancer, the uncertain outcomes may in part be because past trials looked in the wrong place. New research by Fabio Petrocca, MD, and Judy Lieberman, MD, PhD, in Boston Children’s Hospital’s Program in Cellular and Molecular Medicine, suggests that proteasome blockers like Velcade may indeed have a place in the breast oncologist’s armamentarium, but just for a particular aggressive kind of breast cancer called basal-like, triple-negative breast cancer (TNBC). …
It used to be that there were two kinds of lymphoma, a cancer of the white blood cells: Hodgkin’s lymphoma, and everything else (aka non-Hodgkin’s lymphoma). Now doctors recognize more than 20 different types of non-Hodgkin’s lymphoma, based on cell type, genetic/genomic features, what the cells look like under a microscope, where the tumors form, etc.
With greater knowledge of what makes a lymphoma a lymphoma has also come the recognition that each type, subtype and sub-subtype responds to the same treatment differently—or not at all.
That’s led to a more targeted approach to discovering and developing anti-lymphoma drugs, based on the unique molecular features of a particular subtype. A team of researchers including Hao Wu, PhD, of the Program in Cellular and Molecular Medicine at Boston Children’s Hospital, is getting good traction focusing on one especially hard-to-treat lymphoma. …
Leukemia and other cancer cells are really good at hurdling over the obstacles we throw at them. It’s the whole basis of drug resistance: we attack a mutation with one drug, and another mutation arises to cancel out the drug’s effect. Or the cell ramps up other pathways to compensate for the one blocked by the drug.