According to a story from newswise.com, a team of researchers from the University of New Hampshire may have discovered the next new treatment for a rare form of blood cancer called Waldenström’s macroglobulinemia (WM). The approach, which involved targeting certain cell proteins that play a role in controlling DNA information, was able to slow the growth of WM cells. This finding was with a two part drug combination, and results were even more promising when a third therapy was tossed into the mix.
About Waldenström’s Macroglobulinemia (WM)
Waldenström’s macroglobulinemia, which is also known as lymphoplasmacytic lymphoma, is a rare type of blood cancer that affects two types of B lymphocytes, including plasma cells and lymphoplasmacytoid cells. A distinct characteristic of this type of cancer is the presence of a high concentration of IgM antibodies. It is a slow progressing form of blood cancer, and many patients can lead active lives. While it cannot be cured, it is treatable; some patients are able to experience years of remission without symptoms. There are only about 1,500 new cases per year in the U.S. Although it mostly occurs due to sporadic genetic mutations, a family history increases risk. Symptoms include vision loss, headaches, enlargement of the lymph nodes, liver, and spleen, bleeding nose and gums, weight loss, fatigue, and general weakness. To learn more about WM, click here.
Study Findings
The scientists aimed to explore the epigenetic regulation of cancer cells as a potential area of treatment intervention. Epigenetics in this context refers to how DNA ‘opens’ and ‘closes’ to permit the encoding and expression of a given gene. Proteins carry different roles, such as erasing genetic code, the interpretation of the code, or writing the code. The scientists chose to focus in on two proteins: bromodomain and extraterminal (BET). These are interpreting or reading proteins and a prior study has linked them to cancer and other illnesses.
The team selected I-BET-762 and JQ-1 as their therapies of choice, both of which are classified as inhibitors of BET. In the lab setting, WM cells were treated with these inhibitors and both were able to reduce cell proliferation, an effect that was found to be dose dependent. JQ-1 appeared to be the most effective; however, neither drug triggered the death of WM cells. The researchers tested venetoclax, ibrutinib, and panabinostat separately with the BET inhibitors and determined that panabinostat was the most effective when added.
This was the first study that indicates the potential of BET inhibition as an approach for WM. The authors concluded that patients using ibrutinib, which is the only FDA approved therapy for this cancer, may see benefit with the addition of JQ-1.
This study was originally published in the journal Epigenomics.
