Waldenström macroglobulinemia (WM) is a rare variety of lymphoma, and currently, no cure for the disease is present globally; moreover, it only has one FDA-approved treatment. All these problems collectively make it challenging to treat patients suffering from this disease.
A recent study has come up with a solution to this problem, which may turn out to be a significant breakthrough in the Cancer Diagnosis Market. Researchers have introduced drugs that may be successful in reducing WM cancer cells or even completely killing them. The research is the first of its kind and has reported promising results of inhibitors in WM and may open doors for new clinical possibilities.
The team took an innovative approach to the problem and targeted specific cell proteins that control DNA information with the help of inhibitors or drugs. This resulted in effectively reducing the growth of the cancer cells. The team also combined three drugs that could kill WM cancer cells and believe that it could lead to more treatment options.
The study states that targeting different types of proteins within inhibitors may be the way to increase high therapeutic results in different kinds of cancers. However, satisfactory results in WM that researchers have aspired for have been lacking till now.
The team emphasized the epigenetic regulation of WM cancer cells. Epigenetics is a field that explores how DNA is opened and closed to allow particular genes to be encoded or expressed. All proteins have their own exclusive set of tasks to perform, such as writing a code, reading or interpreting it, and some work on erasing the code. Researchers focused on two proteins, namely bromodomain and extra terminal (BET), which work as epigenetic readers and are present in pathological conditions like cancer. The drugs consisting of these proteins can block gene expression that regulates cancer cells by slowing or stopping their growth.
The team treated the WM cancer cells with BET inhibitors I-BET-762 and JQ-1 and concluded that the growth of WM cells present in the lab was reduced. It was noted that the dose-dependent effect was considerable for both drugs. JQ-1 demonstrated the most robust inhibitory impact with a 70% reduction in cell creation at the highest dose. However, neither of the drugs was successful in killing the cell completely.
Researchers then proceeded to add three different drugs, ibrutinib, venetoclax, and panobinostat, with BET inhibitors (JQ-1 and I-BET-762)-This was in various combinations with one drug at a time. After analyzing all three-drug combination separately, they stated that adding panobinostat or venetoclax to the inhibitors was more helpful than adding ibrutinib. Adding panobinostat turned out to be the best combination therapy.