Blood cancer is a type of cancer that affects the blood-forming tissues such as bone marrow and lymphatic system. It is a serious and often life-threatening condition that affects thousands of people each year. However, researchers have identified a new target that may prevent blood cancer from developing. This promising development is seen as a major breakthrough in the field of cancer research and could lead to new treatments that could help save lives. In this article, we will explore this exciting discovery and what it means for the future of blood cancer treatment.
Blood cancer is a complex disease that can affect the production and functionality of blood cells. There are three main types of blood cancer: leukemia, lymphoma, and myeloma, which can manifest in the bone marrow, lymphatic system, or other parts of the body where blood cells are formed. The disease is triggered by the development of cancerous clones of blood stem cells, which undergo explosive clonal expansion, increasing the risk of developing blood cancer and cardiovascular disease. Currently, physicians measure clonal growth rates, which are used to predict blood cancer risk by comparing blood samples taken years apart.
However, a team of global biomedical researchers, led by Alexander Bick, MD, Ph.D., of Vanderbilt University Medical Center, has developed a new method for assessing the growth rate of precancerous blood stem cell clones. The technique, called PACER, measures the number of passenger mutations to determine the expansion rate of cancerous clones at a single time point.
In their research published in Nature, the scientists discovered a gene called TCL1A, which is responsible for driving clonal expansion. The team also found that drugs targeting this gene could reduce clonal growth rates, thus reducing the risk of blood cancer. TCL1A had not previously been related to blood stem cell biology, making it an exciting new drug target for preventing blood cancer.
The PACER technique was tested on 5,000 individuals with non-inherited blood stem cell mutations that triggered clonal hematopoiesis of indeterminate potential (CHIP), but who did not have blood cancer. Using genome-wide association studies, the team discovered TCL1A, a gene linked to abnormal blood stem cell expansion, triggering clonal growth rates. They also found that the TCL1A variant suppressed gene activation, slowing down clone growth rates.
Bick, assistant professor of Medicine in the Division of Genetic Medicine and director of the Vanderbilt Genomics and Therapeutics Clinic notes that the research is ongoing, with the possibilities of discovering more unknown pathways relevant to precancerous growth in other tissues as well as blood.
The research at VUMC is supported by the National Institutes of Health, a Burroughs Wellcome Fund Career Award for Medical Scientists, a Pew-Stewart Scholar for Cancer Research Award, and the Vanderbilt-Ingram Cancer Center. Over 50 institutions in the U.S., Germany, Sweden, and the Netherlands participated in the study. The breakthrough has significant potential to assist physicians in reducing their patients’ risk of developing blood cancer in the future.
In conclusion, the discovery of a new target that may prevent blood cancer is significant progress in the field of medical research. The identification of a specific protein and its role in the development of these diseases may lead to more effective treatments and ultimately, save lives. This breakthrough demonstrates the power of scientific exploration and the potential for advancements in healthcare. As we continue to learn more about the underlying causes of blood cancer, we move closer to a future where these devastating diseases may be cured.
