“`html
A gene known as DNMT3A is crucial for directing blood stem cells to develop into various cell types found in blood, including erythrocytes, leukocytes, and platelets. When this gene acquires mutations — which may happen with aging or due to environmental factors like smoking — an individual’s likelihood of developing blood malignancies, such as acute myeloid leukemia (AML), rises.
DNMT3A functions by affixing chemical markers to the DNA strand through a mechanism referred to as DNA methylation. Up to this point, DNA methylation was the sole recognized role of this gene, but the impact of altered DNA methylation patterns — induced by mutated forms of DNMT3A — on abnormal blood cell development and blood malignancy has been ambiguous.
Currently, fresh research from WashU Medicine researchers presents evidence that DNMT3A possesses previously unrecognized mechanisms of affecting blood stem cell lifespan and genomic stability that are entirely separate from its methylation roles. The study, published in the journal Cell Stem Cell, was spearheaded by Grant A. Challen, a medical professor in the Oncology Division. Challen is also a research member of Siteman Cancer Center, located at Barnes-Jewish Hospital and WashU Medicine.
The research, performed in murine models and human cells, demonstrates that, irrespective of methylation, DNMT3A influences the length of telomeres — the protective caps on DNA strands that shorten with each cell division, restricting the number of divisions possible. When DNMT3A is absent or malfunctioning, telomeres remain prolonged, thereby eliminating replication constraints and permitting blood stem cells to proliferate indefinitely— a characteristic of cancer. Additional experiments also highlighted previously unrecognized functions of this gene in DNA damage response, which also contributes to cancer emergence and advancement. These findings expand the understanding of this gene’s influences in blood malignancies and may aid in the development of novel treatment strategies.
The post Surprising new roles discovered for known cancer gene appeared first on The Source.
“`