Nature Sub-Journal: Blood Cell Precancerous "Clonal Growth"

A study led by researchers at Will Cornell Medical School, New York Presbyterian Hospital, the New York Genome Center, Harvard Medical School, and the Dana-Farber Cancer Institute suggests that spontaneous mutations common in blood stem cells may contribute to the development
of these diseases by altering the gene activity program of stem cells and the mixing of blood cells they produce.

This mutation in blood stem cells, known as DNMT3A R882, causes a massive proliferation of circulating blood cells, or "clonal growth," that also contain this mutation
.

"These findings help us understand how these mutant cells are growing beyond normal cells and pave the way for possible future interventions against these cells to prevent cancer and other clonal growth-related scenarios
.

The study was conducted in
collaboration with Dr.

Dr.

For example, the researchers found that mutated stem cells tend to favor red blood cells and clotting platelets when producing mature blood cells, which provides a potential theoretical basis for a higher risk of cardiovascular disease in patients with clonal hyperplasia in the
blood.

The DNMT3A gene typically encodes an enzyme called methyltransferase, which helps place methylation on DNA
.

"We hope that by discovering such molecular signatures, we will be able to target these clones to grow and prevent the development of cancer in people who are still healthy," said Dr.

The researchers plan to further investigate clonal growth caused by other mutations
.

"We should soon be able to study more cells at the same time and give us a more complete picture of what's happening," said co-first author Neville Dusaj, a student
in the three-institution MD program at Landau Labs.