A new study conducted by University researchers has identified a gene that plays a role in regulating blood-forming stem cells.
The study, published in the Journal of Clinical Investigation, provides new insight into the role of the absent, small or homeotic 1-like (Ash1L) gene in the human blood system. The research sheds new light on the scientific processes involved in both maintaining healthy blood cells and renewing old and diseased ones.
Ivan Maillard, assistant Hematology/Oncology professor and a senior author of the study, said a central feature of the study was the association researchers uncovered between Ash1L and another gene, Mixed Lineage Leukemia 1 — or MLL1 — which belongs to the same family.
“We saw that this gene (Ash1L) was playing an important function in the blood-forming stem cells, but also that it was doing so in conjunction with another member of the same family that has previously been implicated in leukemia,” he said.
Maillard said it is this association between Ash1L and MLL1 that has researchers excited. Finding a link between Ash1L and leukemia creates the possibility of making advances in both diagnosing and treating leukemia.
Rackham student Jennifer Chase, an author of the study, said researchers are looking into how Ash1L and MLL1 cooperate.
“Once we understand the biochemistry behind their interaction, we will be able to make therapeutic approaches toward the diseases that they are involved in,” Chase said.
Researchers used mice to investigate the Ash1L gene. They selectively inhibited Ash1L in one contingent of mice, MLL1 in a second contingent and both in a third contingent. Results showed a mild reduction in blood-forming stem cells in the bone marrow for mice missing either Ash1L or Mll1, but a catastrophic effect for mice missing both.
“When we looked at the bone marrow of the mice and saw no stem cells, that was very unusual,” Chase said. “These experiments showed that the Ash1L gene is critically important in regulating stem cells in mice.”
Maillard said perhaps one of the biggest implications of this study is the potential it creates for future research. One avenue researchers can take is inhibiting the gene, and the proteins it encodes, to further understand its chemical function.
Even more exciting, Maillard said, is that further research may indicate Ash1L plays a role in a host of different diseases.
“Because this gene is so well-conserved in evolution, we think that it is possible for it to have a role in many different human cancers in different organs,” Maillard said.