Myeloid Leukemia Can Now be Put To Stop by Blocking Its Growth Factor

by Rishika Gupta on  April 25, 2018 at 7:55 PM General Health News
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Highlights
  • A new molecular pathway has been discovered that leads to the growth of acute myeloid leukemia (AML).
  • Increase of SHARP1 levels, a circadian clock gene had a two-fold effect on leukemia development.
  • Drug with innovative strategies can be developed to stop this pathway and thereby prevent further development of acute myeloid leukemia.
A new role of a circadian clock protein has been found to assist in the development of acute myeloid leukemia (AML), finds a new study. The name of this protein is SHARP1. The findings of this study are published in the Nature Communications journal.
 Myeloid Leukemia Can Now be Put To Stop by Blocking Its Growth Factor
Myeloid Leukemia Can Now be Put To Stop by Blocking Its Growth Factor

Acute myeloid leukemia is a very rare disease as nearly 1% of all new cancer cases come under these. It is also commonly known as the cancer of blood and bone marrow. The five-year survival rate of this disease is less than twenty percent.

This new molecular pathway involves the circadian clock gene, SHARP1 to assist the growth of AML. New therapeutic strategies can be developed to block this pathway.

The study conducted by researchers at the Cancer Science Institute of Singapore (CSI Singapore) at the National University of Singapore (NUS) took six years.

SHARP1 was previously thought to be responsible for control of the circadian rhythm only. But this study has shown that this particular protein does have a dark side. It was found to assist the AML development.

It was found that Alteration of the MLL gene has helped by SHARP1 as it was its subset. Alteration of these MLL genes are known to cause AML.

"We found that MLL-AF6 binds with SHARP1, leading to an increase in the level of SHARP1. The increase of SHARP1 levels has the two-fold effect of initiating leukemia development, as well as maintaining the growth of leukemic cells. Interestingly, in addition to its own cancer-causing functions, our study also revealed that SHARP1 could act upon other target genes of MLL-AF6 to aggravate the progression of AML. But by removing or reducing the level of SHARP1, the growth of leukemic cells could be stopped, " explained Daniel G. Tenen.

The research team had to employ an array of genetic screening techniques tools to identify this pathway of AML.

Reference
  1. Akihiko Numata, Hui Si Kwok, Akira Kawasaki, Jia Li, Qi-Ling Zhou, Jon Kerry, Touati Benoukraf, Deepak Bararia, Feng Li, Erica Ballabio, Marta Tapia, Aniruddha J. Deshpande, Robert S. Welner, Ruud Delwel, Henry Yang, Thomas A. Milne, Reshma Taneja, Daniel G. Tenen. The basic helix-loop-helix transcription factor SHARP1 is an oncogenic driver in MLL-AF6 acute myelogenous leukemia, Nature Communications (2018).DOI:10.1038/s41467-018-03854-0


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