Turning off the RUNX1 gene improves resistance to cancer cells.

A recent study of the development of gene-related blood cancer has explained why resistance occurs when treated with common anticancer drugs.
team at Douglas University found that a gene called RUNX1 interfered with signaling molecules, so cancer cells became resistant to steroid drugs.
researchers say that if there are drugs that can turn off the gene, it will certainly improve the situation.
the findings were published in the Journal of Biocellular Chemistry.
runtherun series is designed to maintain healthy blood cells, but the abnormal RUNX1 gene plays a vital role in a number of diseases, including leukemia and lymphoma.
they found runX1 inhibits or promotes the growth of cancer, depending on the switch of genes.
the genes of the lipids can alter the balance - "signals" of lipid molecules found in cell membranes that regulate cell procedural death.
runX1 abnormal expression, neuroamine phosphate, a lipid that stimulates cell growth and survival, explains why patients become resistant to dexamethasone, the steroid used to treat cancer.
, if a drug that has been abnormally responsive to RUNX1 is developed, combined with steroids, it will greatly speed up the course of cancer treatment. "Steroids such as dexamethasone are suitable for the treatment of commonly used drugs such as leukemia and lymphoma, and while resistance to dexamethasone is widespread, its root cause is unknown," said the head of the
research team.
the new study not only provides a clearer picture of how this RUNX gene abnormality causes cancer to develop, but also promotes the development of new drugs to prevent resistance to steroids.
" Source: Decoding Medicine.