Listen to a blog summary of a research paper published by Genes & Cancer, entitled, "KDM3A/Ets1/MCAM axis promotes growth and metastatic properties in Rhabdomyosarcoma.”
Rhabdomyosarcoma (RMS) and Ewing Sarcoma are among the most common types of cancer that develop in childhood. In recent years, new studies from researchers at the University of Colorado Denver Anschutz Medical Campus have contributed to the expansion of biomedical knowledge about how these diseases progress—paving a way for novel treatment strategies and therapeutics to inhibit the progression of these diseases.
INTRODUCTION
RMS consists of two predominant and distinct disease subtypes: fusion-positive RMS (FP-RMS) and fusion-negative RMS (FN-RMS). Fusion-positive RMS is the more aggressive subtype and shows a strong metastatic tendency to spread to other parts of the body. The sarcomagenesis of FP-RMS is driven by a genetic mutation that spawns the abnormal cancer-driving protein PAX3/FOXO1, or P3F. These P3F oncofusion genes use transcriptional and epigenetic mechanisms to drive FP-RMS pathogenesis. However, little was previously known about the mechanisms P3F uses for metastasis.
Recently, a team of dedicated researchers—Lays Martin Sobral, Marybeth Sechler, Janet K. Parrish, Tyler S. McCann, Kenneth L. Jones, Joshua C. Black, and Paul Jedlicka—endeavored to better understand the mechanisms and molecular pathways contributing to RMS progression, including the more aggressive FP-RMS subtype. In 2020, their influential research paper was published in Genes & Cancer and entitled, “KDM3A/Ets1/MCAM axis promotes growth and metastatic properties in Rhabdomyosarcoma.”
Full blog - https://www.impactjournals.com/journals/blog/genesandcancer/how-ewing-sarcoma-led-to-discoveries-in-rhabdomyosarcoma/
Keywords - pediatric cancer, rhabdomyosarcoma, KDM3A, Ets1, metastasis
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