Multiple myeloma begins in plasma cells, and affects many of the marrow-containing bones in the body, including arm, pelvis, and leg bones. The number of new cases of myeloma was 6.1 per 100,000 per year based on 2007-2011 cases, and myeloma is most frequently diagnosed among people aged 75-84.
(SEER 18 2007-2011, All Races, Both Sexes)
The estimated incident of myeloma varies across the globe, with the highest rates being reported in the most economically developed regions of the world (e.g. Europe, North America, Australia/New Zealand) and the lowest rates in the least developed regions (e.g. parts of Africa, Asia and parts of Latin America).
Myeloma (C88 and C90), World Age-Standardised Incidence Rates, World Regions, 2008 Estimates
New combination therapy developed for multiple myeloma
Standard treatment for multiple myeloma encompasses chemotherapy, the administration of steroids and the targeted agent Velcade® (bortezomib). However, this form of blood cancer often develops resistance to therapies, which poses a major treatment challenge. Researchers at Virginia Commonwealth University Massey Cancer Center are reporting promising results from laboratory experiments testing a new combination therapy that could potentially overcome the resistance hurdle.
As researches show, multiple myeloma cells are able to survive by increasing the production of a protein known as Mcl-1. The protein regulates a number of processes that promote cell survival and has been implicated in resistance to anti-myeloma drugs that were initially effective. However, a team of researchers demonstrates that a novel drug combination both reduces Mcl-1 expression and disrupts its interactions with other proteins to effectively kill multiple myeloma cells.
The therapy combines a type of drug known as a Chk1 inhibitor with another called a MEK inhibitor. Chk1 inhibitors prevent cells from arresting in stages of the cell cycle that facilitate the repair of DNA damage, while MEK inhibitors prevent cells from activating a variety of proteins that regulate DNA repair processes while promoting the accumulation of pro-death proteins.
“By combining a Chk1 inhibitor with a MEK inhibitor, we have developed one of only a limited number of strategies shown to circumvent therapeutic resistance caused by high expressions of Mcl-1.” says Pei, instructor in the Department of Internal Medicine at the VCU School of Medicine.
Reference:
Circumvention of Mcl-1-Dependent Drug Resistance by Simultaneous Chk1 and MEK1/2 Inhibition in Human Multiple Myeloma Cells. PLoS ONE, 2014; 9 (3): e89064