As cancer research goes, progress is being made against multiple myeloma at light speed. It may not feel that way to anxious patients, but advances are being reported nearly every week.
True, all promising studies don’t produce productive therapies. But some do—many more than for most cancers.
There are politics and funding issues to deal with. FDA mandated delays and red tape don’t help. But the advances I have observed over the past three years have been amazing!
Here are the highlights from a number of these noteworthy studies. Since I did a story about bisphosphonates this weekend, lets start with this Myeloma Beacon article released last week:
Prolia May Delay The Onset Of Bone Complications More Effectively Than Zometa In Multiple Myeloma Patients
By Jessica Langholtz – Oct 27, 2010
The pharmaceutical company Amgen recently announced that its new drug Prolia more effectively prevents bone pain and fractures in patients with advanced bone disease than Zometa. Prolia was noted to have higher efficacy in patients with various types of cancers, including multiple myeloma. The announcement followed the presentation of results from recent Phase 3 trials at the European Society of Medical Oncology Annual Meeting.
How about this, forwarded to me by a reader from a Website called Genetic Engineering and Biotechnology News:
Study identifies key molecules in multiple myeloma
New research links three molecules to a critical tumor suppressor gene that is often turned off in multiple myeloma, a presently incurable cancer of the blood.
The findings might offer a new strategy for treating this disease and other blood cancers, according to researchers at The Ohio State University Comprehensive Cancer Center-Arthur G. James Cancer Hospital and Richard J. Solove Research Institute who led the study.
The silenced molecules are called miR-192, miR-194 and miR-215. All of them are microRNAs, a large class of molecules that are master regulators of many important cell processes.
The study, published in the Oct. 19 issue of Cancer Cell, suggests that re-activating these three molecules triggers expression of the P53 tumor suppressor gene. This, in turn, slows the growth and leads to the death of myeloma cells and could provide a new strategy for treating the disease.
Not technical enough for you? This study implies testing for several genetic abnormalities in multiple myeloma patients may not be necessary:
Translocation t(14;16) and multiple myeloma: is it really an independent prognostic factor?
Blood. 2010 Oct 20
Authors: Avet-Loiseau H, Malard F, Campion L, Magrangeas F, Sebban C, Lioure B, Decaux O, Lamy T, Legros L, Fuzibet JG, Michallet M, Corront B, Lenain P, Hulin C, Mathiot C, Attal M, Facon T, Harousseau JL, Minvielle S, Moreau P
Many trials in myeloma are stratified on cytogenetic abnormalities. Among them, the most commonly chosen are the t(4;14), the del(17p), and the t(14;16). If data are well established for t(4;14) and del(17p), very few data support the use of t(14;16). In order to address this issue, we retrospectively analyzed 1003 patients with newly diagnosed myeloma for this abnormality. We identified 32 patients with the t(14;16). When compared with patients lacking the t(14;16), we did not observe any difference in overall survival (p=.28). Moreover, in multivariate analyses, the t(14;16) was neither prognostic (p=.39). In conclusion, our data do not support the use of t(14;16)-specific probes in the diagnostic panels of multiple myeloma.
OK—my eyes are starting to glaze over. But what amazing stuff! A new bisphosphonate may be available soon. Researchers have discovered that re-activating three molecules could provide a new strategy for treating our cancer. And scientist now know some expensive, additional genetic testing is probably not necessary when evaluating how to treat myeloma patients.
Hopeful advances for all of us! Feel good and keep smiling! Pat