Multiple Myeloma an incurable disease, but I have spent the last 25 years in remission using a blend of conventional oncology and evidence-based nutrition, supplementation, and lifestyle therapies from peer-reviewed studies that your oncologist probably hasn't told you about.
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I try not to use the word “cure” when I’m writing about multiple myeloma (MM). But I can come up with no other outcome for my MM experience. I remain completely MM free and I rely exclusively on evidence-based non-conventional therapies… I believe my multiple myeloma therapies have changed my genetic expression…
Conventional oncology studies chemotherapy and how it affects MM. That’s what they do. The top study below talks about changing MM genetic expression with chemotherapy.
I am a long-term multiple myeloma survivor and MM cancer coach. I have remained in complete remission from my “incurable” cancer since 1999 and I was originally diagnosed in 1994.
Conventional chemotherapy did little to treat my MM. In other words, “killing” my MM cells didn’t work for me. But since 1997, I have undergone a host of therapies all that could have changed how my MM genes expressed themselves aka epigenetics.
I have to be honest and admit that I can’t prove that my evidence-based, anti-MM nutrition, supplementation, bone health, lifestyle and mind-body therapies actually changed my genetic expression. I did not undergo genetic testing when I was first diagnosed. But as the studies linked and excerpted below explain, supplementation, nutrition and lifestyle can change gene expression. I can prove that all of the non-toxic therapies that I pursue daily are evidence-based and are cytotoxic to MM.
And I have had MM since 1994 and I have been in complete remission since early 1999. So what else could be the reason for what can only be called a cure of my multiple myeloma?
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David Emerson
“Moving further into personalized treatment decision making, this mutational profiling may guide therapeutic choice in the future with ever increasing number of available antimyeloma agents or nonmyeloma specific but pathway specific drugs.
In a study of 133 patients with relapsed myeloma treated with single-agent bortezomib, a targeted sequencing of a panel of 41 known oncogenes and tumor suppressor genes was performed [56]. Mutually exclusive mutations of BRAF and RAS were seen in closer to a half of patients and mutations of NRAS (but not KRAS) were associated with lower response rate to bortezomib [56].
On the other hand, mutations in IRF4 which are believed to be the downstream of immunomodulatory drug target of cereblon seem to be associated with better survival [55].
These studies uncovered actionable mutations in multiple myeloma, and coupled with explosion of various pathways and targeted inhibitors there is a growing optimism to hope for mutation specific adapted treatment strategies becoming reality in the near future…”