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.
Click the orange button to the right to learn more about what you can start doing today.
Multi-Drug Resistance (MDR) is the enemy of all multiple myeloma patients, survivors and caregivers. MM survivors are said to have reached MDR when their multiple myeloma no longer responds to conventional therapies.
Consider evidence-based non-conventional therapies that can, according to research, enhance the efficacy of Velcade aka bortezomib regardless of MDR.
One of the most often asked questions that I receive on PeopleBeatingCancer is if supplement __________ could interfere with chemotherapy ___________. It seems to me that the studies linked below clarify the answer to this question.
Thymoquinone not only does not interfere with Velcade, melphalan and doxorubicin, it can enhance the efficacy of those chemotherapy regimens against multiple myeloma.
While I caution all MM patients, survivors and caregivers about the challenges of long-term and/or high-dose toxicity, I have come to view Velcade as being the least of other MM evils.
By this I mean that Velcade has been in clinical practice for more than 10 years. I consider it to be a routine or sort of a backbone MM therapy. Revlimid, Velcade, Dexamethasone is the standard-of-care triplet induction therapy for newly diagnosed MM patients. RVd provides an exceptional overall response rate.
I do not want to come across as a cheerleader for any form of toxic chemotherapy. My point is that the newly diagnosed MM patient must learn about all forms of evidence-based MM therapies including
To learn more about the spectrum of therapies for multiple myeloma scroll down the page, post a question or comment and I will reply to you ASAP.
Hang in there,
“Scientists have found a potential new pathway to stop bortezomib resistance in patients with multiple myeloma (MM).
Researchers suggest that strategies could be developed to use BTZ in combination with existing therapies. They additionally note that MM cells produce insulin-like growth factor 1 (IGF-1). BTZ resistance has been associated with heightened levels of IGF-1 and its receptor.
“The IGF-1R inhibitor OSI-906 can increase the cytotoxicity of BTZ in MM cells, and PI3K and AKT are the downstream targets of IGF1,” they write. “AKT inhibition also causes BTZ-resistant cell death,” said the study authors…”
“CONCLUSIONS- A large volume of research in MM has highlighted the cardinal role of the BMME as a complex signaling molecules network, in which MM onset, progression and DR are regulated by a contact-dependent and -independent interplay between MM cells and their surrounding microenvironment. The role of the BMME network has been seen to be more complex since the discovery of the new players, miRNAs, exosomes and CAFs. The therapeutic failure of novel MM agents (first and second generation proteasome inhibitors, IMIDs, etc.) that target cell adhesion, cytokines secretion and survival pathways may be explained by their involvement. Notably, CAFs, miRNAs deregulation and/or the exosomes cargo (miRNAs/cytokines/proteins) could permit MM cells to achieve apoptotic escape and/or prosurvival autophagy by modulating alternative signaling pathways. Nevertheless, in-depth investigations are needed to better elucidate the role of miRNAs, exosomes and CAFs in affecting a tumor-prone BM niche.
In conclusion, MM drug resistance, being a multistep transformation process in which several players cooperate among themselves, provides the rationale for a multiple targets therapeutic approach with the aim of creating an unsupportive BMME and thereby enabling anti-MM therapies.
” Here we show that HNK significantly induces cytotoxicity in human multiple myeloma (MM) cell lines and tumor cells from patients with relapsed refractory MM. Neither coculture with bone marrow stromal cells nor cytokines (interleukin-6 and insulin-like growth factor-1) protect against HNK-induced cytotoxicity.
Furthermore, HNK enhances MM cell cytotoxicity and apoptosis induced by bortezomib. In addition to its direct cytotoxicity to MM cells, HNK also represses tube formation by endothelial cells, suggesting that HNK inhibits neovascurization in the bone marrow microenvironment.
Taken together, our results provide the preclinical rationale for clinical protocols of HNK to improve patient outcome in MM.”
“However, majority of patients with myeloma suffer relapse or develop chemoresistance to existing therapeutic agents. Thus, there is a need to develop novel alternative therapies for the treatment of MM. Thus in the present study, we investigated whether thymoquinone (TQ), a bioactive constituent of black seed oil, could suppress the proliferation and induce chemosensitization in human myeloma cells and xenograft mouse model. Our results show that TQ inhibited the proliferation of MM cells irrespective of their sensitivity to doxorubicin, melphalan or bortezomib.
Interestingly, TQ treatment also resulted in a significant inhibition in the proliferation of CD138+ cells isolated from MM patient samples in a concentration dependent manner. TQ also potentiated the apoptotic effects of bortezomib in various MM cell lines
Overall, our results demonstrate that TQ can enhance the anticancer activity of bortezomib in vitro and in vivo and may have a substantial potential in the treatment of MM.”