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.
Berberine for myeloma? MM is an incurable blood cancer. Standard-of-care chemotherapy and radiation can cause serious short-term, long-term, and late-stage side effects. Though treatments not approved by the FDA can be a risk, MM patients often look for therapies outside of what their oncologist prescribes to them.
Enter berberine for myeloma. According to the two studies linked below, berberine can help the MM patient manage their incurable cancer while managing possible side effects.
I was diagnosed with chemotherapy-induced cardiomyopathy 15 years after I had my autologous stem cell transplant as well as known cytotoxic chemo regimens of:
I believe my oncologist prescribed known cardiotoxic regimens because he didn’t believe I would live for 15-plus years. As MM patients live longer and longer, I believe more and more MM survivors will be diagnosed with long-term side effects such as chemotherapy-induced cardiomyopathy.
I posted the video below because I felt it was a balanced explanation of berberine’s pros and cons-
Years of experience have shown me that newly diagnosed MM patients must rely on both conventional and non-conventional therapies to manage their incurable blood cancer.
Email me at David.PeopleBeatingCancer@gmail.com to learn more about the full spectrum of MM therapies.
David Emerson
“Background- Current therapies for multiple myeloma (MM) are associated with toxicity and resistance, highlighting the need for novel, effective therapeutics. Berberine (BBR), a botanical alkaloid derived from several Berberis medicinal plants, has exhibited anti-tumor effects, including against multiple myeloma (MM); however, the molecular mechanism underlying the anti-MM effect has not been previously described. This study aimed to identify the target of berberine and related mechanisms involved in its therapeutic activity against MM.
Results- Here, we demonstrated that BBR treatment killed MM cells in vitro and prolonged the survival of mice bearing MM xenografts in vivo. A screening approach integrating surface plasmon resonance (SPR) with liquid chromatography-tandem mass spectrometry (LC-MS/MS) identified UHRF1 (ubiquitin-like with PHD and RING Finger domains 1) as a potential target of BBR. Combining molecular docking and SPR analysis, we confirmed UHRF1 as a BBR-binding protein and discovered that BBR binds UHRF1 in the tandem tudor domain and plant homeodomain (TTD-PHD domain). BBR treatment induced UHRF1 degradation via the ubiquitin-dependent proteasome system and reactivated p16INK4A and p73 in MM cells. Overexpression of UHRF1 promoted the MM cell proliferation and rendered MM cells more resistant to BBR, while silencing of UHRF1 with siRNA attenuated BBR-induced cytotoxicity.
Conclusions- In summary, our study has identified UHRF1 as a direct target of BBR and uncovered molecular mechanisms involved in the anti-MM activity of BBR. Targeting UHRF1 through BBR may be a novel therapeutic strategy against MM…”
Abstract- Berberine (BBR), an isoquinoline alkaloid, exerts protective effects on various cardiac injuries, and also extends the lifespan of individuals. However, the cardioprotective effect of BBR on cardiac senescence remains unknown.
This study investigated the effects of BBR on cardiac senescence and its underlying mechanism. Senescent H9c2 cells induced by doxorubicin (DOX) and naturally aged rats were used to evaluate the protective effects of BBR on cardiac senescence.
The results showed that BBR protected H9c2 cells against DOX-induced senescence. Exogenous Klotho (KL) exerts similar effects to those of BBR. BBR significantly increased in protein expression of KL, while transfection with KL-specific siRNA (siKL) inhibited the protective effect of BBR against senescence.
Both BBR and exogenous KL decreased the levels of reactive oxygen species, inhibited apoptosis, and alleviated mitochondrial dysfunction in these cells; and transfection with siKL attenuated these effects of BBR.
In naturally aged rats, BBR indeed protected the animals from cardiac aging, at least partially, through lowering the levels of cardiac hypertrophy markers, and increased the expression of KL in cardiac tissue.
Additionally, BBR markedly reversed downregulation of sirtuin1 (SIRTI) in the aged heart. In vitro experiments revealed that BBR and exogenous KL also increased the expression of SIRT1, whereas siKL limited this effect of BBR in senescent H9c2 cell.
In summary, BBR upregulated KL expression and prevented heart from cardiac senescence through anti-oxidative and anti-apoptotic effects, as well as alleviation of mitochondrial dysfunction. These effects may be mediated via regulation of the Klotho/SIRT1 signaling pathway…”
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