Recently Diagnosed or Relapsed? Stop Looking For a Miracle Cure, and Use Evidence-Based Therapies To Enhance Your Treatment and Prolong Your Remission

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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Multiple Myeloma Treatment- Long-term Bone Marrow Injury

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“Long-term Bone Marrow (LT-BM) injury is a common cancer treatment-related late effect caused by IR- and chemotherapy-induced damage to HSCs.”

Conventional multiple myeloma treatment is fraught with short, long-term, and late stage side effects.  According to the research linked and excerpted below, chemotherapy and radiation can cause long-term bone marrow injury. The more chemo and radiation you have, the more short and long-term damage is done to bone marrow.


I am a long-term MM survivor. I live with a host of long-term and late stage side effects caused by standard-of-care MM therapies following my diagnosis of MM in early 1994.

The object of this post is to educate newly diagnosed MM patients about long-term bone marrow injury caused by chemotherapy and radiation.

Full disclosure. I don’t understand all of the jargon used in the research below. I understand enough of it, I think, to apply it to my own MM experiences as well as those considering multiple myeloma therapies.

Chemotherapy and radiation can cause a short, long-term and late stage damage to the patient’s bone marrow. That much is clear. As much as I would like to say otherwise, chemotherapy is sometimes the only choice for MM patients with multiple myeloma growing in their bones causing blood, bone and kidney damage.

The two possible solutions? According to the two studies linked below, nutritional anti-oxidant supplementation. The articles specifically cite N-acetyl-cysteine to prevent long-term bone marrow injury. In addition, the article clearly states that chemotherapy causes bone marrow damage in a time and dose dependent manner. Translation? Less is more…

The patient chooses what therapies that he/she undergoes. You can choose NOT to have an autologous stem cell transplant. You can choose to stop induction therapy once you have reached complete remission. Yes, chances are your oncologist will push for more chemotherapy to reach a deeper, longer remission.

But the patient has the final say about his/her body.

Research shows that:

Consider chemo and radiation dose modification. Consider evidence-based anti-oxidant supplementation. Both will reduce your risk of long-term bone marrow damage.

To Learn More about N-Acetyl Cysteine- click now

To learn more about managing your MM, scroll down the page, post a question or comment and I will reply to you ASAP.

Hang in there,

David Emerson

  • MM Survivor
  • MM Cancer Coach
  • Director PeopleBeatingCancer

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Regulation of oxidative stress by ATM is required for self-renewal of haematopoietic stem cells.

“The ‘ataxia telangiectasia mutated’ (Atm) gene maintains genomic stability by activating a key cell-cycle checkpoint in response to DNA damage, telomeric instability or oxidative stress.

Mutational inactivation of the gene causes an

  • autosomal recessive disorder,
  • ataxia-telangiectasia,
  • characterized by immunodeficiency,
  • progressive cerebellar ataxia,
  • oculocutaneous telangiectasia,
  • defective spermatogenesis,
  • premature ageing and
  • a high incidence of lymphoma.

Here we show that ATM has an essential function in the reconstitutive capacity of haematopoietic stem cells (HSCs) but is not as important for the proliferation or differentiation of progenitors, in a telomere-independent manner. Atm-/- mice older than 24 weeks showed progressive bone marrow failure resulting from a defect in HSC function that was associated with elevated reactive oxygen species.

Treatment with anti-oxidative agents restored the reconstitutive capacity of Atm-/- HSCs, resulting in the prevention of bone marrow failure.

These results show that the self-renewal capacity of HSCs depends on ATM-mediated inhibition of oxidative stress.”

Hematopoietic stem cell senescence and cancer therapy-induced long-term bone marrow injury

” Unfortunately, these survivors are at increased risk for developing cancer treatment-related late effects, including ionizing radiation (IR)- and chemotherapy-induced long-term bone marrow (LT-BM) injury.

Because LT-BM injury can deteriorate over time or after the patients receiving additional cancer treatment or undergoing autologous BM transplantation, it may eventually lead to the development of hypoplastic anemia or myelodysplastic syndrome…

…long-term cancer survivors are at increasing risks to develop cancer treatment-related late effects that can adversely affect the quality of life, contribute to the ongoing burden of illness and costs, and decrease length of survival.

One of the common cancer treatment-related late effects is long-term bone marrow (LT-BM) injury resulting from IR- and/or chemotherapy-induced damage to hematopoietic stem cells (HSCs) ()…

Since HSC, MPP and HPC proliferation and differentiation can be stimulated by various hematopoietic growth factors (HGFs) such as

  • granulocyte-colony stimulating factor (G-CSF),
  • granulocyte/macrophage-colony stimulating factor (GM-CSF) or
  • erythropoietin,

these HGFs have been widely used in clinic to promote the recovery of BM hematopoietic function in patients after cancer therapy (). As such, the majority of cancer patients can recover rapidly from acute BM suppression after chemotherapy and/or IR with or without HGF treatment…

Unlike acute BM suppression, LT-BM damage is latent. Patients and animals with LT-BM injury usually have normal blood cell counts under normal homeostatic conditions in spite of a decrease in HSC reserves and an impairment in HSC self-renewal (,).

Because of this latency, the clinical implications of LT-BM injury have been largely overlooked. Moreover, the importance of LT-BM damage is further obscured by the seemingly complete recovery of peripheral blood cell counts, BM cellularity and the number of colony-forming units (CFUs), especially after the use of HGFs…

Impairment in HSC self-renewal has been well documented in patients and animals after exposure to TBI or treatment with various chemotherapeutic agents that can cause LT-BM injury (,,)…

ROS can regulate HSC function in a concentration-dependent manner. Low levels of ROS appear to be required for HSC proliferation, differentiation, and mobilization ()…

However, increased production of ROS can be detrimental to HSCs (,)…

Treatment of ATM−/−(ataxia telangiectasia mutated gene) mice with N-acetyl-cysteine can restore the function of HSCs and prevent the development of BM failure ()…

The induction of chronic oxidative stress by IR and chemotherapy sets in motion a self-perpetuating process of late deleterious effects, including:

  • cellular senescence,
  • genetic instability,
  • inflammation and
  • fibrosis (,,).


LT-BM injury is a common cancer treatment-related late effect caused by IR- and chemotherapy-induced damage to HSCs. Although LT-BM damage is latent, it is long lasting, shows little tendency for recovery, and can lead to hypoplastic anemia and predispose individuals treated with IR and chemotherapy to therapy-related myelodysplastic syndrome and acute myeloid leukemia (,,,).

In this review, we have summarized a number of recent findings regarding the role of oxidative stress in mediating IR- and chemotherapy-induced HSC senescence and LT-BM. These findings provide not only new insights into the molecular mechanisms whereby IR and chemotherapy induce HSC senescence but also potential novel therapeutic strategies that can be exploited to prevent and mitigate IR- and chemotherapy-induced LT-BM injury in cancer patients (Figure 2). Such strategies have the potential to significantly reduce the long-term adverse effects of conventional cancer therapy on the hematopoietic system,












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