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An article was written by Ana Sandoiu and checked by Jasmin Collier, giving some facts on a new innovative way to kill off cancer cells in acute myeloid leukemia. This would occur while preserving and regenerating healthy red blood cells.
The new study was carried out by researchers from the McMaster Stem Cell and Cancer Research Institute at McMaster University in Ontario, Canada. A professor of biochemistry and biomedical sciences at McMaster University and director of the McMaster Stem Cell and Cancer Research Institute, Mick Bhatia, led the investigation. His findings have been published in the journal Nature Cell Biology.
Focusing on targeted leukemic cells is the conventional method for treating leukemia, with little attention to preserving red blood cells. Production of healthy blood cells in the bone marrow is crucial though for preventing leukemia patients from having anemia or fatal infection.
Allison Boy is the first study author and a postdoctoral fellow at the McMaster Stem Cell and kCancer Research Institute. She believes their approach represents a different way of looking at leukemia and they consider the entire bone marrow as an ecosystem, rather than the traditional approach of studying and trying to direct kill the diseased cells themselves. Enough new therapeutic options for patients have not been delivered by these traditional approaches and the standard-of-care for leukemia hasn’t changed in several decades. According to the American Cancer Society (ACS) it was estimated that 21,380 people would be diagnosed with acute myeloid leukemia (AML) during 2017. Seniors tend to be the target for AML.
Bone marrow samples from 34 genetically diverse patients with AML were collected. They examined the patients’ blood cell formation process to compare it with that of healthy donors. They then examined the behavior of individual cells in vitro or in cell cultures, and in vivo, or in mice that had human cells transplanted into them. It was found the disease disrupts the adipotcytic niche in the bone marrow and leukemia suppresses the bone marrow adipocytes that store fat. This led to dysfunction in the stem cells and progenitor cells. This would later go on to form red blood cells in a healthy body, so the maturation of red blood cells were therefore stopped.
A so-called PPAR, gamma agonist, a drug commonly used to treat type 2 diabetes, was administered to mice and found that it restored the fat cells in the bone marrow. This so-called rebirth of fat cells rescued the healthy hematopoietic maturation while repressing leukemic growth. Boosting the fat cells in the bone marrow regenerated the healthy blood cells while killing off the cancerous leukemic ones.
Prof. Bhatia believes the focus of chemotherapy and existing standard-of-care is on killed cancer cells, but instead they took a completely different approach which changes the environment the cancer cells live in. This suppresses the bad cancer cells and also blisters the good healthy cells, allowing them to regenerate in the new drug-induced environment.
They vision this as becoming a potential new therapeutic approach that can either be added to existing treatments or even replace others in the near future. The drug activates blood regeneration to provide benefits for those waiting for bone marrow transplants by activating their own healthy cells.
Dr Fredda Branyon