Blocking cellular 'freecycling' may slow bone marrow scarring in myelofibrosis
In a new study published in Nature Communications, Boston Children's Hospital researchers identified a new target responsible for scar formation in the bone marrow of patients with a type of blood cancer known as myelofibrosis. Combining traditional myelofibrosis therapy with drugs that block scar formation may be a more effective treatment for patients with the disease.
A new study in Nature Communications has identified a potential target for treating bone marrow scarring in myelofibrosis, a type of blood cancer. Myelofibrosis, which typically affects older adults, is often diagnosed when the condition has progressed, resulting in a poor prognosis with an average life expectancy of five to seven years.
The study, led by researchers at Boston Children's Hospital, found that megakaryocytes, platelet-making cells in the bone marrow, release scar-building chemical messages in myelofibrosis patients. These messages, typically recycled within cells, are instead released externally, contributing to the formation of scar tissue and limiting the ability of stem cells to produce healthy new blood cells.
By blocking this "freecycling" activity, drugs such as hydroxychloroquine prevented scar-building messages from reaching the bone marrow space and reduced scar tissue formation in mouse models of myelofibrosis. Combining these drugs with traditional treatments like JAK2 inhibitors, which are currently the first-line treatment for myelofibrosis, further decreased scarring and blood cell abnormalities in mice.
Researchers hope that targeting this mechanism will improve treatment outcomes for myelofibrosis patients by attacking the cancer through multiple mechanisms and potentially outmaneuvering resistance to current therapies.
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