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Chronic Myeloid Leukaemia and Its Impact on Bone Marrow Macrophages

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Ethan Sulliva
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Chronic Myeloid Leukaemia and Its Impact on Bone Marrow Macrophages

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Understanding Chronic Myeloid Leukaemia (CML)

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Chronic myeloid leukaemia (CML) is a type of cancer that starts in the blood-forming cells of the bone marrow and invades the bloodstream. This disease is characterized by the uncontrolled growth of immature cells that form the white blood cells in the bone marrow, leading to an increased number of white blood cells in the circulation. One of the key aspects to consider when understanding CML is the interaction it has with the bone marrow microenvironment and, particularly, with bone marrow (BM) macrophages.

Role of Macrophages in CML

Recent studies have shed light on the crucial role that macrophages play in controlling the progression and burden of CML. Macrophages are immune cells that are heavily involved in the removal of dead cells, foreign substances, and cancer cells. Despite their crucial role, the CML environment can alter the function of BM macrophages. Research has shown that the transcriptional profile and function of BCR ABL1 negative macrophages are altered within the CML bone marrow niche. This alteration leads to the presence of unique subpopulations of immature macrophages in the CML microenvironment.

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Impact of CML on Bone Marrow Microenvironment

A significant impact of CML on the bone marrow microenvironment is the promotion of myelopoiesis of normal hematopoietic stem cells (HSCs). This leads to an increase in the production of neutrophils, monocytes, and macrophages within the bone marrow. This promotion of myelopoiesis may appear beneficial, as these cells are part of the immune system. However, the CML environment also results in the aberrant production of CML secreted factors. These include proteins like lactotransferrin (LTF), which have a suppressive effect on the function of macrophages.

Role of LTF in CML

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Lactotransferrin (LTF) is a protein that is secreted in higher amounts in the CML environment. Studies have found that LTF can suppress CD36 expression, leading to reduced macrophage phagocytosis and efferocytosis. In simpler terms, the presence of LTF impairs the ability of macrophages to clear dead cells and other debris, including cancer cells. This dysregulation in protein secretion from CML stem and progenitor cells can have a significant impact on the progression and burden of the disease.

Future Implications

The understanding of the relationship between CML and BM macrophages is critical for further developments in the treatment and management of CML. Current research is focused on gaining a deeper insight into the altered transcriptional and functional characteristics of macrophages within the CML bone marrow. This could potentially lead to the identification of new therapeutic targets and strategies to control the progression of CML. Moreover, understanding the role of secreted factors like LTF could provide new avenues for therapeutic intervention.

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