Publications by authors named "Mona Mohammadhosseini"
Identifying and targeting microenvironment-driven pathways that are active across acute myeloid leukemia (AML) genetic subtypes should allow the development of more broadly effective therapies. The proinflammatory cytokine interleukin-1β (IL-1β) is abundant in the AML microenvironment and promotes leukemic growth. Through RNA-sequencing analysis, we identify that IL-1β-upregulated ASF1B (antisilencing function-1B), a histone chaperone, in AML progenitors compared with healthy progenitors.
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- Emerging research highlights how factors in the leukemia microenvironment protect cancer cells from treatments and contribute to drug resistance, signaling the need for targeted therapies in acute myeloid leukemia (AML).
- A study involving around 300 AML patient samples found that higher levels of the cytokine CCL2 correlate with reduced effectiveness of MEK inhibitors, leading to further investigations into the mechanisms behind this resistance.
- The findings suggest that targeting both CCL2 and the MEK pathway can improve treatment responses in AML, proposing a combination therapy as a promising strategy to overcome drug resistance and enhance patient outcomes.
Germ line mutations in the RUNX1 gene cause familial platelet disorder (FPD), an inherited disease associated with lifetime risk to hematopoietic malignancies (HM). Patients with FPD frequently show clonal expansion of premalignant cells preceding HM onset. Despite the extensive studies on the role of RUNX1 in hematopoiesis, its function in the premalignant bone marrow (BM) is not well-understood.
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