Autophagy Functions in Hematological Malignancies Biology and Therapy Resistance
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Autophagy".
Deadline for manuscript submissions: closed (20 November 2023) | Viewed by 2579
Special Issue Editors
Interests: autophagy; signaling; metabolism; acute myeloid leukemia
Special Issues, Collections and Topics in MDPI journals
Interests: host autophagy; metabolism; immune response; acute myeloid leukemia
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
While recent approaches to treat hematological cancers hold great promise, therapy resistance is bound to happen and mainly accounts for treatment failure. Therefore, the identification of new targets and resistance mechanisms is urgently needed to improve clinical outcomes. The well-conserved catabolic process, autophagy, has previously been implicated in initiation, progression, and therapeutic resistance of several hematological disorders from myeloproliferative and myelodysplastic syndromes to leukemia and lymphoma. This survival mechanism, characterized by the lysosomal degradation of cytoplasmic content and damaged organelles, ensures energy and cellular homeostasis. In addition, especially through its role in metabolism regulation, autophagy has been increasingly associated with oncogenesis. However, studies to better understand its role and identify through which molecular and cellular mechanisms autophagy regulates hematological malignancies’ biology and response to therapy, especially in vivo, are still necessary.
This Special Issue will investigate, in vitro and in vivo, the contribution of autophagy to hematological malignancies’ development, growth, and relapse depending on the treatments used, in order to understand whether autophagy modulation could be an interesting strategy to improve therapy efficacy.
Dr. Carine Joffre
Dr. Laura Poillet
Guest Editors
Manuscript Submission Information
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Keywords
- autophagy
- hematological cancers
- therapy resistance
- metabolism
