Acute Myeloid Leukemia and Autophagy
A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cell Biology".
Deadline for manuscript submissions: closed (14 May 2021) | Viewed by 3986
Special Issue Editors
Interests: autophagy; chaperone-mediated autophagy; acute myeloid leukemias; breast cancer; retinoids; differentiation therapy; transcription factors
2. ICVS/3B’s-PT Government Associate Laboratory, 4806-909 Braga/Guimarães, Portugal
Interests: acute myeloid leukemia; metabolism; aging; autophagy/mitophagy; cell death programs
Special Issue Information
Dear Colleagues,
Acute myeloid leukemia (AML) is a blood cancer characterized by a block in differentiation of leukemia blast that has acquired aberrant self-renewal potential. With an estimated 5-year overall survival of less than 30%, AML is one of the deadliest cancers. Within the past few years, advanced molecular technology has allowed for a better understanding of AML biology and pathogenesis. Unfortunately, treatment strategies have not significantly changed since 1970, and therapy failure and relapses remain high. The molecular landscape of AML affects key hematopoietic signaling pathways such as apoptosis, proliferation, and differentiation. Therefore, a better understanding of AML biology and pathology will lead to investigating new therapy strategies combining targeted agents with standard chemotherapeutic agents.
Several reports have demonstrated that AML cells have deregulated autophagy. Because of the heterogeneity of the disease, the role of autophagy as a tumor suppressor or promotor in AML is still under debate.
For this Special Issue of Biology, we invite authors to submit original research papers and reviews that cover mechanisms or potential therapy strategies in AML involving autophagy pathways. We look forward to reading your contributions.
Dr. Paula Ludovico
Dr. Magali Humbert
Guest Editors
Manuscript Submission Information
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Keywords
- acute myeloid leukemia
- autophagy
- lysosomes
- blood
- leukemia stem cell
- therapy resistance
- differentiation
- hematopoiesis
