Special Issue "Pathology of Acute Myeloid Leukemia (AML)"

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Pathophysiology".

Deadline for manuscript submissions: 25 April 2024 | Viewed by 193

Special Issue Editor

Dr. Olga K. Weinberg
E-Mail Website
Guest Editor
Division of Pathology, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA
Interests: AML; myeloid neoplasms; biology

Special Issue Information

Dear Colleagues,

Acute myeloid leukemia (AML) is a heterogeneous hematological malignancy characterized by the uncontrolled proliferation of myeloid precursor cells in the bone marrow. This Special Issue will address various topics in the pathogenesis of AML, encompassing the underlying genetic and epigenetic alterations that contribute to disease development and progression.

AML arises from the acquisition of somatic mutations affecting key regulatory genes involved in hematopoietic cell differentiation, self-renewal, and apoptosis. The most frequently mutated genes include FLT3, NPM1, DNMT3A, IDH1/2, and TP53. These mutations disrupt normal cellular signaling pathways, leading to dysregulated proliferation and impaired differentiation of myeloid progenitor cells. In addition, chromosomal aberrations, such as translocations, inversions, and deletions, further contribute to leukemogenesis by disrupting important genes involved in hematopoiesis.

Epigenetic alterations also play a crucial role in AML pathogenesis. Aberrant DNA methylation patterns and histone modifications lead to the silencing of tumor suppressor genes and the activation of oncogenes, promoting leukemic transformation. Furthermore, alterations in microRNA expression profiles can affect critical signaling pathways and contribute to leukemogenesis.

The interaction between leukemic cells and the bone marrow microenvironment is another significant factor in AML pathogenesis. Abnormalities in the bone marrow niche, including changes in cytokine signaling, stromal cell interactions, and angiogenesis, create a supportive environment for leukemic cell survival, proliferation, and chemoresistance.

Understanding the intricate molecular mechanisms underlying AML pathogenesis is crucial for the development of targeted therapies and personalized treatment approaches. Advances in genomic profiling techniques and functional studies are rapidly unraveling the complexities of AML biology, providing opportunities for novel therapeutic strategies that may improve patient outcomes in the future.

Dr. Olga K. Weinberg
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers

This special issue is now open for submission.
Back to TopTop