Epigenetics and Transcription Networks in Leukemia
A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Pathophysiology".
Deadline for manuscript submissions: 30 December 2024 | Viewed by 451
Special Issue Editor
Special Issue Information
Dear Colleagues,
Leukemias are malignant disorders of the blood and bone marrow. Leukemia is the eleventh most common cancer in the United States. In 2023, it is estimated that there will be about 59,610 new cases of leukemia and 23,710 deaths from leukemia in the US. The diseases are largely understood to occur due to alterations in hematopoietic stem cells that cause their transformation into proliferative leukemia stem cells, initiating and maintaining these diseases. Epigenetic and transcription alterations play substantial roles as key functions of leukemia stem cells, such as self-renewal and resistance to standard therapy.
Epigenetic alterations, mainly DNA hypermethylation, histone modifications/remodeling, and aberrant non-coding RNA expressions, are three main epigenetic variations that have been implicated to play a role in leukemia progression. Recently, m6A RNA modification has also been shown to alter the epitranscriptome during leukemogenesis. Different epigenetic-based approaches have been developed and tested to inhibit or reverse the abnormal expression of epigenetic factors in leukemia. A better understanding of epigenetic and transcriptional aspects of leukemogenesis will shed light on new diagnostic and therapeutic approaches, thus greatly improving the outcomes of patients with hematological malignancies.
This special Issue will focus on epigenetic findings elucidating the molecular mechanisms of the development, progression and therapeutic resistance of leukemia. Original research or review articles related to oncogenesis, prognosis, new therapeutic approaches and treatment resistance are welcome.
Dr. Yi Qiu
Guest Editor
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Keywords
- leukemia
- epigenetics
- gene regulation
- genetic mutation
- chemoresistance
- therapy
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