Mitochondria are important cellular organelles that regulate metabolism and survival. These activities are characterized by extensive molecular crosstalk and interactions, e.g., the apoptotic machinery (including apoptosis regulator BCL2) is involved in the regulation of mitochondrial metabolism; the PINK1-Parkin axis regulates mitochondrial recycling, which plays roles in various leukemias; and mitochondria represent the site for oxidative phosphorylation, which provides energy to cells but is also an increasingly recognized target for cancer therapeutics.
Recent literature have highlighted that several mitochondrial functions and metabolism at the first time of diagnosis differs amongst acute myeloid leukemia (AML) patients. Other studies have demonstrated that monocytic AML cell differentiation together with mitochondrial functions are significant for the responsiveness to various forms of antileukemic strategies. This is one of the reasons why oxidative phosphorylation and the mitochondrial respiratory complex are considered a potential therapeutic target in cancer treatment.
In fact, differences in glucose metabolism, lipid and sterol metabolism, and amino acid metabolism that have been shown for cancer cells are likely to play roles in the effectiveness of cancer treatments in different patient populations. Which has done much to support the drive for personalized medical treatment.
Therefore, we are pleased to invite researchers to contribute to this Research Topic which intends to further describe the role of mitochondrial factors in therapy response and survival of AML and other blood malignancies such as acute lymphocytic leukemia (ALL), chronic myeloid leukemia (CML), and myelodysplastic syndromes (MDS).
Manuscripts that accommodate omics technologies and their integration, functional assays and/or bioinformatics and artificial intelligence strategies to identify mitochondrial drug-able proteins and routes, are of interest in this collection. Considerations on the implementation of fast and robust mitochondrial tests in the clinic will be appreciated.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Keywords:
mitochondria, AML, energy metabolism, antileukemic therapy, antileukemic strategies
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Mitochondria are important cellular organelles that regulate metabolism and survival. These activities are characterized by extensive molecular crosstalk and interactions, e.g., the apoptotic machinery (including apoptosis regulator BCL2) is involved in the regulation of mitochondrial metabolism; the PINK1-Parkin axis regulates mitochondrial recycling, which plays roles in various leukemias; and mitochondria represent the site for oxidative phosphorylation, which provides energy to cells but is also an increasingly recognized target for cancer therapeutics.
Recent literature have highlighted that several mitochondrial functions and metabolism at the first time of diagnosis differs amongst acute myeloid leukemia (AML) patients. Other studies have demonstrated that monocytic AML cell differentiation together with mitochondrial functions are significant for the responsiveness to various forms of antileukemic strategies. This is one of the reasons why oxidative phosphorylation and the mitochondrial respiratory complex are considered a potential therapeutic target in cancer treatment.
In fact, differences in glucose metabolism, lipid and sterol metabolism, and amino acid metabolism that have been shown for cancer cells are likely to play roles in the effectiveness of cancer treatments in different patient populations. Which has done much to support the drive for personalized medical treatment.
Therefore, we are pleased to invite researchers to contribute to this Research Topic which intends to further describe the role of mitochondrial factors in therapy response and survival of AML and other blood malignancies such as acute lymphocytic leukemia (ALL), chronic myeloid leukemia (CML), and myelodysplastic syndromes (MDS).
Manuscripts that accommodate omics technologies and their integration, functional assays and/or bioinformatics and artificial intelligence strategies to identify mitochondrial drug-able proteins and routes, are of interest in this collection. Considerations on the implementation of fast and robust mitochondrial tests in the clinic will be appreciated.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Keywords:
mitochondria, AML, energy metabolism, antileukemic therapy, antileukemic strategies
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.