Conclusions
Although the role of autophagy in stem-cell transformation and hematological malignant neoplasms has been investigated in many studies, its role in treatment strategies for these disorders is controversial. Also, autophagy modulation has been reported[59] to play a role in outcomes for hematopoietic malignant neoplasms. Understanding the exact molecular mechanism of autophagy in normal and malignant hematopoiesis can help to provide better treatment strategies for patients. Further, each autophagy pathway in every lineage has a specific characteristic, so targeting theses pathways can result in specific strategies for each type of malignant neoplasms. However, further studies are needed to answer remaining questions in this field.
Abbreviations
ROS, reactive oxygen species; ATG, autophagy-related genes; HSPCs, high self-renewing precursor cells; LSCs, leukemic stem cells; MRD, minimal residual disease; AML, acute myeloid leukemia; APL, acute promyelocytic leukemia; miR, microRNA; FLT3, FMS-like tyrosine kinase 3; ITD, internal tandem duplication; NPM, nucleophosmin 1; PML, promyelocytic leukemia; Akt, serine/threonine-protein kinase; LICs, leukemia-initiating cells; MLL-ENL, mixed lineage leukemia–eleven nineteen lysine-rich leukemia; ATG7, autophagy-related 7; ATG5, autophagy-related 5; AML1-ETO, acute myelogenous leukemia–1 eight-twenty-one oncoprotein; MLL, mixed-lineage leukemia; BM, bone marrow; HLX, H2.0-like homeobox transcription factor; AMPK, AMP-activated protein kinase; CML, chronic myeloid leukemia; BCR-ABL, breakpoint cluster region protein–Abelson murine leukemia; PIK-III, PtIns3P class III inhibitor; CCNG2, Cyclin-G2; MDS, myelodysplastic syndrome; MDS-RS, myelodysplastic syndrome with ring sideroblasts; ATG2B, autophagy-related protein 2 homolog B; GSKIP, GSK3B-interacting protein; ALL, acute lymphoid leukemia; B-ALL, acute lymphoid leukemia in B-cell precursors; T-ALL, acute lymphoid leukemia in thymocytes; BECN1, Beclin-1; pre-B ALL, pre-B acute lymphoblastic leukemia; CLL, chronic lymphoid leukemia; SLL, small lymphocytic lymphoma; B-CLL, B-cell chronic lymphocytic leukemia; TLR9, Toll-like receptor 9; IgM, immunoglobulin M; PI3K, phosphoinositide 3-kinase; PIK3R4, phosphoinositide-3-kinase regulatory subunit 4; DAPK1, death-associated protein kinase 1; CEBP-ATF6, CCAAT-enhancer-binding proteins–activating transcription factor 6; SLAMF1, signaling lymphocytic activation molecule family member 1; DLBCL, diffused large-cell B lymphoma; B-NHL, B–non-Hodgkin lymphoma; FL, follicular lymphoma; WHO, World Health Organization; BCL, B-cell lymphoma; CUL4B, Cullin-4B; JNK, c-Jun N-terminal kinases; MCL, mantle cell lymphoma; TG2, tissue transglutaminase; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; PLSCR1, phospholipid scramblase 1; hH, hedgehog; CXCR-4, C-X-C chemokine receptor type 4; BL, Burkitt lymphoma; MM, multiple myeloma; LC3, light chain 3; MDSCs, myeloid-derived suppressor cells; MALAT-1, metastasis-associated lung adenocarcinoma transcript–1; HMGB1, high mobility group box 1; mTORC, mammalian target of rapamycin complex; ALCL, anaplastic large-cell lymphoma; siRNA, small interfering RNA; HIF-1, hypoxia-inducible factor 1; HSCs, hematopoietic stem cells; FL, follicular lymphoma
Lab Med. 2021;52(1):16-23. © 2021 American Society for Clinical Pathology
