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Article: Diverse pathogenetic roles of SOX genes in acute myeloid leukaemia and their therapeutic implications

TitleDiverse pathogenetic roles of SOX genes in acute myeloid leukaemia and their therapeutic implications
Authors
KeywordsAcute myeloid leukaemia
SOX genes
C/EBPα
β-catenin/Wnt pathway
Hedgehog pathway
TP53 signaling
Issue Date2020
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/semcancer
Citation
Seminars in Cancer Biology, 2020, v. 67 pt. 1, p. 24-29 How to Cite?
AbstractAcute myeloid leukaemia (AML) is a heterogeneous group of diseases with diverse pathogenetic pathways. When treated uniformly with conventional chemotherapy and allogeneic haematopoietic stem cell transplantation (HSCT), it showed variable clinical outcome and prognosis. Members of the SOX [Sry-related high-mobility group (HMG) box] gene family are involved in diverse embryonic and oncogenic processes. The roles of SOX genes in AML are not entirely clear but emerging evidence, including that arising from studies in solid-cancers, showed that SOX genes can function as tumour suppressors or oncogenes and may be involved in key pathogenetic pathways in AML involving C/EBPα mutations, activation of β-catenin/Wnt and Hedgehog pathways and aberrant TP53 signals. Recent data based on genomics and proteomics have identified key interactions between SOX genes and partnering proteins of pathogenetic significance. The observations illustrated the principles and feasibilities of developing lead molecules of potential therapeutic values. Studying the diverse pathogenetic roles of SOX genes in AML may shed lights to the heterogeneity of AML and generate information that can be translated into novel therapeutic strategies.
Persistent Identifierhttp://hdl.handle.net/10722/307904
ISSN
2023 Impact Factor: 12.1
2023 SCImago Journal Rankings: 3.297
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLeung, RKC-
dc.contributor.authorLeung, HC-
dc.contributor.authorLeung, AYH-
dc.date.accessioned2021-11-12T13:39:36Z-
dc.date.available2021-11-12T13:39:36Z-
dc.date.issued2020-
dc.identifier.citationSeminars in Cancer Biology, 2020, v. 67 pt. 1, p. 24-29-
dc.identifier.issn1044-579X-
dc.identifier.urihttp://hdl.handle.net/10722/307904-
dc.description.abstractAcute myeloid leukaemia (AML) is a heterogeneous group of diseases with diverse pathogenetic pathways. When treated uniformly with conventional chemotherapy and allogeneic haematopoietic stem cell transplantation (HSCT), it showed variable clinical outcome and prognosis. Members of the SOX [Sry-related high-mobility group (HMG) box] gene family are involved in diverse embryonic and oncogenic processes. The roles of SOX genes in AML are not entirely clear but emerging evidence, including that arising from studies in solid-cancers, showed that SOX genes can function as tumour suppressors or oncogenes and may be involved in key pathogenetic pathways in AML involving C/EBPα mutations, activation of β-catenin/Wnt and Hedgehog pathways and aberrant TP53 signals. Recent data based on genomics and proteomics have identified key interactions between SOX genes and partnering proteins of pathogenetic significance. The observations illustrated the principles and feasibilities of developing lead molecules of potential therapeutic values. Studying the diverse pathogenetic roles of SOX genes in AML may shed lights to the heterogeneity of AML and generate information that can be translated into novel therapeutic strategies.-
dc.languageeng-
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/semcancer-
dc.relation.ispartofSeminars in Cancer Biology-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectAcute myeloid leukaemia-
dc.subjectSOX genes-
dc.subjectC/EBPα-
dc.subjectβ-catenin/Wnt pathway-
dc.subjectHedgehog pathway-
dc.subjectTP53 signaling-
dc.titleDiverse pathogenetic roles of SOX genes in acute myeloid leukaemia and their therapeutic implications-
dc.typeArticle-
dc.identifier.emailLeung, AYH: ayhleung@hku.hk-
dc.identifier.authorityLeung, AYH=rp00265-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1016/j.semcancer.2019.11.001-
dc.identifier.pmid31698089-
dc.identifier.scopuseid_2-s2.0-85075417429-
dc.identifier.hkuros330178-
dc.identifier.volume67-
dc.identifier.issuept. 1-
dc.identifier.spage24-
dc.identifier.epage29-
dc.identifier.isiWOS:000598178400004-
dc.publisher.placeUnited Kingdom-

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