BCR-ABL (Ph)-like acute leukemia-Pathogenesis, diagnosis and therapeutic options.
Recent comprehensive genetic studies revealed numerous genetic aberrations underlying a group of high-risk leukemias that share a specific activated kinase gene expression pattern. These ALLs were first recognized by the expression profile similar to that of Philadelphia chromosome-positive ALL and currently can be sub-classified by the main aberrantly activated kinase in the leukemic cells. We herein review the biological mechanisms and diagnostic and clinical challenges presented by these leukemias.
Department of Hematology and Bone Marrow Transplantation, Rambam Health Care Campus, Haifa, Israel; Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel. Electronic address: y_ofran@rambam.health.gov.il.
Yishai
Y
Ofran
Department of Pediatric Hemato-Oncology, Edmond and Lily Safra Children's Hospital, Sheba Medical Center, Tel Hashomer, Israel; Department of Human Molecular Genetics And Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
Shai
S
Izraeli
D000818:Animals; D016044:Fusion Proteins, bcr-abl / Q000235:genetics* / Q000378:metabolism; D017353:Gene Deletion; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D006801:Humans; D051740:Ikaros Transcription Factor / Q000235:genetics / Q000378:metabolism; D053612:Janus Kinases / Q000378:metabolism; D010641:Phenotype; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000175:diagnosis / Q000209:etiology* / Q000378:metabolism* / Q000628:therapy; D050791:STAT Transcription Factors / Q000378:metabolism; D015398:Signal Transduction
D050791:STAT Transcription Factors; D051740:Ikaros Transcription Factor; D016044:Fusion Proteins, bcr-abl; D053612:Janus Kinases
BCR-ABL-like ALL; JAK inhibitors; Kinase-driven ALL; Ph-like ALL; Tyrosine kinase inhibitors