Aberrant splicing and drug resistance in AML.
The advent of next-generation sequencing technologies has unveiled a new window into the heterogeneity of acute myeloid leukemia (AML). In particular, recurrent mutations in spliceosome machinery and genome-wide aberrant splicing events have been recognized as a prominent component of this disease. This review will focus on how these factors influence drug resistance through altered splicing of tumor suppressor and oncogenes and dysregulation of the apoptotic signaling network. A better understanding of these factors in disease progression is necessary to design appropriate therapeutic strategies recognizing specific alternatively spliced or mutated oncogenic targets.
Biospecimen Laboratory, Loma Linda University Cancer Center, Loma Linda University School of Medicine, Loma Linda, CA, 92354, USA.
Rosalia
R
de Necochea-Campion
Division of Hematology/Oncology, Loma Linda University School of Medicine, 11175 Campus Street, Chan Shun Pavilion 11015, Loma Linda, CA, 92354, USA.
Geoffrey P
GP
Shouse
Biospecimen Laboratory, Loma Linda University Cancer Center, Loma Linda University School of Medicine, Loma Linda, CA, 92354, USA.
Qi
Q
Zhou
Biospecimen Laboratory, Loma Linda University Cancer Center, Loma Linda University School of Medicine, Loma Linda, CA, 92354, USA.
Saied
S
Mirshahidi
Biospecimen Laboratory, Loma Linda University Cancer Center, Loma Linda University School of Medicine, Loma Linda, CA, 92354, USA. cschen@llu.edu.|Division of Hematology/Oncology, Loma Linda University School of Medicine, 11175 Campus Street, Chan Shun Pavilion 11015, Loma Linda, CA, 92354, USA. cschen@llu.edu.
Chien-Shing
CS
Chen
D017398:Alternative Splicing; D017209:Apoptosis / Q000235:genetics; D019008:Drug Resistance, Neoplasm / Q000235:genetics*; D016147:Genes, Tumor Suppressor; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000235:genetics* / Q000503:physiopathology; D009857:Oncogenes
Chemoresistance; Clonal evolution; Mutation; Splice factor; Target