title: Src family kinases and their role in hematological malignancies.
abstract: The Src family protein tyrosine kinases (SFKs) are non-receptor intracellular kinases that have important roles in both hematopoiesis and leukemogenesis. The derangement of their expression or activation has been demonstrated to contribute to hematological malignancies. This review first examines the mechanisms of SFK overexpression and hyperactivation, emphasizing the dysregulation of the upstream modulators. Subsequently, the role of SFK up-regulation in the initiation, progression and therapy resistance of many hematological malignancies is also analyzed. The presented evidence endeavors to highlight the influence of SFK up-regulation on an extensive number of hematological malignancies and the need to consider them as candidates in targeted anticancer therapy.
authors.affiliation: Haematology Department and Victorian Cancer Cytogenetics Service, St Vincent's Hospital , Fitzroy , Australia.
authors.forename: Matthew
authors.initials: M
authors.lastname: Ku
authors.forename: Meaghan
authors.initials: M
authors.lastname: Wall
authors.forename: Ruth N
authors.initials: RN
authors.lastname: MacKinnon
authors.forename: Carl R
authors.initials: CR
authors.lastname: Walkley
authors.forename: Louise E
authors.initials: LE
authors.lastname: Purton
authors.forename: Constantine
authors.initials: C
authors.lastname: Tam
authors.forename: David
authors.initials: D
authors.lastname: Izon
authors.forename: Lynda
authors.initials: L
authors.lastname: Campbell
authors.forename: Heung-Chin
authors.initials: HC
authors.lastname: Cheng
authors.forename: Harshal
authors.initials: H
authors.lastname: Nandurkar
mesh_terms: D006801:Humans; D007945:Leukemia, Lymphoid / Q000201:enzymology*; D007951:Leukemia, Myeloid / Q000201:enzymology*; D015854:Up-Regulation / Q000502:physiology; D019061:src-Family Kinases / Q000502:physiology*
chemical_list: D019061:src-Family Kinases
keywords: Genetic and other predisposing conditions; lymphoid leukemia; lymphoma and Hodgkin disease; myeloid leukemias and dysplasias; signal transduction; transcription factor changes