Unusual PDGFRB fusion reveals novel mechanism of kinase activation in Ph-like B-ALL

Teresa Sadras, Fatimah B. Jalud, Hansen J. Kosasih, Christopher R. Horne, Lauren M. Brown, Sam El-Kamand, Charles E. de Bock, Lachlan McAloney, Ashley P. Ng, Nadia M. Davidson, Louise E.A. Ludlow, Alicia Oshlack, Mark J. Cowley, Seong L. Khaw, James M. Murphy, Paul G. Ekert

Research output: Contribution to journalArticleOtherpeer-review

7 Citations (Scopus)

Abstract

Philadelphia-like (Ph-like) B-cell precursor acute lymphoblastic leaukemia (B-ALL) is a high-risk subtype of leukaemia [1]. It is characterized by a gene expression profile similar to Philadelphia chromosome positive (Ph+) ALL, but lacking the BCR::ABL1 rearrangement. Instead, Ph-like B-ALL represents a heterogeneous subtype driven by a diverse range of genetic aberrations and chromosomal rearrangements that converge on activated tyrosine kinase signalling [2, 3]. Integration of tyrosine kinase inhibitors into treatment regimens of Ph-like ALL patients has demonstrated early evidence of therapeutic efficacy, although results from larger clinical trials are pending [4].
Original languageEnglish
Pages (from-to)905-909
Number of pages5
JournalLeukemia
Volume37
Issue number4
DOIs
Publication statusPublished - Apr 2023
Externally publishedYes

Cite this