Chinmay Munje
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View article: Tyrosine Kinase Inhibitor Independent Gene Expression Signature in CML Offers New Targets for LSPC Eradication Therapy
Tyrosine Kinase Inhibitor Independent Gene Expression Signature in CML Offers New Targets for LSPC Eradication Therapy Open
Tyrosine kinase inhibitors (TKI) have revolutionised the treatment of CML. However, TKI do not eliminate the leukaemia stem cells (LSC), which can re-initiate the disease. Thus, finding new therapeutic targets in CML LSC is key to finding …
View article: The Spliceosome: A New Therapeutic Target in Chronic Myeloid Leukaemia
The Spliceosome: A New Therapeutic Target in Chronic Myeloid Leukaemia Open
RNA splicing factors are frequently altered in cancer and can act as both oncoproteins and tumour suppressors. They have been found mutated or deregulated, justifying the growing interest in the targeting of splicing catalysis, splicing re…
View article: Tyrosine kinase inhibitor independent gene expression signature in CML offers new targets for LSPC eradication therapy
Tyrosine kinase inhibitor independent gene expression signature in CML offers new targets for LSPC eradication therapy Open
2 Abstract Tyrosine kinase inhibitors (TKI) have revolutionised the treatment of CML. However, TKI do not eliminate the leukaemia stem cells (LSC), which can reinitiate the disease. Thus, finding new therapeutic targets in CML LSC is key t…
View article: Correction: CD93 is expressed on chronic myeloid leukemia stem cells and identifies a quiescent population which persists after tyrosine kinase inhibitor therapy
Correction: CD93 is expressed on chronic myeloid leukemia stem cells and identifies a quiescent population which persists after tyrosine kinase inhibitor therapy Open
An amendment to this paper has been published and can be accessed via a link at the top of the paper.
View article: CD93 is expressed on chronic myeloid leukemia stem cells and identifies a quiescent population which persists after tyrosine kinase inhibitor therapy
CD93 is expressed on chronic myeloid leukemia stem cells and identifies a quiescent population which persists after tyrosine kinase inhibitor therapy Open
The introduction of BCR-ABL tyrosine kinase inhibitors has revolutionized the treatment of chronic myeloid leukemia (CML). A major clinical aim remains the identification and elimination of low-level disease persistence, termed “minimal re…
View article: Integrated nuclear proteomics and transcriptomics identifies S100A4 as a therapeutic target in acute myeloid leukemia
Integrated nuclear proteomics and transcriptomics identifies S100A4 as a therapeutic target in acute myeloid leukemia Open
Inappropriate localization of proteins can interfere with normal cellular function and drive tumor development. To understand how this contributes to the development of acute myeloid leukemia (AML), we compared the nuclear proteome and tra…
View article: S126 COMBINATION OF ASCIMINIB (ABL001) WITH ATP‐COMPETITIVE TYROSINE KINASE INHIBITORS TARGETS EARLY CML PROGENITOR CELLS.
S126 COMBINATION OF ASCIMINIB (ABL001) WITH ATP‐COMPETITIVE TYROSINE KINASE INHIBITORS TARGETS EARLY CML PROGENITOR CELLS. Open
Background: The BCR‐ABL1 chimeric oncoprotein drives chronic myeloid leukaemia (CML) pathogenesis. The introduction of tyrosine kinase inhibitors (TKIs) has transformed clinical outcomes for patients with CML, with over 80% of those treate…
View article: Cord Blood-Derived Quiescent CD34<sup>+</sup> Cells Are More Transcriptionally Matched to AML Blasts Than Cytokine-Induced Normal Human Hematopoietic CD34<sup>+</sup> Cells
Cord Blood-Derived Quiescent CD34<sup>+</sup> Cells Are More Transcriptionally Matched to AML Blasts Than Cytokine-Induced Normal Human Hematopoietic CD34<sup>+</sup> Cells Open
Acute myeloid leukemia (AML) is characterized by developmental arrest, which is thought to arise from transcriptional dysregulation of myeloid development programs. Hematopoietic stem and progenitor cells (HSPCs) isolated from human blood …