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Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE281956 | GEO | 2025/11/12

REPOSITORIES: GEO

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Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 3]

Project description:To unravel the intricate interplay among Oxr1, ROS-induced genetic changes, and dynamics influencing TKI resistance and CML progression

2025-11-12 | GSE281955 | GEO

Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 2]

Project description:To unravel the intricate interplay among Oxr1, ROS-induced genetic changes, and dynamics influencing TKI resistance and CML progression

2025-11-12 | GSE281954 | GEO

Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 1]

Project description:To unravel the intricate interplay among Oxr1, ROS-induced genetic changes, and dynamics influencing TKI resistance and CML progression

2025-11-12 | GSE281856 | GEO

Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia.

Project description:Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia.

| PRJNA1186247 | ENA

Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 2]

Project description:Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 2]

| PRJNA1186250 | ENA

Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 1]

Project description:Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 1]

| PRJNA1186059 | ENA

Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 3]

Project description:Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 3]

| PRJNA1186249 | ENA

Targeting FLT3-TAZ Signaling to Suppress Drug Resistance in Blast Crisis Chronic Myeloid Leukemia

Project description:Although the development of tyrosine kinase inhibitors (TKIs), including BCR-ABL1 targeted therapies, rendered chronic myeloid leukemia (CML) a manageable condition, acquisition of drug resistance during blast crisis (BC) progression remains a critical challenge. Here, we elucidate the significance of FLT3 signaling in the acquisition of drug resistance in BC-CML. Mechanistically, FLT3 expression in CML cells activated FLT3-JAK-STAT3-TAZ-TEAD-CD36 pathway, which conferred resistance to wide range of tyrosine kinase inhibitors (TKIs). Remarkably, a subgroup of BC-CML patients who expressed FLT3 showed strong correlation with the prognostic factors of CML independent of recurrent BCR-ABL1 mutations. We demonstrate that combining FLT3 inhibitors with BCR-ABL1 targeted therapies or single treatment with ponatinib can overcome drug resistance and promote cell death in patient-derived FLT3+ BC-CML cells and mouse xenograft models. Our findings reveal the mechanism of FLT3-mediated drug resistance in BC progression and suggest the inclusion of FLT3 as a therapeutic target for this defined group of patients.

2023-11-15 | GSE226360 | GEO

Blast crisis Ph+ chronic myeloid leukemia with NUP98/HOXA13 up-regulating MSI2.

Project description:BackgroundMusashi2(Msi2)-Numb pathway de-regulation is a molecular mechanism underlying the transition of chronic phase Ph + CML to deadly blast crisis, particularly in cases with a NUP98/HOXA9 fusion from a t(7;11)(p15;p15). This study provides new insights on the mechanisms cooperating in driving MSI2 over-expression and progression of Ph-positive CML.ResultsHerein we describe a t(7;11)(p15;p15) originating a NUP98 fusion with HOXA13, at 7p15, in a 39 year-old man in blast crisis of Ph-positive CML. Both MSI2 and HOXA9 were evaluated by quantitative RT-PCR in our patient and in a series of haematological malignancies. Up-regulation of both genes emerged only in the presence of NUP98/HOXA13 gene fusion. However, over-expression of MSI2, but not HOXA9, was found in 2 cases of Ph + blast crisis with additional chromosome aberrations other than t(7;11). To determine the mechanisms underlying MSI2 over-expression in our patient we performed Chromatin Immunoprecipitation and found that NUP98/HOXA13 fusion protein deregulates MSI2 gene by binding its promoter.ConclusionsTo the best of our knowledge, this is the first molecular characterization of NUP98/HOXA13 fusion in blast crisis of Ph + CML. Our findings suggest cooperative mechanisms of MSI2 over-expression driven by HOXA proteins and strongly supports MSI2 as a prognostic marker and a candidate in target treatment of CML.

| S-EPMC4071805 | biostudies-literature

The B cell mutator AID promotes B lymphoid blast crisis and drug resistance in chronic myeloid leukemia.

Project description:Chronic myeloid leukemia (CML) is induced by BCR-ABL1 and can be effectively treated for many years with Imatinib until leukemia cells acquire drug resistance through BCR-ABL1 mutations and progress into fatal B lymphoid blast crisis (LBC). Despite its clinical significance, the mechanism of progression into LBC is unknown. Here, we show that LBC but not CML cells express the B cell-specific mutator enzyme AID. We demonstrate that AID expression in CML cells promotes overall genetic instability by hypermutation of tumor suppressor and DNA repair genes. Importantly, our data uncover a causative role of AID activity in the acquisition of BCR-ABL1 mutations leading to Imatinib resistance, thus providing a rationale for the rapid development of drug resistance and blast crisis progression.

| S-EPMC2931825 | biostudies-literature

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