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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Safety and efficacy of CYT387, a JAK1 and JAK2 inhibitor, in myelofibrosis

ABSTRACT: 17 patients with myelofibrosis contributed paired research samples; the time points were pre-study and 12 weeks after commencing study treatment with CYT387.Gene expression analysis was investigated to study the effects of drug treatment. Additional analysis invesitigated differences in expression patterns in groups of anemia responders and non-responders following drug treatment. 34 samples representing 17 patients. Each patient submitted 1 pre-treatment sample and 1 post 12 weeks of treatment.

ORGANISM(S): Homo sapiens

SUBMITTER: Animesh Pardanani

PROVIDER: E-GEOD-40841 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Safety and efficacy of CYT387, a JAK1 and JAK2 inhibitor, in myelofibrosis

Project description:17 patients with myelofibrosis contributed paired research samples; the time points were pre-study and 12 weeks after commencing study treatment with CYT387.Gene expression analysis was investigated to study the effects of drug treatment. Additional analysis invesitigated differences in expression patterns in groups of anemia responders and non-responders following drug treatment.

2013-01-14 | GSE40841 | GEO

Safety and efficacy of INCB018424, a JAK1 and JAK2 inhibitor, in myelofibrosis.

Project description: Not available

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Safety and efficacy of CYT387, a JAK1 and JAK2 inhibitor, in myelofibrosis.

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JAK1/2 inhibitor therapy-associated lymphomas in myelofibrosis arising from a pre-existing B-cell clone

Project description:In this study, we elucidated differential gene expression between transformed and untransformed murine Stat1 -/- B cells by RNA sequencing. In addition, clinical samples from 2 lymphoma patients were analyzed. Key results are that 1) JAK1/2 inhibitor treatment in myelofibrosis is associated with an increased risk for aggressive B-cell lymphomas and 2) patients at risk can be identified by screening for pre-existing B-cell clones in peripheral blood or bone marrow.

2019-02-05 | GSE110219 | GEO

Identification of potential new therapeutic approaches for JAK2 V617F mutant patients

Project description:Myelofibrosis is often associated with the myeloproliferative neoplasms and expression of oncogenic JAK2 mutants. Patients with myelofibrosis have diminished quality of life due to systemic symptoms arising from fibrotic changes in the bone marrow. The introduction of the JAK2 inhibitor, ruxolitinib, has been of benefit in the treatment of myelofibrosis patients however, it is not curative and there is still a requirement for new targeted therapies to eradicate the cells at the heart of myelofibrosis pathology. Repurposing drugs bypasses many of the hurdles present in drug development, such as toxicity and pharmacodynamic profiling. To this end we undertook a re-analysis of our pre-existing proteomic data sets to identify perturbed biochemical pathways and their associated drugs/inhibitors to potentially target the cells driving myelofibrosis. This approach identified CBL0137 as a candidate for targeting JAK2 mutant driven malignancies. We therefore assessed CBL0137 as a new agent to extinguish JAK2 mutant primitive cells and show its ability to preferentially target cells from MF patients compared to healthy control cells. Further we define its mechanistic action in primary haemopoietic progenitor cells and demonstrate its ability to reduce splenomegaly and reticulocyte number in a transgenic murine model of myeloproliferative neoplasms.

2022-08-11 | E-MTAB-11653 | biostudies-arrayexpress

ACVR1/JAK1/JAK2 inhibitor momelotinib reverses transfusion dependency and suppresses hepcidin in myelofibrosis phase 2 trial.

Project description: Not available

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Safety and efficacy of TG101348, a selective JAK2 inhibitor, in myelofibrosis.

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Clinical drug response and proteotype profiling elucidates targetable vulnerabilities of myelofibrosis

Project description:Myelofibrosis (MF) is a hematopoietic stem cell disorder belonging to the myeloproliferative neoplasms. MF patients frequently carry driver mutations in JAK2 and Calreticulin (CALR) and have limited therapeutic options. Here, we integrate ex vivo drug response and proteotype analyses across MF patient cohorts to discover targetable vulnerabilities and associated therapeutic strategies. Drug sensitivities of mutated and progenitor cells were measured in patient blood using high-content imaging and single-cell deep learning-based analyses. Integration with matched molecular profiling revealed three therapeutic vulnerabilities. First, CALR mutations drive BET and HDAC inhibitor sensitivity, particularly in the absence of high MAPK-Ras pathway protein levels. Second, an MCM complex-high proliferative signature corresponds to advanced disease and sensitivity to drugs targeting pro-survival signaling and DNA replication. Third, homozygous CALR mutations result in high ER stress, responding to ER stressors and UPR inhibition. Overall, our integrated analyses provide a molecularly-motivated roadmap for individualized MF patient treatment.

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Bone marrow transplantation outcomes in primary myelofibrosis

Project description:Patient samples were analysed for the presence of genomic aberrations prior to ABMT and following relapse, in case it occurred, in patients with primary myelofibrosis.

2020-11-29 | E-MTAB-9110 | biostudies-arrayexpress

MiR-543 regulates the epigenetic landscape of myelofibrosis by targeting TET1 and TET2 [miRNA]

Project description:We analyzed 14 patients with Myelofibrosis (MF) to determine the miRNA profile of patients not responding to current MF treatment. We used Affymetrix miRNA-3 array to profile the differentially expressed miRNA in bone-marrow between patients with MF that respond to current MF treatment and the patients with MF that do not respond to current MF treatment.

2019-12-18 | GSE142239 | GEO

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