P. Brent Ferrell
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View article: CDK8 is a critical effector of cell fate dysregulation in SF3B1-mutant MDS
CDK8 is a critical effector of cell fate dysregulation in SF3B1-mutant MDS Open
Mutations in RNA splicing factor SF3B1 are among the most common in MDS and are strongly associated with MDS with ring sideroblasts (MDS-RS). While aberrant splicing of terminal erythroid regulators has been implicated in MDS pathogenesis,…
View article: The acute myeloid leukemia microenvironment impairs neutrophil maturation and function through NF-κB signaling
The acute myeloid leukemia microenvironment impairs neutrophil maturation and function through NF-κB signaling Open
Acute myeloid leukemia (AML), an aggressive hematological malignancy, is driven by oncogenic mutations in stem and progenitor cells that give rise to AML blasts. Although these mutations are well characterized, their impact on healthy hema…
View article: Incident cytopenia and risk of subsequent myeloid neoplasm in age-related clonal hematopoiesis: a multi-biobank case-control study
Incident cytopenia and risk of subsequent myeloid neoplasm in age-related clonal hematopoiesis: a multi-biobank case-control study Open
National Institutes of Health, Burroughs Wellcome Fund, Edward P. Evans Foundation, Pew Charitable Trusts, Alexander and Margaret Stewart Trust, Beverly and George Rawlings Directorship.
View article: Olutasidenib in combination with azacitidine induces durable complete remissions in patients with relapsed or refractory mIDH1 acute myeloid leukemia: a multicohort open-label phase 1/2 trial
Olutasidenib in combination with azacitidine induces durable complete remissions in patients with relapsed or refractory mIDH1 acute myeloid leukemia: a multicohort open-label phase 1/2 trial Open
NCT02719574.
View article: Germline genetics, disease, and exposure to medication influence longitudinal dynamics of clonal hematopoiesis
Germline genetics, disease, and exposure to medication influence longitudinal dynamics of clonal hematopoiesis Open
Not available.
View article: Distinct Transcriptomic Cell States Differentiate Low-Risk MDS from Healthy Marrow
Distinct Transcriptomic Cell States Differentiate Low-Risk MDS from Healthy Marrow Open
Introduction Myelodysplastic syndromes (MDS) are a group of malignancies that involve ineffective hematopoiesis and often include a large pool of immature blasts. Previous studies have identified malignant ontogeny in hematopoietic stem an…
View article: Supplementary File 1 from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in patients with Myelofibrosis
Supplementary File 1 from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in patients with Myelofibrosis Open
Supplemental Tables S1-S9 Supplemental Figures S1-S2
View article: Data from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in patients with Myelofibrosis
Data from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in patients with Myelofibrosis Open
Purpose: Treatment options are limited beyond JAK inhibitors for patients with primary myelofibrosis (PMF), or secondary MF. Preclinical studies have revealed that PI3Kδ inhibition cooperates with ruxolitinib, a JAK1/2 inhibitor, to reduce…
View article: Supplementary File 1 from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in patients with Myelofibrosis
Supplementary File 1 from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in patients with Myelofibrosis Open
Supplemental Tables S1-S9 Supplemental Figures S1-S2
View article: Immune‐monitoring of myelodysplastic neoplasms: Recommendations from the i4MDS consortium
Immune‐monitoring of myelodysplastic neoplasms: Recommendations from the i4MDS consortium Open
Advancements in comprehending myelodysplastic neoplasms (MDS) have unfolded significantly in recent years, elucidating a myriad of cellular and molecular underpinnings integral to disease progression. While molecular inclusions into progno…
View article: Clonal hematopoiesis and inflammation in the vasculature: CHIVE, a prospective, longitudinal clonal hematopoiesis cohort and biorepository
Clonal hematopoiesis and inflammation in the vasculature: CHIVE, a prospective, longitudinal clonal hematopoiesis cohort and biorepository Open
Clonal hematopoiesis (CH) is an age-associated phenomenon leading to an increased risk of both hematologic malignancy and nonmalignant organ dysfunction. Increasingly available genetic testing has made the incidental discovery of CH clinic…
View article: Olutasidenib in post-venetoclax patients with mutant isocitrate dehydrogenase 1 (m <i>IDH1</i> ) acute myeloid leukemia (AML)
Olutasidenib in post-venetoclax patients with mutant isocitrate dehydrogenase 1 (m <i>IDH1</i> ) acute myeloid leukemia (AML) Open
Olutasidenib, a potent, selective, oral, mutant isocitrate dehydrogenase 1 (mIDH1) inhibitor, is FDA-approved for relapsed/refractory (R/R) acute myeloid leukemia (AML). Here we report efficacy and safety of olutasidenib in 18 patients wit…
View article: Multiomic profiling of human clonal hematopoiesis reveals genotype and cell-specific inflammatory pathway activation
Multiomic profiling of human clonal hematopoiesis reveals genotype and cell-specific inflammatory pathway activation Open
Clonal hematopoiesis (CH) is an age-associated phenomenon that increases the risk of hematologic malignancy and cardiovascular disease. CH is thought to enhance disease risk through inflammation in the peripheral blood.1 Here, we profile p…
View article: Olutasidenib for the Treatment of mIDH1 Acute Myeloid Leukemia in Patients Relapsed or Refractory to Hematopoietic Stem Cell Transplant, Prior mIDH1 Inhibitor, or Venetoclax
Olutasidenib for the Treatment of mIDH1 Acute Myeloid Leukemia in Patients Relapsed or Refractory to Hematopoietic Stem Cell Transplant, Prior mIDH1 Inhibitor, or Venetoclax Open
Introduction. Olutasidenib is a small molecule, oral, mutated-IDH1 (mIDH1) inhibitor approved for the treatment of relapsed/refractory (R/R) acute myeloid leukemia (AML). In the pivotal cohort of the registrational phase 1/2 trial, 51/147 …
View article: Multi-Omics Analysis Reveals That TET2 Loss Epigenetically Primes Monocytes for Inflammatory Responses Via AP-1 Signaling
Multi-Omics Analysis Reveals That TET2 Loss Epigenetically Primes Monocytes for Inflammatory Responses Via AP-1 Signaling Open
Loss of function mutations in TET2 are common in clonal hematopoiesis (CH) and myelodysplastic syndromes (MDS). Increased inflammation and stem cell capacity have been reported in Tet2 KO mouse models, but molecular mechanisms and cell typ…
View article: 1492 Clonal hematopoiesis of indeterminate potential alters solid tumor microenvironment and outcomes in triple negative breast cancer
1492 Clonal hematopoiesis of indeterminate potential alters solid tumor microenvironment and outcomes in triple negative breast cancer Open
Background Clonal hematopoiesis of indeterminate potential (CHIP) is characterized by blood cells with somatic mutations in leukemia-associated genes in patients without hematologic malignancies. The incidence of CHIP increases with age, a…
View article: Data from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in Patients with Myelofibrosis
Data from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in Patients with Myelofibrosis Open
Purpose:Treatment options are limited beyond JAK inhibitors for patients with primary myelofibrosis (MF) or secondary MF. Preclinical studies have revealed that PI3Kδ inhibition cooperates with ruxolitinib, a JAK1/2 inhibitor, to reduce pr…
View article: Supplementary File 1 from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in Patients with Myelofibrosis
Supplementary File 1 from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in Patients with Myelofibrosis Open
Supplemental Tables S1-S9Supplemental Figures S1-S2
View article: Supplementary File 1 from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in Patients with Myelofibrosis
Supplementary File 1 from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in Patients with Myelofibrosis Open
Supplemental Tables S1-S9Supplemental Figures S1-S2
View article: Data from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in Patients with Myelofibrosis
Data from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in Patients with Myelofibrosis Open
Purpose:Treatment options are limited beyond JAK inhibitors for patients with primary myelofibrosis (MF) or secondary MF. Preclinical studies have revealed that PI3Kδ inhibition cooperates with ruxolitinib, a JAK1/2 inhibitor, to reduce pr…
View article: Supplementary File 1 from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in Patients with Myelofibrosis
Supplementary File 1 from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in Patients with Myelofibrosis Open
Supplemental Tables S1-S9 Supplemental Figures S1-S2
View article: Supplementary File 1 from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in Patients with Myelofibrosis
Supplementary File 1 from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in Patients with Myelofibrosis Open
Supplemental Tables S1-S9 Supplemental Figures S1-S2
View article: Data from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in Patients with Myelofibrosis
Data from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in Patients with Myelofibrosis Open
Purpose:Treatment options are limited beyond JAK inhibitors for patients with primary myelofibrosis (MF) or secondary MF. Preclinical studies have revealed that PI3Kδ inhibition cooperates with ruxolitinib, a JAK1/2 inhibitor, to reduce pr…
View article: Supplementary Table from Distinct Patterns of Clonal Evolution Drive Myelodysplastic Syndrome Progression to Secondary Acute Myeloid Leukemia
Supplementary Table from Distinct Patterns of Clonal Evolution Drive Myelodysplastic Syndrome Progression to Secondary Acute Myeloid Leukemia Open
Supplementary Table from Distinct Patterns of Clonal Evolution Drive Myelodysplastic Syndrome Progression to Secondary Acute Myeloid Leukemia
View article: Supplementary Figure from Distinct Patterns of Clonal Evolution Drive Myelodysplastic Syndrome Progression to Secondary Acute Myeloid Leukemia
Supplementary Figure from Distinct Patterns of Clonal Evolution Drive Myelodysplastic Syndrome Progression to Secondary Acute Myeloid Leukemia Open
Supplementary Figure from Distinct Patterns of Clonal Evolution Drive Myelodysplastic Syndrome Progression to Secondary Acute Myeloid Leukemia