Is this you? As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.
Claim your profile
Articles by Christopher Mill
Correction: BET inhibitor-based combinations targeting novel dependencies in MECOM-rearranged (r) AML
In the published version of our article, the (-log10 p-value) on the y-axis for Figure 1D was calculated and displayed incorrectly. We have corrected the panel to show the properly calculated (-log10 p-value) on the y-axis. The original article has been corrected.
"Efficacy of Novel Agents Against Cellular Models of Familial Platelet " by Christopher P Mill, Warren C Fiskus et al.
Blood Cancer Journal 10.1038/s41408-024-00981-4 Post-print Humans, Animals, Mice, Core Binding Factor Alpha 2 Subunit, Leukemia, Myeloid, Acute, Homoharringtonine, Blood Platelets, Blood Platelet Disorders, Proto-Oncogene Proteins c-bcl-2, Targeted therapies, Acute myeloid leukaemia yes Mill, Christopher P; Fiskus, Warren C; DiNardo, Courtney D; et al., "Efficacy of Novel Agents Against Cellular Models of Familial Platelet Disorder With Myeloid Malignancy (FPD-MM)" (2024).
"Causal Linkage of Presence of Mutant NPM1 to Efficacy of Novel Therape" by Christopher P Mill, Warren Fiskus et al.
10.1038/s41375-023-01882-4 Post-print Humans, Aged, Nuclear Proteins, Nucleophosmin, Panobinostat, Neoplasm Recurrence, Local, Mutation, Cytarabine, Leukemia, Myeloid, Acute, fms-Like Tyrosine Kinase 3, Targeted therapies, Acute myeloid leukaemia yes Mill, Christopher P; Fiskus, Warren; Das, Kaberi; et al., "Causal Linkage of Presence of Mutant NPM1 to Efficacy of Novel Therapeutic Agents Against Aml Cells With Mutant NPM1" (2023). Faculty, Staff and Student Publications. 5552.
BET inhibitor-based combinations targeting novel dependencies in MECOM-rearranged (r) AML - Leukemia
Abstract MECOM rearrangement in AML involves either inv(3)(q21;q26.2) or t(3;3)(q21;q26.2), where the dislocated GATA2 enhancer drives overexpression of the transcriptional regulator EVI1, causes concomitant GATA2 repression, and promotes AML progression, aggressive phenotype and therapy refractoriness. Treatment with BET protein inhibitor (BETi) induces in vitro and in vivo efficacy in MECOM-r AML cells.
Unpacking excess mortality in BC
In April 2020, the BC Centre for Disease Control (BCCDC) and the Office of the Provincial Health Officer initiated systematic surveillance of the societal and unintended impacts of the COVID-19 pandemic. Excess mortality was one of the priority metrics of this initiative.
"Effective Therapy for AML With RUNX1 Mutation by Cotreatment With Inhi" by Christopher P Mill, Warren Fiskus et al.
Abstract The majority of RUNX1 mutations in acute myeloid leukemia (AML) are missense or deletion-truncation and behave as loss-of-function mutations. Following standard therapy, AML patients expressing mtRUNX1 exhibit inferior clinical outcome than those without mutant RUNX1.
Superior preclinical efficacy of co-treatment with BRG1/BRM and FLT3 inhibitor against AML cells with FLT3 mutations - Blood Cancer Journal
Abstract Although treatment with standard frontline therapies, including a FLT3 inhibitor (FLT3i) reduces AML burden and achieves clinical remissions, most patients with AML with FLT3 mutation relapse due to therapy-resistant stem/progenitor cells. The core ATPases, BRG1 (SMARCA4) and BRM (SMARCA2) of the canonical (c) BAF (BRG1/BRM-associated factor) complex is a dependency in AML cells, including those harboring FLT3 mutations.
Targeting of Epigenetic Co-dependencies Enhances Anti-AML Efficacy of Menin Inhibitor in AML with MLL1-R or Mutant NPM1
Abstract Monotherapy with Menin inhibitor (MI), e.g., SNDX-5613, induces clinical remissions in patients with relapsed/refractory AML harboring MLL1-r or mtNPM1, but most patients either fail to respond or eventually relapse. Utilizing single-cell RNA-Seq, ChiP-Seq, ATAC-Seq, RNA-Seq, RPPA, and mass cytometry (CyTOF) analyses, present pre-clinical studies elucidate gene-expression correlates of MI efficacy in AML cells harboring MLL1-r or mtNPM1.
Efficacy of novel agents against cellular models of familial platelet disorder with myeloid malignancy (FPD-MM) - Blood Cancer Journal
Abstract Germline, mono-allelic mutations in RUNX1 cause familial platelet disorder (RUNX1-FPD) that evolves into myeloid malignancy (FPD-MM): MDS or AML. FPD-MM commonly harbors co-mutations in the second RUNX1 allele and/or other epigenetic regulators. Here we utilized patient-derived (PD) FPD-MM cells and established the first FPD-MM AML cell line (GMR-AML1).
Preclinical efficacy of targeting epigenetic mechanisms in AML with 3q26 lesions and EVI1 overexpression - Leukemia
Abstract AML with chromosomal alterations involving 3q26 overexpresses the transcription factor (TF) EVI1, associated with therapy refractoriness and inferior overall survival in AML. Consistent with a CRISPR screen highlighting BRD4 dependency, treatment with BET inhibitor (BETi) repressed EVI1, LEF1, c-Myc, c-Myb, CDK4/6, and MCL1, and induced apoptosis of AML cells with 3q26 lesions.
Targeting of epigenetic co-dependencies enhances anti-AML efficacy of Menin inhibitor in AML with MLL1-r or mutant NPM1 - Blood Cancer Journal
Abstract Monotherapy with Menin inhibitor (MI), e.g., SNDX-5613, induces clinical remissions in patients with relapsed/refractory AML harboring MLL1-r or mtNPM1, but most patients either fail to respond or eventually relapse. Utilizing single-cell RNA-Seq, ChiP-Seq, ATAC-Seq, RNA-Seq, RPPA, and mass cytometry (CyTOF) analyses, present pre-clinical studies elucidate gene-expression correlates of MI efficacy in AML cells harboring MLL1-r or mtNPM1.
Causal linkage of presence of mutant NPM1 to efficacy of novel therapeutic agents against AML cells with mutant NPM1 - Leukemia
Abstract In AML with NPM1 mutation causing cytoplasmic dislocation of NPM1, treatments with Menin inhibitor (MI) and standard AML chemotherapy yield complete remissions. However, the causal and mechanistic linkage of mtNPM1 to the efficacy of these agents has not been definitively established.
COVID-19 hospitalisations in immunocompromised individuals in the Omicron era: a population-based observational study using surveillance data in British Columbia, Canada
Summary Background People with immune dysfunction are at higher risk of severe outcomes from COVID-19 infection, but relatively little epidemiologic information is available for mostly vaccinated population in the Omicron era. This population-based study compared relative risk of breakthrough COVID-19 hospitalisation among vaccinated people identified as clinically extremely vulnerable (CEV) vs non-CEV individuals before treatment became more widely available.
RUNX1-targeted therapy for AML expressing somatic or germline mutation in RUNX1
Christopher P. Mill, Warren Fiskus, Courtney D. DiNardo, Yimin Qian, Kanak Raina, Kimal Rajapakshe, Dimuthu Perera, Cristian Coarfa, Tapan M. Kadia, Joseph D. Khoury, Dyana T. Saenz, David N. Saenz, Anuradha Illendula, Koichi Takahashi, Steven M. Kornblau, Michael R. Green, Andrew P. Futreal, John H. Bushweller, Craig M. Crews and Kapil N.
RUNX1 targeted therapy for AML expressing somatic or germline mutation in RUNX1
Christopher P Mill, Warren Fiskus, Courtney D DiNardo, Yimin Qian, Kanak Raina, Kimal Rajapakshe, Dimuthu Perera, Cristian Coarfa, Tapan M Kadia, Joseph D Khoury, Dyana T Saenz, David N Saenz, Anuradha Illendula, Koichi Takahashi, Steven M Kornblau, Michael R Green, Andrew P. Futreal, John H Bushweller, Craig M.
Targeting nuclear β-catenin as therapy for post-myeloproliferative neoplasm secondary AML
Abstract Transformation of post-myeloproliferative neoplasms into secondary (s) AML exhibit poor clinical outcome. In addition to increased JAK-STAT and PI3K-AKT signaling, post-MPN sAML blast progenitor cells (BPCs) demonstrate increased nuclear β-catenin levels and TCF7L2 (TCF4) transcriptional activity. Knockdown of β-catenin or treatment with BC2059 that disrupts binding of β-catenin to TBL1X (TBL1) depleted nuclear β-catenin levels.
Assessing the Diagnostic Properties of a Graded Oral Provocation Challenge for the Diagnosis of Immediate and Nonimmediate Reactions to Amoxicillin in Children | Allergy and Clinical Immunology | JAMA Pediatrics | JAMA Network
Importance The diagnostic properties of a graded provocation challenge (PC) among children presenting with a rash in the course of amoxicillin treatment are currently unknown. Objective To assess the accuracy and the negative predictive value of the PC in a cohort of children referred with suspected allergy to amoxicillin.
Dynamic Regulation of Long-Chain Fatty Acid Oxidation by a Noncanonical Interaction between the MCL-1 BH3 Helix and VLCAD
MCL-1 is a BCL-2 family protein implicated in the development and chemoresistance of human cancer. Unlike its anti-apoptotic homologs, Mcl-1 deletion has profound physiologic consequences, indicative of a broader role in homeostasis. We report that the BCL-2 homology 3 (BH3) ? helix of MCL-1 can directly engage very long-chain acyl-CoA dehydrogenase (VLCAD), a key enzyme of the mitochondrial fatty acid ?-oxidation (FAO) pathway.
JAMA Network | JAMA Pediatrics | Assessing the Diagnostic Properties of a Graded Oral Provocation Challenge for the Diagnosis of Immediate and Nonimmediate Reactions to Amoxicillin in Children
Importance The diagnostic properties of a graded provocation challenge (PC) among children presenting with a rash in the course of amoxicillin treatment are currently unknown. Objective To assess the accuracy and the negative predictive value of the PC in a cohort of children referred with suspected allergy to amoxicillin.
Impact of supervised epinephrine autoinjector administration during food challenges on parent confidence
To view the full text, please login as a subscribed user or purchase a subscription. Click here to view the full text on ScienceDirect. FiguresFigure 1Prechallenge vs postchallenge mean confidence scores in various epinephrine autoinjector confidence domains (n =18).Rapid administration of intramuscular epinephrine is the first-line treatment for anaphylaxis. Patients are prescribed an epinephrine autoinjector (EAI), which may be self- or caregiver administered, depending on the patient's age.
Show More
loading
Actions
Is this you?
As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.Get in touch with Christopher
Contact Christopher, search articles and posts on X, monitor coverage, and track replies from one place.
Learn more about Muck Rack