Kendall Dutchak

ORCID: 0009-0002-0045-3942
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About
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Research Areas
  • Chromatin Remodeling and Cancer
  • Ferroptosis and cancer prognosis
  • Advanced Breast Cancer Therapies
  • Epigenetics and DNA Methylation
  • Lung Cancer Research Studies
  • Radiomics and Machine Learning in Medical Imaging
  • Hippo pathway signaling and YAP/TAZ
  • Cancer, Hypoxia, and Metabolism
  • Histone Deacetylase Inhibitors Research
  • Telomeres, Telomerase, and Senescence
  • Cancer Research and Treatments
  • Mitochondrial Function and Pathology
  • CRISPR and Genetic Engineering
  • Cellular Mechanics and Interactions
  • RNA Interference and Gene Delivery
  • Melanoma and MAPK Pathways
  • Plant Surface Properties and Treatments
  • Virus-based gene therapy research
  • Cancer-related Molecular Pathways

McGill University
2013-2024

Abstract Cyclin-dependent kinase 4/6 (CDK4/6) inhibitors are approved for breast cancer treatment and show activity against other malignancies, including KRAS-mutant non–small cell lung (NSCLC). However, the clinical efficacy of CDK4/6 is limited due to frequent drug resistance their largely cytostatic effects. Through a genome-wide cDNA screen, we identified that bromodomain-containing protein 4 (BRD4) overexpression conferred inhibitor palbociclib in NSCLC cells. Inhibition BRD4, either by...

10.1158/0008-5472.can-23-1749 article EN Cancer Research 2024-01-26

Abstract Oncogenic activation of the RTK–RAS–RAF–MEK–ERK pathway occurs in approximately 25% all human cancers, yet activated RAS, BRAF, or MEK expression primary cells leads to a prolonged and predominantly irreversible cell-cycle arrest termed oncogene-induced senescence (OIS). OIS acts as an intrinsic tumor suppressor mechanism, serving barrier progression. Screening library kinases kinase-regulatory proteins we identified MOB3A, Mps-one binder coactivator (MOB) protein family member,...

10.1158/1541-7786.mcr-21-0767 article EN Molecular Cancer Research 2022-01-19

The ability to express exogenous cDNAs while suppressing endogenous genes via RNAi represents an extremely powerful research tool with the most efficient non-transient approach being accomplished through stable viral vector integration. Unfortunately, since traditional restriction enzyme based methods for constructing such vectors are sequence dependent, their construction is often difficult and not amenable mass production. Here we describe a non-sequence dependent Gateway recombination...

10.1371/journal.pone.0076279 article EN cc-by PLoS ONE 2013-10-11

<div>Abstract<p>Cyclin-dependent kinase 4/6 (CDK4/6) inhibitors are approved for breast cancer treatment and show activity against other malignancies, including <i>KRAS</i>-mutant non–small cell lung (NSCLC). However, the clinical efficacy of CDK4/6 is limited due to frequent drug resistance their largely cytostatic effects. Through a genome-wide cDNA screen, we identified that bromodomain-containing protein 4 (BRD4) overexpression conferred inhibitor palbociclib in...

10.1158/0008-5472.c.7181352.v2 preprint EN 2024-04-15

<div>Abstract<p>Cyclin-dependent kinase 4/6 (CDK4/6) inhibitors are approved for breast cancer treatment and show activity against other malignancies, including <i>KRAS</i>-mutant non–small cell lung (NSCLC). However, the clinical efficacy of CDK4/6 is limited due to frequent drug resistance their largely cytostatic effects. Through a genome-wide cDNA screen, we identified that bromodomain-containing protein 4 (BRD4) overexpression conferred inhibitor palbociclib in...

10.1158/0008-5472.c.7181352 preprint EN 2024-04-15

<div>Abstract<p>Cyclin-dependent kinase 4/6 (CDK4/6) inhibitors are approved for breast cancer treatment and show activity against other malignancies, including <i>KRAS</i>-mutant non–small cell lung (NSCLC). However, the clinical efficacy of CDK4/6 is limited due to frequent drug resistance their largely cytostatic effects. Through a genome-wide cDNA screen, we identified that bromodomain-containing protein 4 (BRD4) overexpression conferred inhibitor palbociclib in...

10.1158/0008-5472.c.7181352.v1 preprint EN 2024-04-15
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