Andrew Dynka

ORCID: 0000-0002-7805-5031
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About
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Research Areas
  • Peptidase Inhibition and Analysis
  • Pancreatic and Hepatic Oncology Research
  • Protease and Inhibitor Mechanisms
  • Cancer Research and Treatments
  • Histone Deacetylase Inhibitors Research
  • CRISPR and Genetic Engineering
  • Immune cells in cancer
  • Phagocytosis and Immune Regulation
  • Sirtuins and Resveratrol in Medicine
  • Cancer Genomics and Diagnostics
  • Cancer Cells and Metastasis
  • Muscle Physiology and Disorders

Roswell Park Comprehensive Cancer Center
2023-2024

VA Western New York Healthcare System
2021

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease that lacks effective treatment options, highlighting the need for developing new therapeutic interventions. Here, we assessed response to pharmacologic inhibition of KRAS, central oncogenic driver PDAC. In a panel PDAC cell lines, KRASG12D with MRTX1133 yielded variable efficacy in suppressing growth and downstream gene expression programs 2D cultures. On basis CRISPR-Cas9 loss-of-function screens, ITGB1 was identified...

10.1158/0008-5472.can-23-2504 article EN cc-by-nc-nd Cancer Research 2024-01-31

Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease for which new therapeutic interventions are needed. Here we assessed the cellular response to pharmacological KRAS inhibition, target central oncogenic factor in PDAC. In a panel of PDAC cell lines, pharmaceutical inhibition G12D allele, with MRTX1133 yields variable efficacy suppression growth and downstream gene expression programs 2D culture. CRISPR screens identify drivers enhanced that regulate focal adhesion signaling...

10.1101/2023.03.18.533261 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-03-22

<div>Abstract<p>Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease that lacks effective treatment options, highlighting the need for developing new therapeutic interventions. Here, we assessed response to pharmacologic inhibition of KRAS, central oncogenic driver PDAC. In a panel PDAC cell lines, KRAS<sup>G12D</sup> with MRTX1133 yielded variable efficacy in suppressing growth and downstream gene expression programs 2D cultures. On basis CRISPR-Cas9...

10.1158/0008-5472.c.7158211 preprint EN 2024-04-01

<div>Abstract<p>Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease that lacks effective treatment options, highlighting the need for developing new therapeutic interventions. Here, we assessed response to pharmacologic inhibition of KRAS, central oncogenic driver PDAC. In a panel PDAC cell lines, KRAS<sup>G12D</sup> with MRTX1133 yielded variable efficacy in suppressing growth and downstream gene expression programs 2D cultures. On basis CRISPR-Cas9...

10.1158/0008-5472.c.7158211.v1 preprint EN 2024-04-01

Background: Mutations in TBCK can generate truncated protein aggregates that abolish the normal function of gene. Alterations have been implicated developmental and neurogenetic disorders, as well progression certain forms cancer. Despite TBCK's involvement various human diseases, underlying mechanism for cancer pathogenesis remains poorly understood. 
 Methods: To further explore loss mutations TBCK, we introduced a CRISPR-mediated knockout system capable deleting...

10.20944/preprints202308.0943.v2 preprint EN 2023-08-29
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