MYH knockdown in pancreatic cancer cells creates an exploitable DNA repair vulnerability

Pancreatic ductal adenocarcinoma (PDAC) has a poor 5-year survival rate of just 13 %. Conventional therapies fail due to acquired chemoresistance. We previously identified MutY-Homolog (MYH), a protein that repairs oxidative DNA damage, as a therapeutic target that induces apoptosis in PDAC cells. H...

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Veröffentlicht in:	Neoplasia (New York, N.Y.) Jg. 61; S. 101138
Hauptverfasser:	Ephraums, James, Youkhana, Janet, Raina, Aparna S., Schulstad, Grace, Croft, Kento, Mawson, Amanda, Kokkinos, John, Gonzales-Aloy, Estrella, Ignacio, Rosa Mistica C., McCarroll, Joshua A., Boyer, Cyrille, Goldstein, David, Pajic, Marina, Haghighi, Koroush S., Johns, Amber, Gill, Anthony J., Erkan, Mert, Initiative (APGI), Australian Pancreatic Cancer Genome, Phillips, Phoebe A., Sharbeen, George
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States Elsevier Inc 01.03.2025 Elsevier
Schlagworte:	Animals Antineoplastic Agents - pharmacology Apoptosis - drug effects Apoptosis - genetics Carcinoma, Pancreatic Ductal - drug therapy Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - pathology Cell Line, Tumor Cell Proliferation - drug effects Chemosensitisation Disease Models, Animal DNA Damage DNA Glycosylases - genetics DNA Glycosylases - metabolism DNA repair DNA Repair - genetics Gene Knockdown Techniques Humans Mice Oxaliplatin Oxidative stress Pancreatic cancer Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - genetics Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Phthalazines - pharmacology Piperazines - pharmacology RNA, Small Interfering - genetics Xenograft Model Antitumor Assays Oxidative stress Chemosensitisation DNA repair Pancreatic cancer
ISSN:	1476-5586, 1476-5586
Online-Zugang:	Volltext
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