Oluwadara Coker

Abstract PR013: Dynamic kinome reprogramming and metabolic rewiring drive adaptive resistance to RAS inhibition in pancreatic cancer

Clint A. Stalnecker, Wen-Hsuan Chang, Brandon L. Mouery, Ryan D. Mouery et autres

Abstract Direct RAS inhibitors are poised to transform the treatment landscape for pancreatic ductal adenocarcinoma (PDAC), where frontline therapy remains cytotoxic chemotherapy with limited clinical benefit. Despite this progress, intrinsic and acquired resistance limit the depth and duration of response. While putative …

us (code pays fourni par la source)

Impact of KRAS codon-specific mutations on survival in metastatic CRC on trifluridine-tipiracil with/without bevacizumab

Giulia Maddalena, Ymke van der Pol, Oscar Eduardo. Villarreal, Oluwadara Coker et autres

BACKGROUND: Clinical benefit from later lines of therapy in metastatic colorectal cancer (mCRC) is limited. Patient selection for treatment is crucial for optimal risk-benefit evaluation. Codon-specific KRAS mutations have been implicated as predictive biomarkers for efficacy of trifluridine/tipiracil (TAS-102). However, their predictive …

us, it (code pays fourni par la source)

Supplementary Figure 1 from Antitumor Efficacy of Dual Blockade with Encorafenib + Cetuximab in Combination with Chemotherapy in Human BRAFV600E-Mutant Colorectal Cancer

Stefania Napolitano, Melanie Nicole Woods, Hey Min Lee, Vincenzo De Falco et autres

Differentially enriched hallmark gene sets after cytotoxic chemotherapy and targeted therapy of B1003b PDX tumor samples.

Proteotranscriptomic Analyses of Microsatellite-Stable Early-Onset Colorectal Cancer

Jumanah Yousef Alshenaifi, Giulia Maddalena, Jessica C. Lal, Oluwadara Coker et autres

PURPOSE The prevalence and death rates of early-onset colorectal cancer (EOCRC) have been increasing at an alarming rate since 1994. Compared with late-onset colorectal cancer (LOCRC), EOCRC is more aggressive and resistant to treatment. Despite KRAS mutations and the mitogen-activated protein kinase/extracellular …

us, sa (code pays fourni par la source)

Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers

Madelaine Skolastika Theardy, Mitsunobu Takeda, Alexey V. Sorokin, Shuaitong Chen et autres

The therapeutic benefit of recently developed mutant KRAS (KRAS∗) inhibitors remains limited by the rapid onset of resistance. Here, we aim to delineate mechanisms underlying acquired resistance and identify actionable targets for overcoming this clinical challenge. Previously, we identified syndecan-1 (SDC1) as …

us (code pays fourni par la source)

Adaptive Plasticity Tumor Cells Modulate MAPK-Targeting Therapy Response in Colorectal Cancer

Oscar Eduardo. Villarreal, Yixin Xu, Ha Tran, Annette A. Machado et autres

mutations in tumors have been found to reduce response in some patients, additional mechanisms underlying the limited response durability of MAPK targeting therapy remain unknown. Here, we denote new contributory tumor biology and provide insight on the impact of tumor plasticity on …

us (code pays fourni par la source)

Supplementary Figure S7 from Epigenome Reprogramming Through H3K27 and H3K4 Trimethylation as a Resistance Mechanism to DNA Methylation Inhibition in BRAFV600E-Mutated Colorectal Cancer

Hey Min Lee, Ajay Kumar Saw, Van Karlyle Morris, Stefania Napolitano et autres

Graphical representation of adaptive epigenome reprogramming upon 5-azacitidine treatment in BRAFV600E CRC

Data from Epigenome Reprogramming Through H3K27 and H3K4 Trimethylation as a Resistance Mechanism to DNA Methylation Inhibition in BRAFV600E-Mutated Colorectal Cancer

Hey Min Lee, Ajay Kumar Saw, Van Karlyle Morris, Stefania Napolitano et autres

AbstractPurpose: BRAFV600E-mutated colorectal cancer exhibits a strong correlation with DNA hypermethylation, suggesting that this subgroup of tumors presents unique epigenomic phenotypes. Nonetheless, 5-azacitidine, which inhibits DNA methyltransferase activity, is not efficacious in BRAFV600E colorectal cancer in vivo. Experimental Design: We randomized and …

Supplementary Figure S4 from Epigenome Reprogramming Through H3K27 and H3K4 Trimethylation as a Resistance Mechanism to DNA Methylation Inhibition in BRAFV600E-Mutated Colorectal Cancer

Hey Min Lee, Ajay Kumar Saw, Van Karlyle Morris, Stefania Napolitano et autres

Differential methylation and histone marks upon 5-azacitidine treatment around 5mC-regulated genes

Supplementary Table S1 from Epigenome Reprogramming Through H3K27 and H3K4 Trimethylation as a Resistance Mechanism to DNA Methylation Inhibition in BRAFV600E-Mutated Colorectal Cancer

Hey Min Lee, Ajay Kumar Saw, Van Karlyle Morris, Stefania Napolitano et autres

Mutation and characteristics of conventional and PDX-derived CRC cell lines

Supplementary Figure S3 from Epigenome Reprogramming Through H3K27 and H3K4 Trimethylation as a Resistance Mechanism to DNA Methylation Inhibition in BRAFV600E-Mutated Colorectal Cancer

Hey Min Lee, Ajay Kumar Saw, Van Karlyle Morris, Stefania Napolitano et autres

Chromatin state profiles of control and 5-azacitidine-treated samples

Supplementary Figure S6 from Epigenome Reprogramming Through H3K27 and H3K4 Trimethylation as a Resistance Mechanism to DNA Methylation Inhibition in BRAFV600E-Mutated Colorectal Cancer

Hey Min Lee, Ajay Kumar Saw, Van Karlyle Morris, Stefania Napolitano et autres

Proteomic analysis of histone post-translational modifications (PTMs), particularly lysine acetylation, upon 5-azacitidine treatment