Charles M. Bowen

ORCID: 0000-0001-5400-4304
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About
Contact & Profiles
Research Areas
  • Genetic factors in colorectal cancer
  • Cancer Genomics and Diagnostics
  • Cancer Cells and Metastasis
  • Cancer, Lipids, and Metabolism
  • RNA modifications and cancer
  • Digestive system and related health
  • Cancer Immunotherapy and Biomarkers
  • Helicobacter pylori-related gastroenterology studies
  • Inflammatory mediators and NSAID effects
  • Colorectal Cancer Screening and Detection
  • Colorectal Cancer Treatments and Studies
  • Colorectal and Anal Carcinomas
  • Mesenchymal stem cell research
  • Ferroptosis and cancer prognosis
  • Cancer-related molecular mechanisms research
  • DNA Repair Mechanisms
  • PARP inhibition in cancer therapy
  • Cancer-related Molecular Pathways
  • Nutrition, Genetics, and Disease
  • Corneal Surgery and Treatments
  • Ovarian cancer diagnosis and treatment
  • Bone Tumor Diagnosis and Treatments
  • Tumors and Oncological Cases
  • Single-cell and spatial transcriptomics
  • Lymphoma Diagnosis and Treatment

The University of Texas MD Anderson Cancer Center
2020-2025

The University of Texas Medical Branch at Galveston
2022-2025

University of Southern California
2018-2019

USC Norris Comprehensive Cancer Center
2019

Background & Aims Lynch syndrome (LS) carriers develop mismatch repair deficient (MMRd) neoplasia with high neoantigen (neoAg) rates. No detailed information on targetable neoAgs from LS pre-cancers exists, which is crucial for vaccine development and immune-interception strategies. We report a focused somatic mutation frameshift-neoAg landscape of microsatellite loci colorectal polyps without malignant potential (PWOMPs), early-stage cancers in carriers. Methods generated paired whole-exome...

10.1053/j.gastro.2024.01.016 article EN cc-by-nc-nd Gastroenterology 2024-01-20

Colorectal pre-cancers in Lynch Syndrome (LS) exhibit a distinct immune profile, presenting unique opportunities for developing immune-interception strategies to prevent carcinogenesis. Epigenetic modulation by EZH2 of immune-related genes is implicated the carcinogenesis different cancer types including colorectal. This study utilizes mouse model LS and ex vivo colonic organoids assess effects inhibitor GSK503 on regulatory pathways, tumorigenesis, epigenetic reprogramming. Our findings...

10.1172/jci.insight.177545 article EN cc-by JCI Insight 2025-02-13

Regardless of the source injury or metabolic dysfunction, fibrosis is a frequent driver liver pathology. Excessive caused by persistent activation hepatic stellate cells (HSCs), which defined myofibroblast (MFA) and epithelial-mesenchymal transition (EMT). Strategies to prevent reverse this HSC phenotype will be critical for successful treatment fibrosis. We have previously shown that full-term, cell-free human amniotic fluid (cfAF) inhibits MFA EMT in fibroblasts vitro. hypothesize cfAF can...

10.1101/2025.02.20.639215 preprint EN cc-by bioRxiv (Cold Spring Harbor Laboratory) 2025-02-20

Colorectal cancer (CRC) remains the third most common in US with 15% of cases displaying Microsatellite Instability (MSI) secondary to Lynch Syndrome (LS) or somatic hypermethylation MLH1 promoter. A cohort rhesus macaques from our institution developed spontaneous mismatch repair deficient (MMRd) CRC a notable fraction harboring pathogenic germline mutation (c.1029C<G, p.Tyr343Ter). Our study aimed provide detailed molecular characterization for cross-comparison human MMRd CRC. We...

10.1371/journal.pgen.1010163 article EN cc-by PLoS Genetics 2022-04-21

Objective Lynch Syndrome (LS) carriers have a significantly increased risk of developing colorectal cancer (CRC) during their lifetimes. Further stratification this patient population may help in identifying additional factors that predispose to carcinogenesis. In most LS patients CRC arise from adenomas, although an alternative non-polypoid carcinogenesis pathway has been proposed for PMS2 carriers. Using data our institutional cohort, aim was describe current screening outcomes with focus...

10.3389/fonc.2023.1146825 article EN cc-by Frontiers in Oncology 2023-04-24

Background Recent clinical trial data from Lynch Syndrome (LS) carriers demonstrated that naproxen administered for 6-months is a safe primary chemoprevention promotes activation of different resident immune cell types without increasing lymphoid cellularity. While intriguing, the precise enriched by remained unanswered. Here, we have utilized cutting-edge technology to elucidate activated in mucosal tissue LS patients. Methods Normal colorectal mucosa samples (pre- and post-treatment)...

10.3389/fimmu.2023.1162669 article EN cc-by Frontiers in Immunology 2023-05-03

Familial adenomatous polyposis (FAP) is a hereditary colorectal cancer syndrome, which results in the development of hundreds polyps carpeting gastrointestinal tract. NSAIDs have reduced polyp burden patients with FAP and synthetic rexinoids demonstrated ability to modulate cytokine-mediated inflammation WNT signaling. This study examined use combination an NSAID (sulindac) rexinoid (bexarotene) as durable approach for reducing colonic prevent development. Whole transcriptomic analysis...

10.1158/1940-6207.capr-20-0496 article EN Cancer Prevention Research 2021-07-15

Myofibroblast activation is a cellular response elicited by variety of physiological or pathological insults whereby cells initiate coordinated intended to eradicate the insult and then revert back basal state. However, an underlying theme in various disease states persistent myofibroblast that fails resolve. Based on multiple observations, we hypothesized secreted factors harvested from co-culturing amniotic stem might mimic anti-inflammatory state cell-free fluid (AF) elicits. We optimized...

10.3390/biomedicines10092189 article EN cc-by Biomedicines 2022-09-05

Abstract Lynch syndrome is the most common cause of hereditary colorectal cancer and secondary to germline alterations in one four DNA mismatch repair (MMR) genes. Here we aimed provide novel insights into initiation MMR-deficient (MMRd) carcinogenesis by characterizing expression profile MMRd intestinal stem cells (ISC). A tissue-specific mouse model (Villin-Cre;Msh2LoxP/LoxP) was crossed with a reporter (Lgr5-EGFP-IRES-creERT2) trace isolate ISCs (Lgr5+) using flow cytometry. Three...

10.1158/0008-5472.can-20-2896 article EN Cancer Research 2021-03-18

Abstract Introduction: Colorectal pre-cancers in Lynch Syndrome (LS) display a distinct immune profile thus presenting unique opportunity to develop novel immune-interception approaches halt carcinogenesis. Epigenetic modulation by EZH2 of immune-related genes has been implicated many cancers including colorectal but it yet be explored LS The main objective this study is test the effect inhibition on cell profiling, carcinogenesis, gene expression, and histone methylation, using ex vivo...

10.1158/1538-7445.am2024-7552 article EN Cancer Research 2024-03-22

Germline pathogenic variants (PVs) in the BRCA1 and BRCA2 genes confer elevated risks of breast, ovarian, other cancers. Lynch syndrome (LS) is associated with increased multiple cancer types including colorectal uterine Current risk mitigation strategies have focused on pharmacologic reduction, enhanced surveillance, preventive surgeries. While these approaches can be effective, they stand to improved because either limited efficacy or undesirable impact quality life. The current review...

10.1200/edbk_433576 article EN American Society of Clinical Oncology Educational Book 2024-06-01

10.4271/2001-01-2184 article EN SAE technical papers on CD-ROM/SAE technical paper series 2001-07-09

<div>Abstract<p>Lynch syndrome is the most common cause of hereditary colorectal cancer and secondary to germline alterations in one four DNA mismatch repair (MMR) genes. Here we aimed provide novel insights into initiation MMR-deficient (MMRd) carcinogenesis by characterizing expression profile MMRd intestinal stem cells (ISC). A tissue-specific mouse model (Villin-Cre;Msh2<sup><i>LoxP/LoxP</i></sup>) was crossed with a reporter...

10.1158/0008-5472.c.6512688.v1 preprint EN 2023-03-31
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