About

Bryson W. Katona, MD, PhD, is the Jeffery and Cynthia King Associate Professor of Lynch Syndrome Research at the University of Pennsylvania's Perelman School of Medicine. He serves as the Director of the Gastrointestinal Cancer Genetics Program and the Gastrointestinal Cancer Risk Evaluation Program at Penn Medicine. His research focuses on hereditary gastrointestinal cancer and polyposis syndromes, with particular emphasis on hereditary colorectal and gastric cancers. Dr. Katona is a member of several research and clinical programs, including the Abramson Cancer Center's Cancer Control Program, the Institute for Translational Medicine and Therapeutics, and the Center for Molecular Studies in Digestive and Liver Diseases. His educational background includes a BA and MS in Chemistry from the University of Pennsylvania and a PhD in Biochemistry, as well as an MD, both from Washington University in St. Louis School of Medicine. His clinical expertise involves hereditary gastrointestinal cancer and polyposis syndromes, and his research aims to improve risk evaluation, screening, and understanding of hereditary cancer syndromes.

Research topics

• Medicine
• Internal medicine
• Biology
• Genetics
• Gastroenterology
• Cancer research
• Bioinformatics
• Oncology

Selected publications

• 460 LYNCH SYNDROME CARRIERS HAVE SIMILAR PREVALENCE OF IBD BUT LOWER OVERALL PREVALENCE OF AUTOIMMUNE DISEASES COMPARED TO CONTROLS

  Gastroenterology · 2026-05-01

  articleSenior author
  PublisherDOI

• 459 ORAL P-HYDROXYBUTYRATE SUPPLEMENTATION ALTERS CIRCULATING METABOLITES TO SUPPRESS COLONIC EPITHELIAL PROLIFERATION IN LYNCH SYNDROME

  Gastrointestinal Endoscopy · 2026-05-01

  articleSenior author
  PublisherDOI

• 459 ORAL P-HYDROXYBUTYRATE SUPPLEMENTATION ALTERS CIRCULATING METABOLITES TO SUPPRESS COLONIC EPITHELIAL PROLIFERATION IN LYNCH SYNDROME

  Gastroenterology · 2026-05-01

  articleSenior author
  PublisherDOI

• Mo1829 IMPACT OF RADIOLIGAND THERAPY-INDUCED HEMATOLOGIC TOXICITY ON ABILITY TO RECEIVE CYTOTOXIC CHEMOTHERAPY IN PATIENTS WITH GASTROENTEROPANCREATIC NEUROENDOCRINE TUMORS

  Gastrointestinal Endoscopy · 2026-05-01

  article
  PublisherDOI

• NANETS Guidelines for the diagnosis and management of stage I–III rectal neuroendocrine tumors

  Endocrine Related Cancer · 2026-01-21

  articleOpen access

  Well-differentiated rectal neuroendocrine tumors (rNETs) are among the most common NETs and account for approximately 12-27% of all gastrointestinal NETs in North America. Significant discrepancies persist in the management of NETs regarding surveillance strategies, staging modalities, high-risk features, and criteria for surgical intervention. This guideline updates current practices of stage I-III rectal NETs with the utilization of GRADE (Grading of Recommendations, Assessment, Development, and Evaluation) methodology and Delphi method of consensus among leading experts in the North American region. We found that several technological advances, such as 68Ga- or 64Cu-DOTATATE SSTR PET/CT, and broad adoption of pelvic MRI have improved staging of rNETs, along with modified endoscopic mucosal and submucosal resection and full-thickness excision techniques that demonstrate efficacy and safety for resection. Pivotal long-term outcome studies provide insight into i) risk factors for regional lymph node metastasis, ii) the impact of R1 excision (endoscopic), iii) best practices for intermediate-sized rNETs (11-20 mm), and iv) risk in small rNETs (≤10 mm). Recommendations were developed upon evidence-based conclusions from the GRADE review to define the role of baseline staging with MRI, advanced endoscopy, and transanal endoscopic surgical methods appropriate for T1 rNETs, the role of salvage therapy in cases of R1 resection, and the consideration of pathologic variables to direct definitive treatment and surveillance. We conclude that advances in screening programs and imaging allow for improved detection and staging of rNETs, while long-term outcome studies can better direct patients toward evidence-based treatment management and rectal organ preservation through less radical resection methods.

  PublisherDOI

• Colorectal Neoplasia Rates in Li-Fraumeni Syndrome

  The American Journal of Gastroenterology · 2026-02-25

  article

  INTRODUCTION: Individuals with Li-Fraumeni syndrome (LFS), a cancer predisposition syndrome caused by TP53 pathogenic germline variants (PGV), have an increased risk of colorectal cancer (CRC). However, limited data exist on colonoscopy metrics, including total neoplasia detection rates, in patients with LFS. METHODS: We conducted a retrospective cohort study of colorectal neoplasia incidence and characteristics in 663 individuals with LFS. We determined total neoplasia detection rate, adenoma detection rate (ADR), advanced ADR, serrated lesion detection rate (SDR), and CRC detection rate, stratified by age, sex, and PGV subtype, in 311 surveillance colonoscopies from 206 adults performed January 2019 to August 2024. RESULTS: CRC was reported in 4.5% of 663 adults and 0.8% of 124 pediatric patients with LFS. Among 206 adults undergoing colonoscopy, total neoplasia detection rate, ADR, SDR, advanced precancerous polyp detection rate, and CRC detection rate were 37%, 27%, 9.3%, 4.5%, and 0.64%, respectively. Detection rates were similar between loss of function and hypomorphic PGVs. Adults aged 45-75 had higher total neoplasia detection rate, ADR, advanced ADR, SDR, and CRC detection rate than those aged 25-45. Male sex was associated with increased total neoplasia detection rate (53.7% vs 30.7%, P = 0.0004), ADR (41.2% vs 22.1%, P = 0.0013), and advanced ADR (7.5% vs 1.3%, P = 0.0105). DISCUSSION: Patients with LFS have comparable ADR and higher SDR with average-risk adults despite earlier, more frequent surveillance, irrespective of TP53 PGV subtype. Our data support current recommendations for earlier and more frequent colonoscopy surveillance than average-risk guidelines, across LFS phenotypes.

  PublisherDOI

• 460 LYNCH SYNDROME CARRIERS HAVE SIMILAR PREVALENCE OF IBD BUT LOWER OVERALL PREVALENCE OF AUTOIMMUNE DISEASES COMPARED TO CONTROLS

  Gastrointestinal Endoscopy · 2026-05-01

  articleSenior author
  PublisherDOI

• Performance of a blood-biomarker test for early detection of pancreatic ductal adenocarcinoma (PDAC) across all stages of disease versus a mixed control population.

  Journal of Clinical Oncology · 2026-01-10

  article

  659 Background: Early detection of pancreatic ductal adenocarcinoma (PDAC) has a significant impact on pancreatic cancer outcomes. Despite this, 4 in 5 patients are diagnosed at later disease stage where surgery is no longer an option. There is a need for more accurate and less burdensome testing methodology. We previously conducted two independent clinical validation studies (CLARITI and VERIFI) where PancreaSure, a serum-based early detection test for PDAC, showed high accuracy in differentiating early-stage disease versus high-risk control patients. To further understand the performance of the test across a varied patient population, we set out to determine test performance in Stage I-IV PDAC and in healthy controls. Methods: PancreaSure, a biomarker signature comprising a mathematical summation of ICAM-1, THSB1, CTSD, TIMP1, and CA19-9 values with a predefined cutoff to differentiate Stage I and Stage II PDAC from controls at high-risk due to genetic/familial background, was assessed for sensitivity and specificity in detecting Stage III and IV PDAC and in normal, healthy controls. Pooled analysis was conducted to determine weighted performance across all stages of PDAC and in high-risk and healthy controls. Results: The study comprised 317 Stage I-II (early stage) and 152 Stage III-IV (late stage) PDAC cases, 1134 high-risk controls, and 295 healthy controls that were collected from US and European sites. PancreaSure overall weighted sensitivity was 79.8% (73.3-86.4% 95% CI). Sensitivity was 77.6% (73.0-82.2%, 95% CI) in early-stage PDAC and 88.2% (81.8-93.0%, 95% CI) in late-stage PDAC. Overall weighted specificity was 90.8% (87.8-93.8% 95% CI). Specificity was 92.2% (90.6-93.7%, 95% CI) in high-risk controls and 97.7% (95.3-99.1%, 95% CI) in healthy controls. Conclusions: Across a robust clinical experience of almost 1900 patients, PancreaSure showed high accuracy across Stage I-IV PDAC, with improved performance in late-stage disease and in healthy controls. These results support the robustness of the test’s performance and can serve as a tool for both early-stage and late-stage PDAC detection in patients at high and normal risk of pancreatic cancer.

  PublisherDOI

• Pediatric Malignancy in the Setting of Lynch Syndrome: A Case Series and Review of the Literature

  Pediatric Blood & Cancer · 2026-01-16

  article

  Lynch Syndrome (LS) is a hereditary cancer predisposition syndrome caused by germline pathogenic/likely pathogenic variants in mismatch repair (MMR) genes. While LS is not traditionally thought to increase childhood cancer risk, some studies have shown an increased prevalence of germline MMR variants in the pediatric oncology population. Herein, we discuss 55 individuals with pediatric cancer and LS. Of these, MSH2 was the most common germline change (36%). Of those tested for loss of heterozygosity (LOH) or microsatellite instability (MSI), the majority had LOH present (78%) and were MSI high (71%), suggesting the contribution of LS to oncogenesis in these individuals.

  PublisherDOI

• Gastric Epithelium from <i>BRCA1</i> and <i>BRCA2</i> Carriers Harbors Increased Double-Stranded DNA Damage and Enhanced Growth Potential

  Molecular Cancer Research · 2026-03-23

  articleOpen accessSenior author

  An accumulating body of evidence suggests carriers of a pathogenic germline variant (PGV) in BRCA1 or BRCA2 have increased gastric cancer (GC) risk. BRCA1 and BRCA2 are tumor suppressor genes involved in promoting homologous recombination to repair double-stranded DNA breaks. The aim of this investigation was to identify differences within the gastric epithelium and in patient-derived gastric organoids (PDGOs) between BRCA1 and BRCA2 carriers and non-carriers to determine if evidence of early gastric carcinogenesis exists amongst these carriers. First, using gastric epithelial biopsies, BRCA2 carriers were found to harbor higher expression of the proliferative marker Ki-67 within the antral gastric epithelium and strikingly, biopsies from both BRCA1 and BRCA2 carriers displayed a marked increase in double-stranded DNA damage. These results were further explored using PDGOs, where a growth advantage was observed for both BRCA1 and BRCA2 PDGOs compared to non-carrier PDGOs. Furthermore, both BRCA1 and BRCA2 PDGOs displayed a more pronounced enhancement of Ki-67 expression as well as increased double stranded DNA damage compared to non-carrier PDGOs. Importantly, none of the PDGOs showed signs of BRCA1 or BRCA2 loss of heterozygosity, potentially indicating a haploinsufficient phenotype. Taken together, these novel findings suggest that haploinsufficiency in BRCA1 and BRCA2 carriers may lead to DNA damage in the gastric epithelium, which may serve as an early event contributing to GC development. Implications: The elevated risk in GC for BRCA1 and BRCA2 PGV carriers may be due to haploinsufficiency and warrants further investigation into BRCA1 and BRCA2-associated GC.

  PublisherOA PDFDOI

Recent grants

• Menin/MLL promotes cell survival in the setting of EGFR inhibition

  NIH · $819k · 2015–2020

• Menin regulates colonic epithelial cell growth through LXR repression

  NIH · $243k · 2019–2021

Frequent coauthors

• Rachel Hodan

  Cancer Genetics (United States)

  89 shared

• Eduardo Vilar

  83 shared

• Xianxin Hua

  University of Pennsylvania

  82 shared

• Zijie Feng

  Second Affiliated Hospital of Xi'an Jiaotong University

  73 shared

• Xin He

  68 shared

• Xianxin Hua

  65 shared

• Yan Cao

  Changchun University of Chinese Medicine

  64 shared

• Yuan Wu

  Hubei Cancer Hospital

  63 shared

Education

• MD, PhD

  Washington University in Saint Louis School of Medicine

  2009

• BA, MS

  University of Pennsylvania

  2002