Obesity has become one of the leading preventable causes of cancer, and weight-loss (bariatric) surgery is the most effective long-term treatment we have for it. Patients who undergo these operations go on to develop far fewer obesity-related cancers — liver cancer risk falls by roughly half, and ovarian cancer risk by even more. Why this happens is largely unknown, and explaining it is the central goal of the Dang Lab.
We believe much of the answer lies in the gut. Bariatric surgery changes far more than how much a person eats: it rewires how the intestine, its hormones, and the trillions of bacteria living inside it signal to the rest of the body. Our laboratory follows those signals from the gut to fat tissue, to the immune system, and finally into a tumor. Using animal models in which we perform the same operations our patients receive, we have found that sleeve gastrectomy reshapes the gut bacterial community, quiets inflammation, and switches off a specific tumor signal that pulls harmful immune cells into liver cancers — even in animals that regain the weight they lost. That last detail matters, because it suggests surgery is doing something beyond weight loss alone.
That distinction has become urgent. New weight-loss medications are now used by millions of people, and we do not yet know whether they deliver everything surgery does. We test the two head-to-head — in cancer models in the laboratory, and in patients with obesity-related heart failure, where we measure how much exercise capacity and heart function recover after surgery versus medication.
The lab also asks whether gut bacteria can be harnessed to treat gastroparesis, a disabling condition — common in people with diabetes — in which the stomach empties far too slowly.
Our goal is to identify which gut signals do the protective work, so the benefits of surgery can one day reach patients who cannot or should not have an operation.
Jerry Dang, MD, PhD, FRCSC, FACS, FASMBS, is a bariatric, foregut, and flexible endoscopic surgeon at Cleveland Clinic and Associate Professor of Surgery at the Cleveland Clinic Lerner College of Medicine of Case Western Reserve University. He is staff in the Department of Microbial Sciences in Health within Cleveland Clinic Research, where he leads a laboratory studying how metabolic surgery and the gut microbiome reprogram host immunity and metabolism to suppress obesity-driven cancer.
Dr. Dang completed a Bachelor of Science in Mechanical Engineering at the University of Calgary and worked as a production and project engineer before entering medicine. He earned his medical degree and completed general surgery residency at the University of Alberta, where he also completed the Royal College Clinician Investigator Program and a PhD in Surgery, with a thesis on the Intestinal Physiology of Bariatric Surgery. He then completed fellowship training in Advanced Laparoscopic Surgery and Flexible Surgical Endoscopy at Cleveland Clinic's Digestive Disease Institute and joined the staff in 2023. He is board certified by the American Board of Surgery and the Royal College of Physicians and Surgeons of Canada.
Clinically, he specializes in primary and revisional bariatric surgery, complex foregut and hernia reconstruction, and therapeutic endoscopy, including gastric per-oral endoscopic myotomy (G-POEM) for gastroparesis.
Dr. Dang has authored more than 150 peer-reviewed publications and several textbook chapters, serves on multiple editorial boards, and chairs the Emerging Technology and Procedures Committee of the American Society for Metabolic and Bariatric Surgery. His research has been supported by the ASMBS, SAGES, the Central Surgical Association, Alberta Innovates, the Canadian Institutes of Health Research, and Cleveland Clinic's Digestive Disease Institute
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The Dang Lab, in Cleveland Clinic Research (Microbial Sciences in Health), asks how metabolic surgery and the gut microbiome reprogram host immunity, metabolism, and end-organ function — and how much of that benefit weight loss alone reproduces.
Bariatric surgery and hepatocellular carcinoma. In a DMBA/high-fat-diet model with tumors detected by ultrasound before surgery, sleeve gastrectomy (SG) reduces tumor multiplicity and normalizes liver weight despite later weight regain. Paired metagenomics with cecal, adipose, non-tumor liver, and tumor transcriptomics converge on an SG-associated microbial program (glycan biosynthesis, inositol degradation) tracking with lower cecal IL-6–JAK–STAT3 and PI3K–mTOR signaling, reduced adipose inflammatory and coagulation tone, and suppressed tumor CCL2/MCP-1. Current work tests temporal order, microbiome sufficiency by FMT, and whether the CCL2/CCR2 axis is a required terminal effector (R01 in preparation).
Weight loss versus surgery in ovarian cancer. In diet-induced obese mice bearing luciferase-tagged ID8-Trp53-/- tumors, SG and Roux-en-Y gastric bypass are benchmarked by longitudinal bioluminescence–CT against a graded incretin series (semaglutide, tirzepatide, retatrutide) and weight-matched pair-feeding, quantifying surgery-specific effects as deviation from the fitted weight-loss–response curve.
Microbiome modulation in diabetic gastroparesis. A factorial FMT x fermentable-fiber design tests whether SCFA-driven microbial shifts restore gastric emptying and neuroimmune integrity (ICC/c-Kit, nNOS, CD206+/HO-1+ muscularis macrophages).
Clinical translation. A prospective HFpEF cohort phenotypes cardiopulmonary and structural recovery by CPET, strain echocardiography, and DXA at baseline, 10% weight loss, and nadir, comparing surgery with incretin pharmacotherapy. A second pilot tests concurrent sleeve gastrectomy at liver transplantation. Registry and AI studies run in parallel.
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