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About

Stanley R. Hamilton, MD, FCAP, AGAF, is a digestive system and molecular pathologist and Professor and Chair of the Department of Pathology at the City of Hope National Medical Center since 2000. A native of Indiana, Dr. Hamilton received his medical degree at the Indiana University School of Medicine, followed by internship and residency in Pathology and Laboratory Medicine at the Johns Hopkins University School of Medicine and Hosptial in Baltimore and a fellowship at St. Mark’s Hospital in London. He remained at Johns Hopkins as a faculty member until he was recruited to the University of Texas MD Anderson Cancer Center in 1998 as Professor and Head of Pathology and Laboratory Medicine. He is internationally known as an expert in gastrointestinal pathology with focus on colorectal cancer. Stanley R. Hamilton, M.D., is one of the premier pathologists of his generation and a nationally known leader who built the pathology and laboratory medicine department at MD Anderson Cancer Center into a world class facility. He now brings more than four decades of expertise to City of Hope as chair of the Department of Pathology. A native of Indiana, Dr. Hamilton received his medical degree at Indiana University, continued his training at Johns Hopkins University in Baltimore, then helped grow the Hopkins pathology department for the next 20 years before moving on to MD Anderson in 1998. Along the way he became nationally known as an expert in gastro-intestinal/colon cancer pathology. Dr. Hamilton is excited to join the City of Hope family, which he describes as “great people, all dedicated to the mission. It's a wonderful environment.” He plans to leverage the digital transformation now taking place in his field, bringing state-of-the-art pathology services to every patient at every City of Hope community practice site, while improving and enhancing the biomarker data used in clinical trials, and further integrating digital pathology into the overall informatics of the institution.

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Skills

Experience

Professor of Pathology

City of Hope, California

Jan-2024 to Present

Publication

  • dott image February, 2005

Contribution of bone marrow–derived endothelial cells to human tumor vasculature

It has been shown that bone marrow–derived stem cells can form a major fraction of the tumor endothelium in mouse tumors. To determine the role of such cells in human tumor angiogenesis, w...

  • dott image February, 2001

Top-down morphogenesis of colorectal tumors

One of the fundamental tenets of oncology is that tumors arise from stem cells. In the colon, stem cells are thought to reside at the base of crypts. In the early stages of tumorigenesis, ho...

Evaluation of candidate tumour suppressor genes on chromosome 18 in colorectal cancers

Chromosome deletions are the most common genetic events observed in cancer1–4. These deletions are generally thought to reflect the existence of a tumour suppressor gene within the lost re...

Mad-related genes in the human

Resistance to the growth inhibitory effects of TGF-β is common in human cancers1,2. However, the mechanism(s) by which tumour cells become resistant to TGF-β are generally unknown. We have...

Topological Control of p21WAF1/CIP1 Expression in Normal and Neoplastic Tissues1

The p53-regulated gene product p21WAF1/CIP1 is the prototype of a family of small proteins that negatively regulate the cell cycle. To learn more about p21WAF1/CIP1 regulation in vivo, monoc...

  • dott image January, 1995

Mismatch repair gene defects in sporadic colorectal cancers with microsatellite instability

Microsatellite instability has been observed in both sporadic and hereditary forms of colorectal cancer. In the hereditary form, this instability is generally due to germline mutations in mi...

  • dott image November, 1994

Molecular Determinants of Dysplasia in Colorectal Lesions1

One hallmark of malignant potential is dysplasia, the disruption of normal morphology. While it is generally recognized that cancer is the result of a series of genetic changes, the relation...

  • dott image September, 1994

hMSH2 Mutations in Hereditary Nonpolyposis Colorectal Cancer Kindreds1

It has recently been shown that hereditary nonpolyposis colorectal cancer (HNPCC) is caused by hereditable defects in DNA mismatch repair genes. However, the fraction of HNPCC due to defects...

Allelic Loss of Chromosome 18q and Prognosis in Colorectal Cancer

Background Colorectal cancer occurs in approximately 150,000 people each year in the United States. Prognostic assessment influences the treatment of patients with colorectal cancer, includ...

  • dott image April, 1994

Replication Errors in Benign and Malignant Tumors from Hereditary Nonpolyposis Colorectal Cancer Patients1

A replication error (RER) phenotype has been documented both in sporadic colorectal tumors and in tumors from patients with hereditary nonpolyposis colorectal cancer (HNPCC). In the current ...