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James Howe

Professor,  Surgery

Contact Information

Phone: +1 319 356 1727
Email: james-howe@uiowa.edu


MD, University of Vermont College of Medicine
Residency, Barnes Hospital/Washington University
Fellowship, Surgical Oncology, Research Fellow, Washington University
Fellowship, Surgical Oncology, Memorial Sloan-Kettering Center


Primary: Surgery

Centers and Program Affiliations

Research Interests

juvenile polyposis, genetic marker, polyp

MeSH Terms from Publications

Research Summary

Understanding the Genetic Basis of Juvenile Polyposis

Work in the Surgical Oncology Molecular Biology lab is focused upon understanding and defining the genetic basis of Juvenile Polyposis (JP). The main objective of our current studies is to identify the third causative gene for this inherited cancer predisposition syndrome. To this end, a large Iowa JP family is being tested using a comprehensive panel of genetic markers derived from all the human chromosomes to determine the chromosomal location of this gene. When candidate genes from this region are found, they will be tested for mutations in this JP family, and a panel of over 90 different JP families. In addition to this research focus, we have also been studying how the mutations in people born with JP lead to the formation of polyps. To do this, we have taken both normal and polyp tissues obtained from surgery or endoscopy in JP patients with mutations in the three different JP genes. From these we have performed microarray analysis, which allows us to compare the level of expression of all human genes. These patterns of changes in gene expression between the different JP genes will help us to understand which genetic pathways are involved in polyp development. We are also systematically examining the effects of the DNA mutations in JP patients upon the RNA messages and protein products that result from them. To do this, we have established cell lines from the white blood cells from a large number of JP patients, which gives us a repository of renewable cells for future studies. This will help to clarify the effects of mutations in some JP patients, while in others in whom no mutations have been found by sequencing, may suggest alterative mechanisms of how the JP genes are inactivated. It will also make in vitro studies possible, which will give us a way to determine the effects of various drugs on cells, so that we may develop treatments that will suppress the development of polyps and cancers.

Recent Publications

Show publications
  1. Differentiation of small bowel and pancreatic neuroendocrine tumors by gene-expression profiling. Surgery 152(6):998-1007, 2012. [PubMed]
  2. Invasion in follicular thyroid cancer cell lines is mediated by EphA2 and pAkt. Surgery 152(6):1218-24, 2012. [PubMed]
  3. Risk of subsequent primary thyroid cancer after another malignancy: latency trends in a population-based study. Ann Surg Oncol 19(6):1887-96, 2012. [PubMed]
  4. Germline mutations in SMAD4 disrupt bone morphogenetic protein signaling. J Surg Res 174(2):211-4, 2012. [PubMed]
  5. Comparison of clinicopathologic factors in 122 patients with resected pancreatic and ileal neuroendocrine tumors from a single institution. Ann Surg Oncol 19(3):966-72, 2012. [PubMed]
  6. Juvenile polyposis and other intestinal polyposis syndromes with microdeletions of chromosome 10q22-23. Clin Genet 81(2):110-6, 2012. [PubMed]
  7. SP1 regulates the transcription of BMPR1A. J Surg Res 171(1):e15-20, 2011. [PubMed]
  8. Discovery of SMAD4 promoters, transcription factor binding sites and deletions in juvenile polyposis patients. Nucleic Acids Res 39(13):5369-78, 2011. [PubMed]
  9. Surveillance and intervention after thyroid lobectomy. Ann Surg Oncol 18(6):1729-33, 2011. [PubMed]
  10. Neto2 modulation of kainate receptors with different subunit compositions. J Neurosci 31(22):8078-82, 2011. [PubMed]