James Howe

Summary

Affiliation: University of Iowa
Country: USA

Publications

  1. Keck K, Maxwell J, Utria A, Bellizzi A, Dillon J, O Dorisio T, et al. The Distal Predilection of Small Bowel Neuroendocrine Tumors. Ann Surg Oncol. 2018;25:3207-3213 pubmed publisher
    ..SBNETs are less prevalent proximally in the small bowel, which may result from anatomic differences in enterochromaffin cell density, hormonal factors, or environmental exposures in the distal SB. ..
  2. Sherman S, Maxwell J, Qian Q, Bellizzi A, Braun T, Iannettoni M, et al. Esophageal cancer in a family with hamartomatous tumors and germline PTEN frameshift and SMAD7 missense mutations. Cancer Genet. 2015;208:41-6 pubmed publisher
  3. Maxwell J, Sherman S, Li G, Choi A, Bellizzi A, O Dorisio T, et al. Somatic alterations of CDKN1B are associated with small bowel neuroendocrine tumors. Cancer Genet. 2015;: pubmed publisher
    ..8%; 95% CI -0.44-10%). Alterations of cell-cycle control due to alterations in CDKN1B may be one mechanism by which SBNETs develop, which could have implications for new treatment modalities. ..
  4. Maxwell J, Sherman S, Stashek K, O Dorisio T, Bellizzi A, Howe J. A practical method to determine the site of unknown primary in metastatic neuroendocrine tumors. Surgery. 2014;156:1359-65; discussion 1365-6 pubmed publisher
    ..The algorithm identified the primary tumor site in all cases in which IHC failed. Performing IHC, followed by GEC for indeterminate cases, identifies accurately the primary site in SBNET and PNET metastases in virtually all patients. ..
  5. Maxwell J, Sherman S, O Dorisio T, Bellizzi A, Howe J. Liver-directed surgery of neuroendocrine metastases: What is the optimal strategy?. Surgery. 2016;159:320-33 pubmed publisher
    ..PSD procedures are safe and can achieve significant cytoreduction, which is associated with improved survival. Lowering the debulking target threshold to 70% may benefit NET patients by increasing eligibility for cytoreduction. ..
  6. Maxwell J, O Dorisio T, Howe J. Biochemical Diagnosis and Preoperative Imaging of Gastroenteropancreatic Neuroendocrine Tumors. Surg Oncol Clin N Am. 2016;25:171-94 pubmed publisher
    ..This review discusses the biomarkers important for the diagnosis of these tumors and the imaging modalities needed. ..
  7. Maxwell J, Sherman S, Howe J. Translational Diagnostics and Therapeutics in Pancreatic Neuroendocrine Tumors. Clin Cancer Res. 2016;22:5022-5029 pubmed
    ..Clin Cancer Res; 22(20); 5022-9. ©2016 AACR SEE ALL ARTICLES IN THIS CCR FOCUS SECTION, "ENDOCRINE CANCERS REVISING PARADIGMS". ..
  8. Keck K, Choi A, Maxwell J, Li G, O Dorisio T, Breheny P, et al. Increased Grade in Neuroendocrine Tumor Metastases Negatively Impacts Survival. Ann Surg Oncol. 2017;24:2206-2212 pubmed publisher
    ..Determining the grade in both the primary tumor and a metastasis is important for estimating prognosis and to help inform decisions regarding additional therapies. ..
  9. request reprint
    Howe J, Roth S, Ringold J, Summers R, Järvinen H, Sistonen P, et al. Mutations in the SMAD4/DPC4 gene in juvenile polyposis. Science. 1998;280:1086-8 pubmed
    ..The mutant SMAD4 proteins are predicted to be truncated at the carboxyl-terminus and lack sequences required for normal function. These results confirm an important role for SMAD4 in the development of gastrointestinal tumors. ..

More Information

Publications16

  1. request reprint
    Howe J, Bair J, Sayed M, Anderson M, Mitros F, Petersen G, et al. Germline mutations of the gene encoding bone morphogenetic protein receptor 1A in juvenile polyposis. Nat Genet. 2001;28:184-7 pubmed
    ..These findings indicate involvement of an additional gene in the transforming growth factor-beta (TGF-beta) superfamily in the genesis of JP, and document an unanticipated function for BMP in colonic epithelial growth control. ..
  2. Howe J, Shellnut J, Wagner B, Ringold J, Sayed M, Ahmed A, et al. Common deletion of SMAD4 in juvenile polyposis is a mutational hotspot. Am J Hum Genet. 2002;70:1357-62 pubmed
  3. Howe J, Sayed M, Ahmed A, Ringold J, Larsen Haidle J, Merg A, et al. The prevalence of MADH4 and BMPR1A mutations in juvenile polyposis and absence of BMPR2, BMPR1B, and ACVR1 mutations. J Med Genet. 2004;41:484-91 pubmed
    ..Since mutations were not found in more than half the JP patients, either additional genes predisposing to JP remain to be discovered, or alternate means of inactivation of the two known genes are responsible for these JP cases. ..
  4. Howe J, Chinnathambi S, Calva D, Bair J, Pechman B, Salamon A, et al. A family with two consecutive nonsense mutations in BMPR1A causing juvenile polyposis. Cancer Genet Cytogenet. 2008;181:52-4 pubmed publisher
    ..This mutation caused protein truncation, and represents a novel case of consecutive nonsense mutations in human disease. ..
  5. Sherman S, Maxwell J, Carr J, Wang D, O DORISIO M, O Dorisio T, et al. GIPR expression in gastric and duodenal neuroendocrine tumors. J Surg Res. 2014;190:587-93 pubmed publisher
    ..1 versus 3.5-fold overexpression). We conclude that GIPR could provide an improved signal-to-noise ratio for imaging versus SSTR2 and represents a promising novel therapeutic target in GDNETs. ..
  6. Keck K, Breheny P, Braun T, Darbro B, Li G, Dillon J, et al. Changes in gene expression in small bowel neuroendocrine tumors associated with progression to metastases. Surgery. 2018;163:232-239 pubmed publisher
    ..Differential expression of various genes, including PMP22, SYT13 and SERPINA10, are associated with the progression of SBNETs and warrant further investigation. ..
  7. Keck K, Maxwell J, Menda Y, Bellizzi A, DILLON J, O Dorisio T, et al. Identification of primary tumors in patients presenting with metastatic gastroenteropancreatic neuroendocrine tumors. Surgery. 2017;161:272-279 pubmed publisher
    ..Preoperative testing facilitated operative planning, allowing for resection of the primary and hepatic debulking in most patients. ..