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The joint IAEA, EANM, and SNMMI practical guidance on peptide receptor radionuclide therapy (PRRNT) in neuroendocrine tumours
TLDR
This guidance covers the rationale, indications and contraindications for PRRNT, assessment of treatment response and patient follow-up, and is aimed at guiding nuclear medicine specialists in selecting likely candidates to receive PRR NT and to deliver the treatment in a safe and effective manner. Expand
Mutations in the RET proto-oncogene are associated with MEN 2A and FMTC.
TLDR
Evidence is presented that sequence changes within the coding region of the RET proto-oncogene, a putative transmembrane tyrosine kinase, may be responsible for the development of neoplasia in these inherited disorders. Expand
Mutations in the SMAD4/DPC4 gene in juvenile polyposis.
TLDR
It is shown that a subset of juvenile polyposis families carry germ line mutations in the gene SMAD4 (also known as DPC4), located on chromosome 18q21.1, that encodes a critical cytoplasmic mediator in the transforming growth factor-beta signaling pathway. Expand
Germline mutations of the gene encoding bone morphogenetic protein receptor 1A in juvenile polyposis
TLDR
Findings indicate involvement of an additional gene in the transforming growth factor-β (TGF-β) superfamily in the genesis of JP, and document an unanticipated function for BMP in colonic epithelial growth control. Expand
The risk of gastrointestinal carcinoma in familial juvenile polyposis
TLDR
The risk of gastrointestinal malignancy in affected members of this JP kindred exceeds 50%. Expand
Factors predictive of survival in ampullary carcinoma.
TLDR
Reviewing the recent Memorial Sloan-Kettering Cancer Center experience with adenocarcinoma of the ampulla of Vater and identifying clinicopathologic factors that have an impact on patient survival found factors predictive of improved survival in ampullary carcinoma include resection, negative margins, and negative nodes. Expand
The prevalence of MADH4 and BMPR1A mutations in juvenile polyposis and absence of BMPR2, BMPR1B, and ACVR1 mutations
TLDR
The prevalence of germline MADH4 and BMPR1A mutations is approximately 20% for each gene, which means 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. Expand
The North American Neuroendocrine Tumor Society Consensus Guidelines for Surveillance and Medical Management of Midgut Neuroendocrine Tumors
TLDR
The medical aspects of these guidelines (focusing on systemic treatment, nonsurgical liver-directed therapy, and postoperative surveillance) are summarized in this article and surgical guidelines are described in a companion article. Expand
The American College of Surgeons Commission on Cancer and the American Cancer Society. Adenocarcinoma of the small bowel: review of the National Cancer Data Base, 1985-1995.
TLDR
SBA is found most commonly in the duodenum, and patient DSS is reduced at this site compared with those patients with jejunal or ileal tumors, and this reduction in survival was associated with a lower percentage of cancer-directed surgery. Expand
GermlineSMAD4 orBMPRIA mutations and phenotype of juvenile polyposis
TLDR
Patients with germlineSMAD4 orBMPR1A mutations have a more prominent JP phenotype than those without, and SMAD4 mutations predispose to UGI polyposis. Expand
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