Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

A Parathyroid-Gut Axis: Hypercalcemia and the Pathogenesis of Gastrinoma in Multiple Endocrine Neoplasia 1.

Molecular cancer research : MCR - 1 Jun 2021

Hackeng Wenzel M, Dreijerink Koen M A, Offerhaus G Johan A, Brosens Lodewijk A A

Abstract excerpt

Patients with multiple endocrine neoplasia 1 (MEN1) syndrome have a germline mutation in the MEN1 gene. Loss of the wild-type allele can initiate endocrine tumorigenesis. Microscopic and macroscopic pituitary, parathyroid, and pancreatic tumors (referred to as the 3 P's) show loss of the wild-type MEN1 allele up to 100%. In contrast, the duodenal gastrinoma pathogenesis in MEN1 syndrome follows a...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Duodenum
Share to Germ-Line Mutation
Share to Hypercalcemia

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Models, Genetic

Share to Multiple Endocrine Neoplasia Type 1

Share to Pancreatic Neoplasms

Share to Parathyroid Glands

Share to Proto-Oncogene Proteins

Source

Identifiers

PMID: 33771883
DOI: 10.1158/1541-7786.MCR-21-0073

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A Parathyroid-Gut Axis: Hypercalcemia and the Pathogenesis of Gastrinoma in Multiple Endocrine Neoplasia 1.PMID 33771883Read ↗

Multiple Endocrine Neoplasia type 1.Semantic proximity Read ↗

Molecular Pathophysiology of Parathyroid Tumorigenesis-The Lesson from a Rare Disease: The "MEN1 Model".Semantic proximity Read ↗

Endocrine Precursor Lesions and Microadenomas of the Duodenum and Pancreas with and without MEN1: Criteria, Molecular Concepts and Clinical SignificanceSemantic proximity Read ↗

Molecular Pathophysiology of Parathyroid Tumorigenesis—The Lesson from a Rare Disease: The “MEN1 Model”Semantic proximity Read ↗

Multiple Endocrine Neoplasia—Syndromes of the Twentieth CenturySemantic proximity Read ↗

Tracing Early Molecular Drivers of Gastrinoma in MEN1: A Systematic Review for Precision Surveillance and Improved Patient OutcomesSemantic proximity Read ↗

[Multiple endocrine neoplasia syndroms. Type 1].Semantic proximity Read ↗

Evolution of Our Understanding of the Hyperparathyroid Syndromes: A Historical PerspectiveSemantic proximity Read ↗

Concepts for screening and diagnostic follow-up in multiple endocrine neoplasia type 1 (MEN1).Semantic proximity Read ↗

Hyperparathyroidism in hereditary syndromes: special expressions and special managements.Semantic proximity Read ↗

Conditional deletion of menin results in antral G cell hyperplasia and hypergastrinemia.Semantic proximity Read ↗

Multiple endocrine neoplasia type 1 gene mutations in sporadic gastrinomas in Japan.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.