Evidence map›Paper›PMID 22943010›Full record

ArticleJournal of gastrointestinal oncology2012

Molecular pathology of pancreatic neuroendocrine tumors.

Mingyi Chen, Michael Van Ness, Yangtong Guo, Jeffrey Gregg

Open access · greenAbstract read
In one paragraph

Article in Journal of gastrointestinal oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.3field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Von Hippel-Lindau Disease.Journal of pediatric genetics · 2016
    Review
  10. Article
  11. Article
  12. Expression of CK19 and KIT in resectable pancreatic neuroendocrine tumors.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Article
  13. Expression of PTEN and mTOR in pancreatic neuroendocrine tumors.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Article
  14. Article
  15. Review
  16. Article
  17. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Mingyi ChenDepartment of Pathology and Laboratory Medicine, University of California Davis Medical Center, Sacramento, California, USA.
Michael Van Ness
Yangtong Guo
Jeffrey Gregg
University of California, Davis · USUniversity of California Davis Medical Center · US

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI PRIMO N. LARA · 2002 to 2026
$84.9M
NCI NIH HHS P30 CA093373
6 · The paper itself

Abstract

Pancreatic endocrine tumors (PETs) are rare neoplasms which account for 1% to 2% of all pancreatic malignancies. The diagnostic, grading and prognostic criteria for PETs have been controversial in surgical pathology and clinical medicine. The newly updated 2010 WHO classification introduced in clinical practice will give more insight into genetic and molecular changes related to PET subtypes. These neoplasms can be graded into 1 of 3 tiers, based on histologic characteristics in likeness to epithelial neuroendocrine tumors in other anatomic sites. Most PETs are sporadic, however, some of them, may occur as part of familial tumors (inherited syndromes) such as multiple endocrine neoplasia type 1 (MEN1 syndrome), von Hippel-Lindau disease (VHL), neurofibromatosis type 1 (NF-1), and tuberous sclerosis (TSC). In sporadic endocrine pancreatic tumors, losses of chromosome 1 and 11q as well as gain on 9q appear to be early events in the development of pancreatic tumors. Multiple genetic defects may accumulate with time and result in pancreatic neuroendocrine tumor progression and malignancy. Although PETs may be similar or identical in histologic appearance to neuroendocrine tumors of the gastrointestinal tract, differences in their underlying biology and likely differences in response to therapeutic agents suggest that they should be treated and investigated as a distinct entity. The correlation of PI3K/Akt/mTOR pathway in the pathogenesis of PETs has been reported, and clinical trials data of mTOR inhibitors is promising.

Indexed as

molecular pathology and diagnosisPancreatic neuroendocrine tumors (PNET)tumorigenesis

Identifiers

PMID22943010
PMCPMC3418536
OpenAlexW1943511012

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.