Evidence map›Paper›PMID 36621763›Full record

ArticleMolecular metabolism2023

Islet amyloid polypeptide does not suppress pancreatic cancer.

Austin J Taylor, Evgeniy Panzhinskiy, Paul C Orban, Francis C Lynn, David F Schaeffer, James D Johnson, Janel L Kopp, C Bruce Verchere

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Select Endocrine Disorders and Exosomes in Early PDAC Diagnosis.International journal of molecular sciences · 2024
    Review
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

8 authors at 1 institution in 1 country.

Austin J TaylorBC Children's Hospital Research Institute, Vancouver, BC, Canada; Centre for Molecular Medicine and Therapeutics, Vancouver, BC, Canada; Department of Pathology and Laboratory Medicine, University of British Columbia, BC, Canada.
Evgeniy PanzhinskiyLife Sciences Institute, University of British Columbia, BC, Canada; Department of Biochemistry, University of British Columbia, BC, Canada.
Paul C OrbanBC Children's Hospital Research Institute, Vancouver, BC, Canada; Centre for Molecular Medicine and Therapeutics, Vancouver, BC, Canada; Department of Surgery, University of British Columbia, BC, Canada.
Francis C LynnBC Children's Hospital Research Institute, Vancouver, BC, Canada; Department of Surgery, University of British Columbia, BC, Canada; Department of Cellular and Physiological Sciences, University of British Columbia, BC, Canada.
David F SchaefferDepartment of Pathology and Laboratory Medicine, University of British Columbia, BC, Canada; Pancreas Centre BC, Vancouver, BC, Canada.
James D JohnsonLife Sciences Institute, University of British Columbia, BC, Canada; Department of Cellular and Physiological Sciences, University of British Columbia, BC, Canada.
Janel L KoppLife Sciences Institute, University of British Columbia, BC, Canada; Department of Cellular and Physiological Sciences, University of British Columbia, BC, Canada.
C Bruce VerchereBC Children's Hospital Research Institute, Vancouver, BC, Canada; Centre for Molecular Medicine and Therapeutics, Vancouver, BC, Canada; Department of Pathology and Laboratory Medicine, University of British Columbia, BC, Canada; Department of Surgery, University of British Columbia, BC, Canada. Electronic address: bverchere@bcchr.ca.
University of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesPancreatic cancer risk is elevated approximately two-fold in type 1 and type 2 diabetes. Islet amyloid polypeptide (IAPP) is an abundant beta-cell peptide hormone that declines with diabetes progression. IAPP has been reported to act as a tumour-suppressor in p53-deficient cancers capable of regressing tumour volumes. Given the decline of IAPP during diabetes development, we investigated the actions of IAPP in pancreatic ductal adenocarcinoma (PDAC; the most common form of pancreatic cancer) to determine if IAPP loss in diabetes may increase the risk of pancreatic cancer.

methodsPANC-1, MIA PaCa-2, and H1299 cells were treated with rodent IAPP, and the IAPP analogs pramlintide and davalintide, and assayed for changes in proliferation, death, and glycolysis. An IAPP-deficient mouse model of PDAC (Iapp

resultsIAPP did not impact glycolysis in MIA PaCa-2 cells, and did not impact cell death, proliferation, or glycolysis in PANC-1 cells or in H1299 cells, which were previously reported as IAPP-sensitive. Iapp deletion in Kras

conclusionsIn contrast to previous reports, we find that IAPP does not function as a tumour suppressor. This suggests that loss of IAPP signalling likely does not increase the risk of pancreatic cancer in individuals with diabetes.

Indexed as

Diabetes Mellitus, Type 2Pancreatic NeoplasmsAnimalsCerebellumDiabetes MellitusFaciesFetal Growth RetardationIslet Amyloid PolypeptideMiceProto-Oncogene Proteins p21(ras)Islet Amyloid PolypeptideProto-Oncogene Proteins p21(ras)AmylinDiabetesIslet amyloid polypeptidePancreatic ductal adenocarcinomaTumor suppressor

Identifiers

PMID36621763
PMCPMC9938314
OpenAlexW4313575227

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.