Evidence map›Paper›PMID 23639840›Full record

ReviewBiochimica et biophysica acta2013

A molecular rheostat at the interface of cancer and diabetes.

Mahasin A Osman, Fazlul H Sarkar, Enrique Rodriguez-Boulan

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Inhibition of induced-hepatic cancerFrontiers in oncology · 2022
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. GTP-Dependent K-Ras Dimerization.Structure (London, England : 1993) · 2015
    Article
  14. Review
  15. Article
  16. Review
  17. G-protein-coupled receptor GPR161 is overexpressed in breast cancer and is a promoter of cell proliferation and invasion.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  18. 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

3 authors at 3 institutions in 1 country.

Mahasin A OsmanWarren Alpert Medical School, Division of Biology and Medicine, Molecular Pharmacology, Physiology and Biotechnology, Brown University, Providence, RI 02912, USA. Mahasin_Osman@Brown.edu
Fazlul H Sarkar
Enrique Rodriguez-Boulan
Brown University · USCornell University · USThe Barbara Ann Karmanos Cancer Institute · US

Funding

SORTING OF PLASMA MEMBRANE PROTEINS IN EPITHELIAL CELLSR01GM034107 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI RODRIGUEZ-BOULAN, ENRIQUE J · 1985 to 2019
$9.6M
Roles of IQGAPs in polarity and cytokinesisK22CA104285 · NCI · CORNELL UNIVERSITY ITHACA · PI OSMAN, MAHASIN · 2004 to 2006
$403k
NCI NIH HHS CA104285NCI NIH HHS K22 CA104285NIGMS NIH HHS R01 GM034107
6 · The paper itself

Abstract

Epidemiology studies revealed the connection between several types of cancer and type 2 diabetes (T2D) and suggested that T2D is both a symptom and a risk factor of pancreatic cancer. High level of circulating insulin (hyperinsulinemia) in obesity has been implicated in promoting aggressive types of cancers. Insulin resistance, a symptom of T2D, pressures pancreatic β-cells to increase insulin secretion, leading to hyperinsulinemia, which in turn leads to a gradual loss of functional β-cell mass, thus indicating a fine balance and interplay between β-cell function and mass. While the mechanisms of these connections are unclear, the mTORC1-Akt signaling pathway has been implicated in controlling β-cell function and mass, and in mediating the link of cancer and T2D. However, incomplete understating of how the pathway is regulated and how it integrates body metabolism has hindered its efficacy as a clinical target. The IQ motif containing GTPase activating protein 1 (IQGAP1)-Exocyst axis is a growth factor- and nutrient-sensor that couples cell growth and division. Here we discuss how IQGAP1-Exocyst, through differential interactions with Rho-type of small guanosine triphosphatases (GTPases), acts as a rheostat that modulates the mTORC1-Akt and MAPK signals, and integrates β-cell function and mass with insulin signaling, thus providing a molecular mechanism for cancer initiation in diabetes. Delineating this regulatory pathway may have the potential of contributing to optimizing the efficacy and selectivity of future therapies for cancer and diabetes.

Indexed as

AnimalsDiabetes ComplicationsDiabetes Mellitus, Type 2HumansNeoplasmsras GTPase-Activating ProteinsSignal TransductionIQ motif containing GTPase activating protein 1ras GTPase-Activating Proteins

Identifiers

PMID23639840
PMCPMC3667713
OpenAlexW1966254873

What OpenQuestion holds

Textmetadata
LicenceTDM
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.