Evidence map›Paper›PMID 25919692›Full record

ArticlePloS one2015

Modulation of the leptin receptor mediates tumor growth and migration of pancreatic cancer cells.

Alisha M Mendonsa, Madeleine C Chalfant, Lee D Gorden, Michael N VanSaun

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

46 citing papers in PubMed, 62 citations in OpenAlex.

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  9. Dietary fat and lipid metabolism in the tumor microenvironment.Biochimica et biophysica acta. Reviews on cancer · 2023
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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.

Alisha M MendonsaDepartment of Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.
Madeleine C ChalfantDepartment of Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.
Lee D GordenDepartment of Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America; Department of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.
Michael N VanSaunDepartment of Surgery, Division of Surgical Oncology, University of Miami, Sylvester Cancer Center, Miami, Florida, United States of America.
Vanderbilt University Medical Center · USSylvester Comprehensive Cancer Center · US

Funding

Molecular Determinants of Tumor Progression in A Steatolic Liver MicroenvironmentU01CA143072 · NCI · VANDERBILT UNIVERSITY · PI GORDEN, DAVID L, MOSES, HAROLD L · 2009 to 2013
$1.4M
NCI NIH HHS 5U01CA143072NCI NIH HHS U01 CA143072
6 · The paper itself

Abstract

Obesity has been implicated as a significant risk factor for development of pancreatic cancer. In the setting of obesity, a systemic chronic inflammatory response is characterized by alterations in the production and secretion of a wide variety of growth factors. Leptin is a hormone whose level increases drastically in the serum of obese patients. High fat diet induced obesity in mice leads to an overall increased body weight, pancreatic weight, serum leptin, and pancreatic tissue leptin levels. Here we report the contribution of obesity and leptin to pancreatic cancer growth utilizing an in vivo orthotopic murine pancreatic cancer model, which resulted in increased tumor proliferation with concomitant increased tumor burden in the diet induced obese mice compared to lean mice. Human and murine pancreatic cancer cell lines were found to express the short as well as the long form of the leptin receptor and functionally responded to leptin induced activation through an increased phosphorylation of AKT473. In vitro, leptin stimulation increased cellular migration which was blocked by addition of a PI3K inhibitor. In vivo, depletion of the leptin receptor through shRNA knockdown partially abrogated increased orthotopic tumor growth in obese mice. These findings suggest that leptin contributes to pancreatic tumor growth through activation of the PI3K/AKT pathway, which promotes pancreatic tumor cell migration.

Indexed as

Cell MovementAdiposityAnimalsCell Line, TumorCell ProliferationDiet, High-FatGene Knockdown TechniquesHumansLeptinMaleMice, Inbred C57BLObesityPancreatic NeoplasmsReceptors, LeptinLeptinReceptors, Leptin

Identifiers

PMID25919692
PMCPMC4412670
OpenAlexW2015349322

What OpenQuestion holds

Textmetadata
LicenceCC0
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.