Evidence map›Paper›PMID 33019728›Full record

ArticleCells2020

The Relationship between Leptin, the Leptin Receptor and FGFR1 in Primary Human Breast Tumors.

Wyatt Boothby-Shoemaker, Vanessa Benham, Shreya Paithankar, Rama Shankar, Bin Chen, Jamie J Bernard

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.0field-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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Wyatt Boothby-ShoemakerDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824, USA.
Vanessa BenhamDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824, USA.
Shreya PaithankarDepartment of Pediatrics and Human Development, Michigan State University, Grand Rapids, MI 49503, USA.
Rama ShankarDepartment of Pediatrics and Human Development, Michigan State University, Grand Rapids, MI 49503, USA.
Bin ChenDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824, USA.
Jamie J BernardDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824, USA.
Michigan State University · US

Funding

Repurpose open data to discover therapeutics for understudied diseasesR01GM134307 · NIGMS · MICHIGAN STATE UNIVERSITY · PI CHEN, BIN · 2019 to 2023
$2.5M
Mechanistic role of obesity in benzo(a)pyrene-initiated cancerR01ES030695 · NIEHS · MICHIGAN STATE UNIVERSITY · PI BERNARD, JAMIE J · 2020 to 2023
$1.5M
The Role of Fat in Tumor FormationR00CA177868 · NCI · MICHIGAN STATE UNIVERSITY · PI BERNARD, JAMIE J · 2015 to 2017
$699k
NCI NIH HHS R00 CA177868NIEHS NIH HHS R01 ES030695NIGMS NIH HHS R01 GM134307
6 · The paper itself

Abstract

Obesity is associated with increased breast cancer risk and poorer cancer outcomes; however, the precise etiology of these observations has not been fully identified. Our previous research suggests that adipose tissue-derived fibroblast growth factor-2 (FGF2) promotes the malignant transformation of epithelial cells through the activation of fibroblast growth factor receptor-1 (FGFR1). FGF2 is increased in the context of obesity, and increased sera levels have been associated with endocrine-resistant breast cancer. Leptin is a marker of obesity and promotes breast carcinogenesis through several mechanisms. In this study, we leverage public gene expression datasets to evaluate the associations between FGFR1, leptin, and the leptin receptor (LepR) in breast cancer. We show a positive association between FGFR1 and leptin protein copy number in primary breast tumors. These observations coincided with a positive association between Janus kinase 2 (Jak2) mRNA with both leptin receptor (LepR) mRNA and FGFR1 mRNA. Moreover, two separate Jak2 inhibitors attenuated both leptin+FGF2-stimulated and mouse adipose tissue-stimulated MCF-10A transformation. These results demonstrate how elevated sera FGF2 and leptin in obese patients may promote cancer progression in tumors that express elevated FGFR1 and LepR through Jak2 signaling. Therefore, Jak2 is a potential therapeutic target for FGFR1 amplified breast cancer, especially in the context of obesity.

Indexed as

Body Mass IndexBreast NeoplasmsFemaleHumansLeptinReceptor, Fibroblast Growth Factor, Type 1Receptors, LeptinFGFR1 protein, humanLEPR protein, humanLeptinReceptor, Fibroblast Growth Factor, Type 1Receptors, Leptinbody fatnessbody mass indexFGF2FGFR1leptinleptin receptorobesityoverweight

Identifiers

PMID33019728
PMCPMC7600295
OpenAlexW3091066250

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.