Evidence map›Paper›PMID 23500888›Full record

ReviewBiochimica et biophysica acta2013

Adipose tissue and adipocytes support tumorigenesis and metastasis.

Kristin M Nieman, Iris L Romero, Bennett Van Houten, Ernst Lengyel

Abstract 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 457 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
457citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

457 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Toward targeted therapeutics for lobular breast cancer.The Journal of clinical investigation · 2026
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397 more citing papers are in PubMed but not listed here.

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.

Kristin M NiemanDepartment of Obstetrics and Gynecology, Center for Integrative Science, University of Chicago, Chicago, IL, USA.
Iris L Romero
Bennett Van Houten
Ernst Lengyel

Funding

REPRODUCTIVE SCIENTIST TRAINING PROGRAMK12HD000849 · NICHD · WASHINGTON UNIVERSITY · PI Danny J Schust · 1988 to 2026
$33.2M
Regulation of Adhesion and Proteolysis in Ovarian CancerR01CA111882 · NCI · UNIVERSITY OF CHICAGO · PI LENGYEL, ERNST · 2006 to 2016
$2.8M
Metabolic changes in ovarian cancer cells initiated by metastasis to adipose tissR01CA169604 · NCI · UNIVERSITY OF CHICAGO · PI LENGYEL, ERNST · 2013 to 2017
$1.7M
A Role for Fatty Acid Binding Protein 4 in Ovarian Cancer MetastasisF32CA168309 · NCI · UNIVERSITY OF CHICAGO · PI NIEMAN, KRISTIN · 2012 to 2012
$41k
NCI NIH HHS F32 CA168309NCI NIH HHS L30 CA153336NCI NIH HHS R01 CA111882NCI NIH HHS R01 CA169604NICHD NIH HHS K12 HD000849
6 · The paper itself

Abstract

Adipose tissue influences tumor development in two major ways. First, obese individuals have a higher risk of developing certain cancers (endometrial, esophageal, and renal cell cancer). However, the risk of developing other cancers (melanoma, rectal, and ovarian) is not altered by body mass. In obesity, hypertrophied adipose tissue depots are characterized by a state of low grade inflammation. In this activated state, adipocytes and inflammatory cells secrete adipokines and cytokines which are known to promote tumor development. In addition, the adipocyte mediated conversion of androgens to estrogen specifically contributes to the development of endometrial cancer, which shows the greatest relative risk (6.3-fold) increase between lean and obese individuals. Second, many tumor types (gastric, breast, colon, renal, and ovarian) grow in the anatomical vicinity of adipose tissue. During their interaction with cancer cells, adipocytes dedifferentiate into pre-adipocytes or are reprogrammed into cancer-associated adipocytes (CAA). CAA secrete adipokines which stimulate the adhesion, migration, and invasion of tumor cells. Cancer cells and CAA also engage in a dynamic exchange of metabolites. Specifically, CAA release fatty acids through lipolysis which are then transferred to cancer cells and used for energy production through β-oxidation. The abundant availability of lipids from adipocytes in the tumor microenvironment, supports tumor progression and uncontrolled growth. Given that adipocytes are a major source of adipokines and energy for the cancer cell, understanding the mechanisms of metabolic symbiosis between cancer cells and adipocytes, should reveal new therapeutic possibilities. This article is part of a Special Issue entitled Lipid Metabolism in Cancer.

Indexed as

Cell Transformation, NeoplasticNeoplasm MetastasisAdipocytesAdipose TissueDisease ProgressionHumansNeoplasmsObesityTumor MicroenvironmentAdipocytesCancerMetabolic symbiosisMetastasisObesityVisceral adipose tissue

Identifiers

PMID23500888
PMCPMC3742583

What OpenQuestion holds

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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.