Evidence map›Paper›PMID 26454069›Full record

ReviewSeminars in cancer biology2015

Dysregulated metabolism contributes to oncogenesis.

Matthew D Hirschey, Ralph J DeBerardinis, Anna Mae E Diehl, Janice E Drew, Christian Frezza, Michelle F Green, Lee W Jones, Young H Ko, Anne Le, Michael A Lea and 16 more

Open access · hybridAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 193 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
193citing papers in PubMed, 2 pooled it
10.9field-weighted citation impact, top 1% 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

193 citing papers in PubMed, 2 syntheses or guidelines pooled it, 314 citations in OpenAlex.

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133 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

26 authors at 15 institutions in 3 countries.

Matthew D HirscheyDepartment of Medicine, Duke University Medical Center, Durham, NC 27710, USA; Duke Molecular Physiology Institute, Duke University Medical Center, Durham, NC 27701, USA; Department of Pharmacology & Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA. Electronic address: matthew.hirschey@duke.edu.
Ralph J DeBerardinisChildren's Medical Center Research Institute, University of Texas - Southwestern Medical Center, Dallas, TX 75390, USA.
Anna Mae E DiehlDepartment of Medicine, Duke University Medical Center, Durham, NC 27710, USA.
Janice E DrewRowett Institute of Nutrition and Health, University of Aberdeen, Aberdeen, Scotland, United Kingdom.
Christian FrezzaMRC Cancer Unit, University of Cambridge, Hutchison/MRC Research Centre, Cambridge, United Kingdom.
Michelle F GreenDuke Molecular Physiology Institute, Duke University Medical Center, Durham, NC 27701, USA.
Lee W JonesDepartment of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.
Young H KoUniversity of Maryland BioPark, KoDiscovery, Baltimore, MD 20201, USA.
Anne LeThe Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.
Michael A LeaNew Jersey Medical School, Rutgers University, Newark, NJ 07103, USA.
Jason W LocasaleDepartment of Pharmacology & Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA; Division of Nutritional Sciences, Cornell University, Ithaca, NY 14850, USA; Field of Genetics, Genomics, and Development, Cornell University, Ithaca, NY 14850, USA.
Valter D LongoAndrus Gerontology Center, Division of Biogerontology, University of Southern California, Los Angeles, CA 90089, USA.
Costas A LyssiotisDepartment of Molecular and Integrative Physiology and Department of Internal Medicine, University of Michigan, Ann Arbor 48109, USA.
Eoin McDonnellDuke Molecular Physiology Institute, Duke University Medical Center, Durham, NC 27701, USA.
Mahya MehrmohamadiField of Genetics, Genomics, and Development, Cornell University, Ithaca, NY 14850, USA.
Gregory MichelottiDepartment of Medicine, Duke University Medical Center, Durham, NC 27710, USA.
Vinayak MuralidharKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139, USA; Harvard-MIT Division of Health Sciences and Technology, Harvard Medical School, Boston, MA 02115, USA.
Michael P MurphyMRC Mitochondrial Biology Unit, Wellcome Trust-MRC Building, Cambridge, United Kingdom.
Peter L PedersenDepartment of Biological Chemistry and Department of Oncology, Johns Hopkins University, Baltimore, MD 21205, USA.
Brad PooreThe Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.
Lizzia RaffaghelloLaboratory of Oncology, Istituto Giannina Gaslini, Genoa, Italy.
Jeffrey C RathmellDuke Molecular Physiology Institute, Duke University Medical Center, Durham, NC 27701, USA; Department of Pharmacology & Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA.
Sharanya SivanandDepartment of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.
Matthew G Vander HeidenKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139, USA; Harvard-MIT Division of Health Sciences and Technology, Harvard Medical School, Boston, MA 02115, USA; Dana-Farber Cancer Institute, Boston, MA 02115, USA.
Kathryn E WellenDepartment of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.
Target Validation Team
Duke Medical Center · USJohns Hopkins University · USCancer Research Institute · USCornell University · USHarvard University · USChildren's Medical Center · USIstituto Giannina Gaslini · ITMemorial Sloan Kettering Cancer Center · USMRC Mitochondrial Biology Unit · GBRutgers, The State University of New Jersey · USUniversity of Aberdeen · GBUniversity of Cambridge · GBUniversity of Maryland, Baltimore · USUniversity of Michigan · USUniversity of Southern California · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI FRANCESCA M GANY · 1985 to 2026
$347.4M
Studies on the Mechanisms by which SIRT5 Regulates Aging and DiseaseR01AG045351 · NIA · DUKE UNIVERSITY · PI HIRSCHEY, MATTHEW D · 2014 to 2023
$4.4M
CANCER BIOLOGY TRAINING GRANTT32CA059365 · NCI · DUKE UNIVERSITY · PI WANG, XIAO-FAN · 1993 to 2014
$4.4M
Understanding metabolic flux and the control of mammalian cell growthR00CA168997 · NCI · DUKE UNIVERSITY · PI LOCASALE, JASON W. · 2013 to 2015
$695k
Medical Research Council MC_U105663142Medical Research Council MC_UP_1101/3Medical Research Council MC_UU_12022/6NCI NIH HHS P30 CA008748NCI NIH HHS R00 CA168997NCI NIH HHS T32 CA059365NIA NIH HHS R01 AG045351
6 · The paper itself

Abstract

Cancer is a disease characterized by unrestrained cellular proliferation. In order to sustain growth, cancer cells undergo a complex metabolic rearrangement characterized by changes in metabolic pathways involved in energy production and biosynthetic processes. The relevance of the metabolic transformation of cancer cells has been recently included in the updated version of the review "Hallmarks of Cancer", where dysregulation of cellular metabolism was included as an emerging hallmark. While several lines of evidence suggest that metabolic rewiring is orchestrated by the concerted action of oncogenes and tumor suppressor genes, in some circumstances altered metabolism can play a primary role in oncogenesis. Recently, mutations of cytosolic and mitochondrial enzymes involved in key metabolic pathways have been associated with hereditary and sporadic forms of cancer. Together, these results demonstrate that aberrant metabolism, once seen just as an epiphenomenon of oncogenic reprogramming, plays a key role in oncogenesis with the power to control both genetic and epigenetic events in cells. In this review, we discuss the relationship between metabolism and cancer, as part of a larger effort to identify a broad-spectrum of therapeutic approaches. We focus on major alterations in nutrient metabolism and the emerging link between metabolism and epigenetics. Finally, we discuss potential strategies to manipulate metabolism in cancer and tradeoffs that should be considered. More research on the suite of metabolic alterations in cancer holds the potential to discover novel approaches to treat it.

Indexed as

CarcinogenesisCell ProliferationCell Transformation, NeoplasticEnergy MetabolismEpigenesis, GeneticHumansMetabolic Networks and PathwaysMitochondriaNeoplasmsCancer metabolismCancer therapyHost metabolismMitochondriaWarburg

Identifiers

PMID26454069
PMCPMC4656121
OpenAlexW1940930637

What Socratic 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 Socratic graph.