Evidence map›Paper›PMID 28561705›Full record

ReviewAmerican Society of Clinical Oncology educational book. American Society of Clinical Oncology. Annual Meeting2017

Metabolic Alterations in Cancer and Their Potential as Therapeutic Targets.

Jamie D Weyandt, Craig B Thompson, Amato J Giaccia, W Kimryn Rathmell

Abstract readReview
In one paragraph

Review in American Society of Clinical Oncology educational book. American Society of Clinical Oncology. Annual Meeting, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–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

26 citing papers in PubMed.

  1. Article
  2. Beyond DNA damage: 3D tumor models and the integrin mechanobiology of radioresistance.Journal of experimental & clinical cancer research : CR · 2026
    Review
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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.

Jamie D WeyandtFrom the Department of Medicine, Division of Hematology and Oncology, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN; Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY; Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA.
Craig B ThompsonFrom the Department of Medicine, Division of Hematology and Oncology, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN; Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY; Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA.
Amato J GiacciaFrom the Department of Medicine, Division of Hematology and Oncology, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN; Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY; Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA.
W Kimryn RathmellFrom the Department of Medicine, Division of Hematology and Oncology, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN; Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY; Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA.

Funding

TUMOR HYPOXIA--MOLECULAR STUDIES &CLINICAL EXPLOITATIONP01CA067166 · NCI · STANFORD UNIVERSITY · PI LE, QUYNH-THU XUAN · 1996 to 2017
$25.5M
BIOCHEMICAL &CHEMICAL TRAINING FOR CANCER RESEARCHT32CA009582 · NCI · VANDERBILT UNIVERSITY · PI David K Cortez · 1987 to 2026
$8.8M
NCI NIH HHS P01 CA067166NCI NIH HHS T32 CA009582
6 · The paper itself

Abstract

Otto Warburg's discovery in the 1920s that tumor cells took up more glucose and produced more lactate than normal cells provided the first clues that cancer cells reprogrammed their metabolism. For many years, however, it was unclear as to whether these metabolic alterations were a consequence of tumor growth or an adaptation that provided a survival advantage to these cells. In more recent years, interest in the metabolic differences in cancer cells has surged, as tumor proliferation and survival have been shown to be dependent upon these metabolic changes. In this educational review, we discuss some of the mechanisms that tumor cells use for reprogramming their metabolism to provide the energy and nutrients that they need for quick or sustained proliferation and discuss the potential for therapeutic targeting of these pathways to improve patient outcomes.

Indexed as

Cell ProliferationCellular ReprogrammingEnergy MetabolismHumansMetabolic Networks and PathwaysNeoplasms

Identifiers

PMID28561705
PMCPMC5954416

What OpenQuestion holds

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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.