Evidence map›Paper›PMID 22237205›Full record

ReviewCell death & disease2012

Cancer metabolism: current perspectives and future directions.

C Muñoz-Pinedo, N El Mjiyad, J-E Ricci

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 199 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
199citing 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

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

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139 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

3 authors.

C Muñoz-PinedoCell Death Regulation Group, IDIBELL (Bellvitge Biomedical Research Institute), Gran Via de L'Hospitalet 199, L'Hospitalet, Barcelona 08908 Spain. cmunoz@idibell.cat
N El Mjiyad
J-E Ricci

Funding

Worldwide Cancer Research 08-0621
6 · The paper itself

Abstract

Cellular metabolism influences life and death decisions. An emerging theme in cancer biology is that metabolic regulation is intricately linked to cancer progression. In part, this is due to the fact that proliferation is tightly regulated by availability of nutrients. Mitogenic signals promote nutrient uptake and synthesis of DNA, RNA, proteins and lipids. Therefore, it seems straight-forward that oncogenes, that often promote proliferation, also promote metabolic changes. In this review we summarize our current understanding of how 'metabolic transformation' is linked to oncogenic transformation, and why inhibition of metabolism may prove a cancer's 'Achilles' heel'. On one hand, mutation of metabolic enzymes and metabolic stress sensors confers synthetic lethality with inhibitors of metabolism. On the other hand, hyperactivation of oncogenic pathways makes tumors more susceptible to metabolic inhibition. Conversely, an adequate nutrient supply and active metabolism regulates Bcl-2 family proteins and inhibits susceptibility to apoptosis. Here, we provide an overview of the metabolic pathways that represent anti-cancer targets and the cell death pathways engaged by metabolic inhibitors. Additionally, we will detail the similarities between metabolism of cancer cells and metabolism of proliferating cells.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBiomedical ResearchCell CommunicationCell ProliferationCell Transformation, NeoplasticGlucoseHumansMetabolic Networks and PathwaysMiceMitochondriaNeoplasmsOncogenesProto-Oncogene Proteins c-bcl-2Signal TransductionGlucoseProto-Oncogene Proteins c-bcl-2

Identifiers

PMID22237205
PMCPMC3270265

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.