Targeting metabolic transformation for cancer therapy.

Tennant DA; Durán RV; Gottlieb E

doi:10.1038/nrc2817

Targeting metabolic transformation for cancer therapy.

Tennant DA ¹,

Durán RV ,

Gottlieb E

Affiliations

1. Cancer Research UK, The Beatson Institute for Cancer Research, Glasgow, UK.
Authors
Tennant DA¹
(1 author)

ORCIDs linked to this article

Nature reviews. Cancer, 19 Mar 2010, 10(4):267-277
https://doi.org/10.1038/nrc2817 PMID: 20300106

Review

Abstract

Cancer therapy has long relied on the rapid proliferation of tumour cells for effective treatment. However, the lack of specificity in this approach often leads to undesirable side effects. Many reports have described various 'metabolic transformation' events that enable cancer cells to survive, suggesting that metabolic pathways might be good targets. There are currently several drugs under development or in clinical trials that are based on specifically targeting the altered metabolic pathways of tumours. This Review highlights pathways against which there are already drugs in different stages of development and also discusses additional druggable targets.

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Read article at publisher's site: https://doi.org/10.1038/nrc2817

References

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Search life-sciences literature (45,103,589 articles, preprints and more)

Targeting metabolic transformation for cancer therapy.

Affiliations

Authors

ORCIDs linked to this article

Abstract

Full text links

References

The biology of cancer: metabolic reprogramming fuels cell growth and proliferation.

Metabolic transformation in cancer.

Glucose metabolism and programmed cell death: an evolutionary and mechanistic perspective.

Hypoxia response elements in the aldolase A, enolase 1, and lactate dehydrogenase A gene promoters contain essential binding sites for hypoxia-inducible factor 1.

Fatty acid synthase expression in endometrial carcinoma: correlation with cell proliferation and hormone receptors.

Elevated expression of fatty acid synthase and fatty acid synthetic activity in colorectal neoplasia.

An integrated genomic analysis of human glioblastoma multiforme.

IDH1 and IDH2 mutations in gliomas.

Mutations in SDHD, a mitochondrial complex II gene, in hereditary paraganglioma.

Germline mutations in FH predispose to dominantly inherited uterine fibroids, skin leiomyomata and papillary renal cell cancer.

Citations & impact

Impact metrics

Citations of article over time

Alternative metrics

Smart citations by scite.ai
Explore citation contexts and check if this article has been supported or disputed.
https://scite.ai/reports/10.1038/nrc2817

Article citations

Withaferin A decreases glycolytic reprogramming in breast cancer.

Natural Products and Altered Metabolism in Cancer: Therapeutic Targets and Mechanisms of Action.

Glycolysis and chemoresistance in acute myeloid leukemia.

Targeting cellular adaptive responses to glutaminolysis perturbation for cancer therapy.

Controlling glycolysis to generate characteristic volatile organic compounds of lung cancer cells.

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Targeting metabolic transformation for cancer therapy.

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