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Cited by 271

The DOI matches its Crossref record; 66 of the 66 references it cites were found in a registry or an index.

Revisiting the TCA cycle: signaling to tumor formation

Open access
Raimundo, Nuno, Baysal, Bora E., Shadel, Gerald S.·2011·Trends in Molecular Medicine

Abstract

A role for mitochondria in tumor formation is suggested by mutations in enzymes of the TCA cycle: isocitrate dehydrogenase (IDH), succinate dehydrogenase (SDH) and fumarate hydratase (FH). Although they are all components of the TCA cycle, the resulting clinical presentations do not overlap. Activation of the hypoxia pathway can explain SDH phenotypes, but recent data suggest that FH and IDH mutations lead to tumor formation by repressing cellular differentiation. Here we discuss recent findings in the context of both mitochondrial and cytoplasmic components of the TCA cycle, and we propose that extra-metabolic roles of TCA cycle metabolites result in the reduced cellular differentiation. Furthermore, the activation of the pseudo-hypoxia pathway likely promotes the growth of these neoplasias into tumors.

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Metadata

Authors
Raimundo, N., Baysal, B. E., & Shadel, G. S.
Venue
Trends in Molecular Medicine
Publisher
Elsevier BV
Published
2011-11
Volume
17
Issue
11
Pages
641-649
ISSN
1471-4914 (ISSN-L)
OpenAlex
W1963894699
Cited by
271
References
66
FWCI
0.91
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Revisiting the TCA cycle: signaling to tumor formation. https://app.cochat.ai/papers/10.1016/j.molmed.2011.06.001
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Raimundo, N., Baysal, B. E., & Shadel, G. S. (2011). Revisiting the TCA cycle: signaling to tumor formation. Trends in Molecular Medicine. https://doi.org/10.1016/j.molmed.2011.06.001

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.