2026-05-17T01:16:03Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/260742025-12-18T12:56:23Zcom_20.500.12105_2273com_20.500.12105_2202col_20.500.12105_19571
Repisalud
author
Cascon Soriano, Alberto
author
Robledo Batanero, Mercedes
funder
Instituto de Salud Carlos III
funder
Fundación Mutua Madrileña
2025-01-20T15:49:19Z
2025-01-20T15:49:19Z
2012-07-01
Cancer Res . 2012 Jul 1;72(13):3119-24.
Cancer Research
22706201
https://hdl.handle.net/20.500.12105/26074
The overexpression of MYC, which occurs in many tumors, dramatically disrupts the equilibrium between activation and repression of the oncogenic MYC/MYC-associated protein X (MAX)/MAX dimerization protein 1 (MXD1) network, favoring MYC-MAX complexes and thereby impairing differentiation and promoting cell growth. Although for some time it has appeared that MAX is necessary for both the activation and repression of the axis, recent evidence shows that MYC retains considerable biologic function in the absence of MAX. The presence of germline MAX mutations in patients with hereditary pheochromocytoma supports the predominant role of MAX as a negative regulator of the network and suggests that MYC deregulation plays a role in hereditary cancer predisposition. This finding also confirms the importance of impairment of the MYC/MAX/MXD1 axis in the development of aggressive neural tumors, because MYCN overexpression is an established genetic hallmark of malign neuroblastoma, and it is likely that MXI1 plays a relevant role in the development of medulloblastoma and glioblastoma. Finally, the likely malignant behavior of tumors with mutations in MAX points to MYC as a candidate therapeutic target in the treatment of metastatic pheochromocytoma.
eng
C-MYC
NEUROBLASTOMA
CELLS
GENE
TRANSCRIPTION
PHEOCHROMOCYTOMA
INACTIVATION
PROTEINS
GROWTH
MAX and MYC: a heritable breakup.
research article
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URL
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MAXANDMYC-2012.pdf
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