Wnt/β-catenin pathway deregulation in childhood adrenocortical tumors

Leal, Letícia F.; Mermejo, Lívia M.; Ramalho, Leandra Z.; Martinelli, Carlos E.; Yunes, José A.; Seidinger, Ana Luiza; Mastellaro, Maria José; Cardinalli, Izilda A.; Brandalise, Silvia R.; Moreira, Ayrton C.; Tone, Luiz G.; Scrideli, Carlos A.; Castro, Margaret; Antonini, Sonir R.

doi:10.1210/jc.2011-0363

Cited by 55Adrenal and Paraganglionic TumorsWnt/β-catenin signaling in development and cancerChromatin Remodeling and Cancer

Wnt/β-catenin pathway deregulation in childhood adrenocortical tumors

Leal, Letícia F., Mermejo, Lívia M., Ramalho, Leandra Z., Martinelli, Carlos E., Yunes, José A., Seidinger, Ana Luiza, Mastellaro, Maria José, Cardinalli, Izilda A. +6 more·2011·The Journal of Clinical Endocrinology & Metabolism

DOI 10.1210/jc.2011-0363

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Abstract

CONTEXT: CTNNB1/β-catenin mutations and activation of Wnt/β-catenin pathway are frequent in adult adrenocortical tumors (ACT), but data on childhood ACT are lacking. OBJECTIVE: The aim of the study was to investigate the presence of Wnt/β-catenin pathway abnormalities in childhood ACT. PATIENTS AND METHODS: Clinicopathological findings and outcome of 62 childhood ACT patients were analyzed regarding CTNNB1 mutations and the expression of Wnt-related genes (CTNNB1; WNT4, a Wnt ligand; SFRP1, DKK3, and AXIN1, Wnt inhibitors; TCF7, a transcription factor; and MYC and WISP2, target genes) by quantitative PCR and immunohistochemistry. RESULTS: CTNNB1-activating mutations were found in only four of 62 ACT (6%), all of them harboring TP53 mutation. There was association between the presence of CTNNB1 mutations and death (P = 0.02). Diffuse β-catenin accumulation was found in 71% of ACT, even in ACT without CTNNB1 mutations. Compared to normal adrenals, ACT presented increased expression of CTNNB1 (P = 0.008) and underexpression of Wnt inhibitor genes: DKK3 (P < 0.0001), SFRP1 (P = 0.05), and AXIN1 (P = 0.04). With regard to Wnt/β-catenin target genes, ACT presented increased expression of WISP2 but lower expression of MYC. Higher overall survival was associated with underexpression of SFRP1 (P = 0.01), WNT4 (P = 0.004), and TCF7 (P < 0.01). CONCLUSIONS: CTNNB1 mutations are not common in childhood ACT but appear to associate with poor prognosis. Nevertheless, most ACT exhibit increased expression of β-catenin and WISP2 and reduced expression of Wnt inhibitor genes (DKK3, SFRP1, and AXIN1). Thus, in addition to CTNNB1 mutations, other genetic events affecting the Wnt/β-catenin pathway may be involved in childhood adrenocortical tumorigenesis.

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High-grade ACCs are enriched for mutations of TP53 and/or CTNNB1, and these mutations tend to be mutually exclusive.
“High-grade ACCs are enriched for mutations of TP53 (14, 140–142) and/or CTNNB1 (143–149), and these mutations tend to be mutually exclusive (reviewed in Ref. 150).”
From Adrenocortical carcinoma (2014) · cites this paper as [145]

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Authors: Leal, L. F., Mermejo, L. M., Ramalho, L. Z., Martinelli, C. E., Yunes, J. A., Seidinger, A. L., Mastellaro, M. J., Cardinalli, I. A., Brandalise, S. R., Moreira, A. C., Tone, L. G., Scrideli, C. A., Castro, M., & Antonini, S. R.
Affiliations: Universidade de São Paulo (BR)
Centro Infantil Boldrini (BR)
ORCID: Leal, Letícia F.
Mermejo, Lívia M.
Martinelli, Carlos E.
Yunes, José A.
Mastellaro, Maria José
Cardinalli, Izilda A.
Moreira, Ayrton C.
Scrideli, Carlos A.
Castro, Margaret
Antonini, Sonir R.
Venue: The Journal of Clinical Endocrinology & Metabolism
Publisher: The Endocrine Society
Published: 2011-10
Volume: 96
Issue: 10
Pages: 3106-3114
ISSN: 0021-972X (ISSN-L)
1945-7197
DOI: 10.1210/jc.2011-0363
OpenAlex: W2052990651
Cited by: 55
References: 39
Citations by year: 2026: 3 · 2025: 1 · 2024: 4 · 2023: 1 · 2022: 5 · 2021: 2 · 2020: 2 · 2019: 7 · 2018: 2 · 2017: 3 · 2016: 8 · 2015: 6 · 2014: 6 · 2013: 3 · 2012: 1
FWCI: 3.60
Type: journal article
Language: en
Open access: closed
Locations: The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
PubMed (publishedVersion)
Funders: Universidade de São Paulo
Topics: Health Sciences › Medicine › Surgery › Adrenal and Paraganglionic Tumors
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
Keywords: Wnt/β-catenin signaling, CTNNB1 mutation, beta-catenin accumulation, Wnt inhibitors, DKK3, SFRP1, AXIN1, WISP2, c-Myc, TCF1, Wnt4, TP53 mutation, prognosis, adrenocortical tumorigenesis
MeSH terms: Adolescent, Adrenal Cortex Neoplasms, Child, Child, Preschool, DNA, Female, Humans, Immunohistochemistry, Infant, Male, Mutation, Repressor Proteins, RNA, Messenger, Transcription Factors, Cohort Studies, Signal Transduction, Survival Analysis, Tumor Suppressor Protein p53, Proto-Oncogene Proteins c-myc, Treatment Outcome, Reverse Transcriptase Polymerase Chain Reaction, Intercellular Signaling Peptides and Proteins, Wnt Proteins, beta Catenin, T Cell Transcription Factor 1, CCN Intercellular Signaling Proteins, Axin Protein, Wnt4 Protein

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Wnt/β-catenin pathway deregulation in childhood adrenocortical tumors

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