The role of fibroblast growth factor receptor 4 overexpression and gene amplification as prognostic markers in pediatric and adult adrenocortical tumors
- Luciana Pinto Brito*,
- Tamaya Castro Ribeiro*,
- Madson Q Almeida1,
- Alexander Augusto de Lima Jorge2,
- Iberê Cauduro Soares3,
- Ana Claudia Latronico,
- Berenice Bilharinho Mendonca,
- Maria Candida Barisson Villares Fragoso1 and
- Antonio Marcondes Lerario1
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Unidade de Endocrinologia do Desenvolvimento, Laboratorio de Hormonios e Genetica Molecular LIM/42, Faculdade de Medicina da Universidade de Sao Paulo, Avenida Dr Enéas
de Carvalho Aguiar, No. 155 PAMB, 2° Andar, Bloco 6, Sao Paulo CEP 05403-900, Brazil
1Unidade de Suprarrenal, Disciplina de Endocrinologia
2Unidade de Endocrinologia Genética LIM/25, Disciplina de Endocrinologia and
3Divisão de Anatomia Patológica do Hospital das Clínicas LIM/14, Faculdade de Medicina da Universidade de Sao Paulo, Sao Paulo, Brazil
- (Correspondence should be addressed to A M Lerario; Email: amlerario{at}gmail.com)
Dear Editor
In the last decade, relevant progresses in the molecular basis of adrenocortical tumors (ACTs) were achieved and abnormalities involving growth pathway deregulation were frequently associated with malignancy. Remarkably, upregulation of insulin-like growth factor 2 (IGF2) and its receptor (IGF1R) has been demonstrated in a significant proportion of ACTs, and the presence of these abnormalities has both prognostic and therapeutic implications (Almeida et al. 2008). In fact, clinical trials involving pharmacological blockade of IGF1R are currently under process. Besides the IGF system, other growth signaling pathways have been suggested to be important for ACC progression and are possible therapeutic targets. Among these, fibroblast growth factor receptor 4 (FGFR4) overexpression has been observed in both adult and pediatric ACT by genome-wide expression studies in the same extent as the IGF system (de Fraipont et al. 2005, Laurell et al. 2009). However, these data have not been validated in an independent cohort and the molecular mechanisms responsible for FGFR4 …
