A Novel TP53 Mutation Associated with TWIST1 and SIP1 Expression in an Aggressive Adrenocortical Carcinoma.
Daniel BulzicoDavi Coe TorresGerson Moura FerreiraBruno Ricardo Barreto PiresPaulo Antônio Silvestre de FariaRocio HassanEliana AbdelhayMario VaismanLeonardo Vieira NetoPublished in: Endocrine pathology (2018)
Adrenocortical carcinomas (ACC) are very rare tumors related to TP53 mutations mostly in childhood onset cases. Epithelial-mesenchymal transition (EMT) transcription factors TWIST1 and Smad interacting protein 1 (SIP1) are related to poorer outcomes in other malignancies, but their role in ACC is unknown. We describe a case of an advanced metastatic ACC (Weiss-score of 9) in a patient at age 76. After primary tumor resection, mitotane therapy was started as palliation to low-volume liver metastasis. After a 2-year period of stable disease, the patient died due to brain metastasis. Somatic gene sequencing revealed a novel TP53 mutation in DNA extracted from paraffin-embedded tissue, a deletion of 8bp in exon 8 (c.811_818del8; GAGGTGCG/-) in homo or hemizygosis causing a subsequent frameshift and premature stop codon at position 302. Immunohistochemistry of P53 and p-Ser-15 P53 showed absent tumoral staining. In addition, immunohistochemical analysis showed an increased expression of the mesenchymal markers vimentin and fibronectin. At last, EMT transcription factors TWIST1 and SIP1 were also overexpressed in tumoral cells. This case report describes an aggressive ACC with not only a novel somatic mutation, but also a novel International Agency for Research on Cancer database 8 base-pair deletion in TP53 exon 8. In addition, the expression of EMT inducers TWIST1 and SIP1 have been reported for the first time in an ACC case. Further investigation is needed to clarify the biologic significance of this new TP53 mutation and its role in the EMT process.
Keyphrases
- epithelial mesenchymal transition
- case report
- transforming growth factor
- poor prognosis
- signaling pathway
- transcription factor
- binding protein
- induced apoptosis
- copy number
- squamous cell carcinoma
- rheumatoid arthritis
- bone marrow
- single cell
- stem cells
- type diabetes
- genome wide identification
- mesenchymal stem cells
- small molecule
- single molecule
- young adults
- genome wide
- dna methylation
- cell cycle arrest
- childhood cancer
- pi k akt
- smoking cessation
- endoplasmic reticulum stress
- glycemic control