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DIFFERENTIAL GENE EXPRESSION OF MEDULLARY THYROID CARCINOMA REVEALS SPECIFIC MARKERS ASSOCIATED WITH GENETIC CONDITIONS.

ABSTRACT: Transcriptional analysis of 49 primary medullary thyroid carcinoma tumors. Comparisons MTCM918T vs MTC634 and MTCM918T vs MTCWT. 49 (52 hybridized tumors with 3 replicates) primary Medullary Thyroid Carcinoma (MTC) cases were hybridized onto a cDNA microarray in order to identify the unique markers for specific genetic classes of MTC.

ORGANISM(S): Homo sapiens

SUBMITTER: Mercedes Robledo

PROVIDER: E-GEOD-32662 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Differential gene expression of medullary thyroid carcinoma reveals specific markers associated with genetic conditions.

Maliszewska Agnieszka A Leandro-Garcia Luis J LJ Castelblanco Esmeralda E Macià Anna A de Cubas Aguirre A Goméz-López Gonzalo G Inglada-Pérez Lucía L Inglada-Pérez Lucía L Álvarez-Escolá Cristina C De la Vega Leticia L Letón Rocío R Gómez-Graña Álvaro Á Landa Iñigo I Cascón Alberto A Rodríguez-Antona Cristina C Borrego Salud S Zane Mariangela M Schiavi Francesca F Merante-Boschin Isabella I Pelizzo Maria R MR Pisano David G DG Opocher Giuseppe G Matias-Guiu Xavier X Encinas Mario M Robledo Mercedes M

The American journal of pathology 20121128 2

Medullary thyroid carcinoma accounts for 2% to 5% of thyroid malignancies, of which 75% are sporadic and the remaining 25% are hereditary and related to multiple endocrine neoplasia type 2 syndrome. Despite a genotype-phenotype correlation with specific germline RET mutations, knowledge of pathways specifically associated with each mutation and with non-RET-mutated sporadic MTC remains lacking. Gene expression patterns have provided a tool for identifying molecular events related to specific tum ...[more]

PMID: 23201134

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DIFFERENTIAL GENE EXPRESSION OF MEDULLARY THYROID CARCINOMA REVEALS SPECIFIC MARKERS ASSOCIATED WITH GENETIC CONDITIONS.

Project description:Transcriptional analysis of 49 primary medullary thyroid carcinoma tumors. Comparisons MTCM918T vs MTC634 and MTCM918T vs MTCWT.

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Integration of miRNA, mRNA and methylation profiling reveals genes aberrantly regulated associated to RETM918T mutation in Medullary Thyroid Carcinoma [miRNA component]

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Integration of miRNA, mRNA and methylation profiling reveals genes aberrantly regulated associated to RETM918T mutation in Medullary Thyroid Carcinoma [methylation component]

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Overexpression of microRNA-375 in medullary thyroid carcinoma cells hinders cell proliferation and improves the vandetanib efficacy effect in vitro

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Transcriptional Targeting Of Oncogene Addiction In Medullary Thyroid Cancer [RNA-Seq]

Project description:Metastatic medullary thyroid cancer (MTC) is a currently incurable disease. FDA approved therapies that target RET, a commonly mutated receptor tyrosine kinase in MTC, and other receptor tyrosine kinases, do not result in complete responses and acquired resistance is universal due to “gatekeeper” mutation in Ret or overactivation of alternative signaling pathways. Based on data from human MTCs and a number of murine models, the CDK/RB cell cycle pathway is a potential alternative target for MTC. The objective of this study was to determine if CDKs represent therapeutic targets for MTC and to define mechanisms of activity. We demonstrate that targeting the CDK/RB pathway with Palbociclib (CDK4/6 inhibitor) is not cytotoxic to MTC cells but that Dinaciclib (CDK1/2/5/9 inhibitor) remarkably reduced cell viability and proliferation at low doses in two MTC cell lines accompanied by loss of CDK9 and RET protein and mRNA levels. In human tumors, CDK9 protein was highly expressed and array CGH demonstrated copy number gain in 11/30 analyzed tumors. RNA sequencing demonstrated that RNA polymerase II-dependent transcription was markedly reduced by Dinaciclib, consistent with transcriptional mode of action. Subsequent studies using the CDK7 inhibitor, THZ1, demonstrated high potency vs. the MTC cell lines and marked loss of RET mRNA and protein. In silico analysis, and CHIP-Sequencing using H3K27Ac antibody confirmed that RET is associated with a super-enhancer in RET-mutated MTC cells. In summary, this study reveals a novel mechanism of RET transcription regulation that represents a potentially translatable finding for new therapeutic approaches for RET-mutated MTC.

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