Dataset Information

Transcription profiling of mouse thyroid from Slc26a4 animals vs. heterzygous controls.

ABSTRACT: Determination of differential expression of genes in the thyroid of pendrin (Slc26a4) heterozygous and knockout mice at a time point corresponding to maximal thyroid gland activity, postnatal day 15 (P15). Experiment Overall Design: A total of Six samples of thyroid RNA obtained from P15 mice were analyzed. Triplicates from pendrin (Slc26a4) heterozygous and knockout mice were run and analyzed.

INSTRUMENT(S): 418 [Affymetrix]

SUBMITTER: Philine Wangemann

PROVIDER: E-GEOD-10589 | ArrayExpress | 2009-03-01

SECONDARY ACCESSION(S): GSE10589PRJNA107741

REPOSITORIES: GEO, ArrayExpress

ACCESS DATA

Dataset's files

Source:

Items per page:

1 - 5 of 6

Similar Datasets

Project description:Thyroid cancer is the most common form of endocrine cancer, and it is a disease whose incidence is rapidly rising. Well-differentiated epithelial thyroid cancer can be divided into papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC). Although FTC is less common, patients with this condition have more frequent metastasis and a poorer prognosis than those with PTC.The objective of this study was to characterize the molecular mechanisms contributing to the development and metastasis of FTC.We developed and characterized mice carrying thyroid-specific double knockout of the Prkar1a and Pten tumor suppressor genes and compared signaling alterations observed in the mouse FTC to the corresponding human tumors.The study was conducted at an academic research laboratory. Human samples were obtained from academic hospitals.Deidentified, formalin-fixed, paraffin-embedded (FFPE) samples were analyzed from 10 control thyroids, 30 PTC cases, five follicular variant PTC cases, and 10 FTC cases.There were no interventions.Mouse and patient samples were analyzed for expression of activated cAMP response element binding protein, AKT, ERK, and mammalian target of rapamycin (mTOR). Murine FTCs were analyzed for differential gene expression to identify genes associated with metastatic progression.Double Prkar1a-Pten thyroid knockout mice develop FTC and recapitulate the histology and metastatic phenotype of the human disease. Analysis of signaling pathways in FTC showed that both human and mouse tumors exhibited strong activation of protein kinase A and mTOR. The development of metastatic disease was associated with the overexpression of genes required for cell movement.These data imply that the protein kinase A and mTOR signaling cascades are important for the development of follicular thyroid carcinogenesis and may suggest new targets for therapeutic intervention. Mouse models paralleling the development of the stages of human FTC should provide important new tools for understanding the mechanisms of FTC development and progression and for evaluating new therapeutics.

			Action	DRS
	E-GEOD-10589.README.txt	Txt
	E-GEOD-10589.eSet.r	Other
	E-GEOD-10589.idf.txt	Idf
	E-GEOD-10589.processed.1.zip	Processed
	E-GEOD-10589.raw.1.zip	Raw

Dataset Information

Transcription profiling of mouse thyroid from Slc26a4 animals vs. heterzygous controls.

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure