Biomarker identification of medullary thyroid carcinoma from gene expression profiles considering without-treatment and with-treatment studies-A bioinformatics approach.

Adv Protein Chem Struct Biol

Laboratory of Integrative Genomics, Department of Integrative Biology, School of BioSciences and Technology, Vellore Institute of Technology (VIT), Vellore, Tamil Nadu, India. Electronic address:

Published: July 2024

AI Article Synopsis

  • - Medullary thyroid carcinoma (MTC) is a type of cancer that arises from specific thyroid cells, and its genetic mutations significantly impact diagnosis and treatment outcomes.
  • - This research focuses on identifying key biomarker genes and microRNAs to improve the diagnosis and treatment of MTC by analyzing gene expression profiles from treated and untreated datasets.
  • - Significant findings include the upregulation of the RET gene in untreated cases and its downregulation following dinaciclib treatment, highlighting the need for further investigation into how RET's expression is controlled for better therapeutic strategies.

Article Abstract

Medullary thyroid carcinoma (MTC) is a neuroendocrine tumor derived from parafollicular thyroid gland cells. In both hereditary MTC and sporadic forms, genetic changes result in fundamental changes, and prognosis and mutational status are highly correlated. In this work, biomarker genes (DEGs and DEmiRNAs) for MTC will be computationally identified in order to help in their diagnosis and treatment. The gene expression profiles of two different types of studies, namely without-treatment (wo-trt) and with-treatment (w-trt), are considered for discovering biomarkers. The datasets were retrieved from the GEO database, and the DEGs and DEmiRNAs were analyzed using ExpressAnalyst and GEO2R. The functional analysis of DEGs and DEmiRNAs was performed, and most of the pathways enriched related to thyroid oncological pathways such as MAPK pathway,mTOR pathway, and PI3K-AKT Signaling pathway. Through this conclusion, the RET gene was upregulated wo-trt; the dinaciclib treatment RET gene was down-regulated computationally. To optimize the therapeutic targeting of RET, greater research into the mechanisms regulating RET transcription is necessary.

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Source
http://dx.doi.org/10.1016/bs.apcsb.2023.12.011DOI Listing

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