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Krystian Jazdzewski

Researcher at University of Warsaw

Publications -  37
Citations -  3718

Krystian Jazdzewski is an academic researcher from University of Warsaw. The author has contributed to research in topics: Thyroid cancer & Thyroid carcinoma. The author has an hindex of 22, co-authored 35 publications receiving 3476 citations. Previous affiliations of Krystian Jazdzewski include Ohio State University & Medical University of Warsaw.

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The role of microRNA genes in papillary thyroid carcinoma

TL;DR: It is concluded that up-regulation of several miRs and regulation of KIT are involved in PTC pathogenesis, and that sequence changes in genes targeted by miRNAs can contribute to their regulation.
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Common SNP in pre-miR-146a decreases mature miR expression and predisposes to papillary thyroid carcinoma

TL;DR: The data suggest that a common polymorphism in pre-miR-146a affects the miR expression, contributes to the genetic predisposition to PTC, and plays a role in the tumorigenesis through somatic mutation.
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Polymorphic mature microRNAs from passenger strand of pre-miR-146a contribute to thyroid cancer

TL;DR: It is proposed that contrary to previously held views transcripts from the passenger strand of miRs can profoundly affect the downstream effects of genes within the premiR sequence, which can cause epistasis through the production of additional mature miRs.
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In-Depth Characterization of the MicroRNA Transcriptome in Normal Thyroid and Papillary Thyroid Carcinoma

TL;DR: Almost all microRNAs exhibit isoforms of variable length and potentially distinct function in thyroid tumorigenesis, and numerous isomiRs had altered seed sequences, which led to a different set of target genes.
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Interleukin (IL)-23 receptor is a major susceptibility gene for Graves' ophthalmopathy: the IL-23/T-helper 17 axis extends to thyroid autoimmunity.

TL;DR: Variants in the IL-23R gene are strongly associated with Graves' disease (GD) and Graves' ophthalmopathy (GO), and these variants may predispose to GO by changing the expression and/or function of IL- 23R, thereby promoting a proinflammatory signaling cascade.