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JAK Pseudokinase Domain Variants Highlight nRTK VUSs Identified with Next-Generation Sequencing in Solid Tumor Patients

JAK Pseudokinase Domain Variants Highlight nRTK VUSs Identified with Next-Generation Sequencing... Pathology & Oncology Research (2019) 25:817–818 https://doi.org/10.1007/s12253-018-0443-3 LETTER TO THE EDITOR JAK Pseudokinase Domain Variants Highlight nRTK VUSs Identified with Next-Generation Sequencing in Solid Tumor Patients 1,2 3 1 Matthew K. Stein & Lindsay K. Morris & Mike G. Martin Received: 21 November 2017 /Accepted: 30 May 2018 /Published online: 3 June 2018 Arányi Lajos Foundation 2018 Main Text undetermined significance (VUS) were included. All variants had >99% detection confidence based upon allele frequency Non-receptor tyrosine kinase (nRTK) pathways are aberrantly and amplicon coverage. In order to classify VUS, in silico activated in cancer, and mutations in nRTKs have potential analysis with PolyPhen-2 was utilized to predict pathogenicity therapeutic and prognostic importance. Consisting of 10 fam- [2]. Any VUS predicted-damaging with in silico analysis we ilies, the 32 known human nRTKs each include a TKD made denote VUSp. VUSs were then classified as occurring within of N and C-terminal lobes necessary for catalytic activity, as or outside of the TKD; PSKD lesions were also detailed for well as varying regulatory regions including Src homology 2 JAK1–3. (SH2) and 3 (SH3), and in the case of the Janus kinases a 346 patients (79 breast, 110 colon and 157 non-small cell http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Pathology & Oncology Research Springer Journals

JAK Pseudokinase Domain Variants Highlight nRTK VUSs Identified with Next-Generation Sequencing in Solid Tumor Patients

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Publisher
Springer Journals
Copyright
Copyright © 2018 by Arányi Lajos Foundation
Subject
Biomedicine; Cancer Research; Oncology; Pathology; Immunology; Biomedicine, general
ISSN
1219-4956
eISSN
1532-2807
DOI
10.1007/s12253-018-0443-3
Publisher site
See Article on Publisher Site

Abstract

Pathology & Oncology Research (2019) 25:817–818 https://doi.org/10.1007/s12253-018-0443-3 LETTER TO THE EDITOR JAK Pseudokinase Domain Variants Highlight nRTK VUSs Identified with Next-Generation Sequencing in Solid Tumor Patients 1,2 3 1 Matthew K. Stein & Lindsay K. Morris & Mike G. Martin Received: 21 November 2017 /Accepted: 30 May 2018 /Published online: 3 June 2018 Arányi Lajos Foundation 2018 Main Text undetermined significance (VUS) were included. All variants had >99% detection confidence based upon allele frequency Non-receptor tyrosine kinase (nRTK) pathways are aberrantly and amplicon coverage. In order to classify VUS, in silico activated in cancer, and mutations in nRTKs have potential analysis with PolyPhen-2 was utilized to predict pathogenicity therapeutic and prognostic importance. Consisting of 10 fam- [2]. Any VUS predicted-damaging with in silico analysis we ilies, the 32 known human nRTKs each include a TKD made denote VUSp. VUSs were then classified as occurring within of N and C-terminal lobes necessary for catalytic activity, as or outside of the TKD; PSKD lesions were also detailed for well as varying regulatory regions including Src homology 2 JAK1–3. (SH2) and 3 (SH3), and in the case of the Janus kinases a 346 patients (79 breast, 110 colon and 157 non-small cell

Journal

Pathology & Oncology Research – Springer Journals

Published: Jun 3, 2018

References

  • Structure of the pseudokinase-kinase domains from protein kinase TYK2 reveals a mechanism for Janus kinase (JAK) autoinhibition
    Lupardus, PJ; Ultsch, M; Wallweber, H
  • Sunyaev SR
    Adzhubei, IA; Schmidt, S; Peshkin, L; Ramensky, VE; Gerasimova, A; Bork, P; Kondrashov, AS
  • Structural modeling of JAK1 mutations in T-cell acute lymphoblastic leukemia reveals a second contact site between pseudokinase and kinase domains
    Canté-Barrett, K; Uitdehaag, JC; Meijerink, JP
  • Mutated JAK kinases and deregulated STAT activity are potential therapeutic targets in cutaneous T-cell lymphoma
    Perez, C; Gonzalez-Rincon, J; Onaindia, A