1 Ocak 2017 Dergi makalesi Açık Erişim

Hu, Xiaozhou; Baytak, Esra; Li, Jinnan; Akman, Burcu; Okay, Kaan; Hu, Genfu; Scuto, Anna; Zhang, Wenyan; Kucuk, Can

DataCite XML

<?xml version='1.0' encoding='utf-8'?>
<resource xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns="http://datacite.org/schema/kernel-4" xsi:schemaLocation="http://datacite.org/schema/kernel-4 http://schema.datacite.org/meta/kernel-4.1/metadata.xsd">
  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/43897</identifier>
  <creators>
    <creator>
      <creatorName>Hu, Xiaozhou</creatorName>
      <givenName>Xiaozhou</givenName>
      <familyName>Hu</familyName>
      <affiliation>Dokuz Eylul Univ, Izmir Int Biomed &amp; Genome Inst iBG Izmir, Izmir, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Baytak, Esra</creatorName>
      <givenName>Esra</givenName>
      <familyName>Baytak</familyName>
    </creator>
    <creator>
      <creatorName>Li, Jinnan</creatorName>
      <givenName>Jinnan</givenName>
      <familyName>Li</familyName>
      <affiliation>Sichuan Univ, West China Hosp, Dept Pathol, Chengdu, Guangxi, Peoples R China</affiliation>
    </creator>
    <creator>
      <creatorName>Akman, Burcu</creatorName>
      <givenName>Burcu</givenName>
      <familyName>Akman</familyName>
      <affiliation>Dokuz Eylul Univ, Izmir Int Biomed &amp; Genome Inst iBG Izmir, Izmir, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Okay, Kaan</creatorName>
      <givenName>Kaan</givenName>
      <familyName>Okay</familyName>
      <affiliation>Dokuz Eylul Univ, Izmir Int Biomed &amp; Genome Inst iBG Izmir, Izmir, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Hu, Genfu</creatorName>
      <givenName>Genfu</givenName>
      <familyName>Hu</familyName>
    </creator>
    <creator>
      <creatorName>Scuto, Anna</creatorName>
      <givenName>Anna</givenName>
      <familyName>Scuto</familyName>
      <affiliation>City Hope Med Ctr, Dept Pathol, Duarte, CA USA</affiliation>
    </creator>
    <creator>
      <creatorName>Zhang, Wenyan</creatorName>
      <givenName>Wenyan</givenName>
      <familyName>Zhang</familyName>
      <affiliation>Sichuan Univ, West China Hosp, Dept Pathol, Chengdu, Guangxi, Peoples R China</affiliation>
    </creator>
    <creator>
      <creatorName>Kucuk, Can</creatorName>
      <givenName>Can</givenName>
      <familyName>Kucuk</familyName>
    </creator>
  </creators>
  <titles>
    <title>The Relationship Of Rel Proto-Oncogene To Pathobiology And Chemoresistance In Follicular And Transformed Follicular Lymphoma</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2017</publicationYear>
  <dates>
    <date dateType="Issued">2017-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/43897</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1016/j.leukres.2017.01.001</relatedIdentifier>
  </relatedIdentifiers>
  <rightsList>
    <rights rightsURI="http://www.opendefinition.org/licenses/cc-by">Creative Commons Attribution</rights>
    <rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights>
  </rightsList>
  <descriptions>
    <description descriptionType="Abstract">Follicular lymphoma (FL) is a common type of indolent lymphoma that occasionally transforms to more aggressive B-cell lymphomas. These transformed follicular lymphomas (tFL) are often associated with chemoresistance whose mechanisms are currently unknown. REL, a proto-oncogene located on frequently amplified 2p16.1-p15 locus, promotes tumorigenesis in many cancer types through deregulation of the NF-KB pathway; however, its role in FL pathobiology or chemoresistance has not been addressed. Here, we evaluated REL gene copy number by q-PCR on FFPE FL tumor samples, and observed REL amplification in 30.4% of FL cases that was associated with weak elevation of transcript levels. PCR-Sanger analysis did not show any somatic mutation in FL tumors. In support of a marginal oncogenic role, a REL-transduced FL cell line was positively selected under limiting serum conditions. Interestingly, reanalysis of previously reported gene expression profiles revealed significant enrichment of DNA damage-induced repair and cell cycle arrest pathways in tFL tumors with high REL expression compared to those with low REL expression consistent with the critical role of c-REL in genotoxicity-induced NF-KB signaling, which was reported to lead to drug resistance. In addition to DNA damage repair genes such as ATM and BRCA1, anti-apoptotic BCL2 was significantly elevated in REL-high FL and tFL tumors. Altogether these data suggest that other genes located in amplified 2p16.1-p15 locus may have more oncogenic role in FL etiology; however, high REL expression may be useful as a predictive biomarker of response to immunochemotherapy, and inhibition of c-REL may potentially sensitize resistant FL or tFL cells to chemotherapy. (C) 2017 Elsevier Ltd. All rights reserved.</description>
  </descriptions>
</resource>