<clinical_study>
  <!-- This xml conforms to an XML Schema at:
    https://clinicaltrials.gov/ct2/html/images/info/public.xsd -->
  <required_header>
    <download_date>ClinicalTrials.gov processed this data on September 20, 2023</download_date>
    <link_text>Link to the current ClinicalTrials.gov record.</link_text>
    <url>https://clinicaltrials.gov/ct2/show/NCT01694342</url>
  </required_header>
  <id_info>
    <org_study_id>ramona 1.0</org_study_id>
    <nct_id>NCT01694342</nct_id>
  </id_info>
  <brief_title>Telomere Parameters in Patients With Nonalcoholic Fatty Liver</brief_title>
  <acronym>telomereFL</acronym>
  <official_title>Telomere Parameters Like Telomere Length, Telomerase Expression, Telomere Capture and Aneuploidy in Patients With Nonalcoholic Fatty Liver</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>Meir Medical Center</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>Meir Medical Center</source>
  <oversight_info>
    <has_dmc>No</has_dmc>
  </oversight_info>
  <brief_summary>
    <textblock>
      Telomerase, through its regulatory function on telomere length may play an important role in&#xD;
      immune function, cellular replicative life span, and carcinogenesis. Non-alcoholic fatty&#xD;
      liver disease (NAFLD) is considered a benign condition, but in some cases, it may progress to&#xD;
      cirrhosis and hepatocellular carcinoma. The risk factors for that evolution are not fully&#xD;
      understood.&#xD;
&#xD;
      Our group showed in a previous study, that hTERT mRNA expression is lower in peripheral&#xD;
      lymphocytes of patients with fatty liver, compared to healthy controls. This finding could&#xD;
      explain the telomere shortening found previously in these patients by our group [20] and&#xD;
      others [21]. Furthermore, we found higher rates of TC in these patients, probably due to an&#xD;
      attempt to counteract the shortening of the telomeres and to stabilize them. This is through&#xD;
      a different mechanism that is not telomerase-mediated.&#xD;
&#xD;
      Telomere capture is considered an alternative way to maintain telomere length and chromosomal&#xD;
      stability [3]. It is a more common mechanism for chromosome stabilization and repair, in&#xD;
      contrast to the telomerase-mediated process of chromosome healing and elongation This study&#xD;
      aimed to evaluate mechanisms of telomere homeostasis like telomere shortening, telomerase&#xD;
      activity, telomere capture and aneuploidy in patients with NAFLD in order to explain previous&#xD;
      findings of telomere shortening in these patients.&#xD;
    </textblock>
  </brief_summary>
  <overall_status>Unknown status</overall_status>
  <last_known_status>Not yet recruiting</last_known_status>
  <start_date>September 2012</start_date>
  <study_type>Observational</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <observational_model>Cohort</observational_model>
    <time_perspective>Prospective</time_perspective>
  </study_design_info>
  <enrollment type="Anticipated">30</enrollment>
  <condition>FATTY LIVER</condition>
  <condition>NO MALIGNANCY</condition>
  <condition>NO DECOMPENSATED ILLNESS</condition>
  <eligibility>
    <study_pop>
      <textblock>
        Individuals - over 18 years old that were diagnosed with nonalcoholic fatty liver and are&#xD;
        on follow-up in our liver unit&#xD;
      </textblock>
    </study_pop>
    <sampling_method>Probability Sample</sampling_method>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          -  age over 18&#xD;
&#xD;
          -  diagnosis of fatty liver&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          -  no malignancy&#xD;
&#xD;
          -  no eligible to sign the consent paper&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>18 Years</minimum_age>
    <maximum_age>75 Years</maximum_age>
    <healthy_volunteers>Accepts Healthy Volunteers</healthy_volunteers>
  </eligibility>
  <overall_contact>
    <last_name>Yona Kitay-Cohen, MD</last_name>
    <phone>+97297471560</phone>
    <email>yonaki@clalit.org.il</email>
  </overall_contact>
  <location>
    <facility>
      <name>Meir Hospital</name>
      <address>
        <city>Kefar Saba</city>
        <country>Israel</country>
      </address>
    </facility>
    <contact>
      <last_name>Yona Kitay-Cohen, MD</last_name>
      <phone>+97297471560</phone>
      <email>yonaki@clalit.org.il</email>
    </contact>
    <investigator>
      <last_name>Yona Kitay-Cohen, MD</last_name>
      <role>Principal Investigator</role>
    </investigator>
  </location>
  <location_countries>
    <country>Israel</country>
  </location_countries>
  <verification_date>July 2012</verification_date>
  <study_first_submitted>September 23, 2012</study_first_submitted>
  <study_first_submitted_qc>September 26, 2012</study_first_submitted_qc>
  <study_first_posted type="Estimate">September 27, 2012</study_first_posted>
  <last_update_submitted>September 26, 2012</last_update_submitted>
  <last_update_submitted_qc>September 26, 2012</last_update_submitted_qc>
  <last_update_posted type="Estimate">September 27, 2012</last_update_posted>
  <responsible_party>
    <responsible_party_type>Sponsor</responsible_party_type>
  </responsible_party>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Fatty Liver</mesh_term>
    <mesh_term>Non-alcoholic Fatty Liver Disease</mesh_term>
  </condition_browse>
  <!-- Results have not yet been posted for this study                                          -->
</clinical_study>


download date: ClinicalTrials.gov processed this data on September 20, 2023
link text: Link to the current ClinicalTrials.gov record.
url: https://clinicaltrials.gov/ct2/show/NCT01694342
org study id: ramona 1.0
nct id: NCT01694342
lead sponsor: 
has dmc: No
Telomerase, through its regulatory function on telomere length may play an important role in
      immune function, cellular replicative life span, and carcinogenesis. Non-alcoholic fatty
      liver disease (NAFLD) is considered a benign condition, but in some cases, it may progress to
      cirrhosis and hepatocellular carcinoma. The risk factors for that evolution are not fully
      understood.

      Our group showed in a previous study, that hTERT mRNA expression is lower in peripheral
      lymphocytes of patients with fatty liver, compared to healthy controls. This finding could
      explain the telomere shortening found previously in these patients by our group [20] and
      others [21]. Furthermore, we found higher rates of TC in these patients, probably due to an
      attempt to counteract the shortening of the telomeres and to stabilize them. This is through
      a different mechanism that is not telomerase-mediated.

      Telomere capture is considered an alternative way to maintain telomere length and chromosomal
      stability [3]. It is a more common mechanism for chromosome stabilization and repair, in
      contrast to the telomerase-mediated process of chromosome healing and elongation This study
      aimed to evaluate mechanisms of telomere homeostasis like telomere shortening, telomerase
      activity, telomere capture and aneuploidy in patients with NAFLD in order to explain previous
      findings of telomere shortening in these patients.
observational model: Cohort
time perspective: Prospective
study pop: 
sampling method: Probability Sample
criteria: 
gender: All
minimum age: 18 Years
maximum age: 75 Years
healthy volunteers: Accepts Healthy Volunteers
last name: Yona Kitay-Cohen, MD
phone: +97297471560
email: yonaki@clalit.org.il
facility: 
contact: 
investigator: 
country: Israel
responsible party type: Sponsor
mesh term: Fatty Liver
mesh term: Non-alcoholic Fatty Liver Disease