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Related Concept Videos

Non-LTR Retrotransposons03:18

Non-LTR Retrotransposons

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As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
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Isolation and Quantification of Epstein-Barr Virus from the P3HR1 Cell Line
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SSTR2 expression in EBV-positive and EBV-negative lymphomas.

Nivaz Brar1, Juan Carlos Barrios-Menéndez2, Gregory W Charville1

  • 1Department of Pathology, Stanford University, 300 Pasteur Drive, Lane 235, Stanford, CA, 94305-5324, USA.

Journal of Hematopathology
|April 10, 2026
PubMed
Summary
This summary is machine-generated.

Epstein-Barr virus (EBV) is necessary for Somatostatin receptor 2 (SSTR2) upregulation in classic Hodgkin lymphoma, but not other EBV-associated lymphomas. SSTR2 is also linked to higher-grade B-cell lymphomas in EBV-negative cases.

Keywords:
EBVHodgkinLymphomaSSTR2

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Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • Somatostatin receptor 2 (SSTR2) protein is often overexpressed in tumors.
  • SSTR2 can be targeted for diagnosis and therapy using specific molecules.

Purpose of the Study:

  • To examine SSTR2 expression in a large cohort of hematopoietic proliferations.
  • To investigate the link between Epstein-Barr virus (EBV) and SSTR2 in EBV-associated lymphomas to understand SSTR2 upregulation mechanisms.

Main Methods:

  • Retrospective analysis of 407 lymphoma cases from Guatemala.
  • Immunohistochemistry used to assess SSTR2 protein expression.
  • In situ hybridization used to detect EBV-associated small RNAs.

Main Results:

  • SSTR2 was expressed in 43% of EBV-positive classic Hodgkin lymphomas (cHL) but none of the EBV-negative cHL cases.
  • Most other EBV-associated lymphomas were negative for SSTR2.
  • In EBV-negative non-Hodgkin lymphomas, SSTR2 was found in 33% of DLBCL/HGBL with specific rearrangements and 17% of DLBCL and follicular lymphomas.

Conclusions:

  • EBV infection is a prerequisite for SSTR2 upregulation in classic Hodgkin lymphoma (cHL).
  • EBV is not sufficient for SSTR2 upregulation in cHL and does not drive it in other EBV-associated lymphomas.
  • SSTR2 expression correlates with higher-grade germinal center-derived B-cell lymphomas in EBV-negative cases.