Evidence map›Paper›PMID 41963561›Full record

ArticleJournal of hematopathology2026

SSTR2 expression in EBV-positive and EBV-negative lymphomas.

Nivaz Brar, Juan Carlos Barrios-Menéndez, Gregory W Charville, Edward L Briercheck, Yasodha Natkunam, Fabiola Valvert, Oscar Silva

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Article in Journal of hematopathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

7 authors.

Nivaz BrarDepartment of Pathology, Stanford University, 300 Pasteur Drive, Lane 235, Stanford, CA, 94305-5324, USA.
Juan Carlos Barrios-MenéndezLaboratorio de Investigacíon Biológica en Cáncer, Liga Nacional Contra El Cáncer, El Instituto de Cancerologia y Hospital Dr. Bernardo del Valle, Guatemala City, Guatemala.
Gregory W CharvilleDepartment of Pathology, Stanford University, 300 Pasteur Drive, Lane 235, Stanford, CA, 94305-5324, USA.
Edward L BriercheckDepartment of Medical Oncology & Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Yasodha NatkunamDepartment of Pathology, Stanford University, 300 Pasteur Drive, Lane 235, Stanford, CA, 94305-5324, USA.
Fabiola ValvertLaboratorio de Investigacíon Biológica en Cáncer, Liga Nacional Contra El Cáncer, El Instituto de Cancerologia y Hospital Dr. Bernardo del Valle, Guatemala City, Guatemala.
Oscar SilvaDepartment of Pathology, Stanford University, 300 Pasteur Drive, Lane 235, Stanford, CA, 94305-5324, USA. osilva@stanford.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSomatostatin receptor 2 (SSTR2) protein expression is aberrantly upregulated in various tumors and can be visualized using scintigraphy or radiological techniques and therapeutically targeted using octreotide-based molecules. PURPOSE: In this study, we assessed SSTR2 expression in the largest cohort of hematopoietic proliferations examined to date and interrogated the relationship between EBV and SSTR2 in EBV-associated lymphomas as a possible mechanism for SSTR2 upregulation.

methodsWe retrospectively identified 407 cases of lymphoma from Guatemala, a country with a high prevalence of EBV-associated lymphomas. SSTR2 protein expression was assessed by immunohistochemistry, while EBV was assessed by in situ hybridization for EBV-associated small RNAs.

resultsWe found SSTR2 expression in 43% (20/47) of EBV-positive classic Hodgkin lymphomas (cHL) and 0% (0/12) of EBV-negative cHL cases. All but one of the other EBV-associated lymphomas (n = 53) were negative for SSTR2. Within the EBV-negative non-Hodgkin lymphomas assessed, 33% (1/3) of diffuse large B-cell lymphoma (DLBCL)/high-grade B-cell lymphoma (HGBL) with MYC and BCL2 rearrangement, 17% (25/149) of DLBCL not otherwise specified, and 17% (5/29) of follicular lymphomas showed SSTR2 expression. All other lymphomas showed no significant SSTR2 expression.

conclusionsOur study demonstrates that EBV infection is required, but not sufficient, to upregulate SSTR2 in classic Hodgkin lymphoma, but not in other EBV-associated lymphomas. We also provide data to suggest that SSTR2 is associated with "higher-grade" germinal center-derived B-cell lymphomas in EBV-negative non-Hodgkin lymphomas.

Indexed as

Epstein-Barr Virus InfectionsHerpesvirus 4, HumanLymphomaReceptors, SomatostatinAdultAgedFemaleGene Expression Regulation, NeoplasticHodgkin DiseaseHumansImmunohistochemistryLymphoma, Large B-Cell, DiffuseMaleMiddle AgedRetrospective StudiesReceptors, Somatostatinsomatostatin receptor 2SSTR2 protein, humanEBVHodgkinLymphomaSSTR2

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.