blood-cancer

EBV infection is required—but not sufficient—to trigger a specific therapeutic receptor marker in Hodgkin lymphoma.

Study of 407 lymphoma cases from Guatemala found SSTR2 expression in 43% of EBV-positive classical Hodgkin lymphoma vs. 0% of EBV-negative cHL. Other EBV-associated lymphomas were largely SSTR2-negative. In EBV-negative NHL, SSTR2 associated with higher-grade B-cell lymphomas (17% of DLBCL, 17%…

Dan Manning

Dan Manning

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EBV infection is required—but not sufficient—to trigger a specific therapeutic receptor marker in Hodgkin lymphoma.

EBV infection is required—but not sufficient—to trigger a specific therapeutic receptor marker in Hodgkin lymphoma.

Study of 407 lymphoma cases from Guatemala found SSTR2 expression in 43% of EBV-positive classical Hodgkin lymphoma vs. 0% of EBV-negative cHL. Other EBV-associated lymphomas were largely SSTR2-negative. In EBV-negative NHL, SSTR2 associated with higher-grade B-cell lymphomas (17% of DLBCL, 17% follicular lymphoma).

Key Findings

  • 43% of EBV-positive cHL expressed SSTR2 vs. 0% EBV-negative cHL
  • EBV is necessary but not sufficient for SSTR2 upregulation in cHL
  • Most other EBV-associated lymphomas were SSTR2-negative
  • In EBV-negative NHL, SSTR2 associated with higher-grade B-cell lymphomas
  • Largest lymphoma SSTR2 cohort studied to date (n=407)

Implications

SSTR2 status in EBV-positive cHL could guide use of somatostatin-based imaging or targeted therapy. Understanding co-factors for SSTR2 upregulation may reveal new therapeutic targets.

Caveats

Retrospective study from Guatemala; abstract-only. No treatment outcomes data. SSTR2 targeting in lymphoma remains investigational.

Source: Journal of hematopathology — 2026-04-10

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