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<p>Galectin-1 (LGALS1) secreted by tumor cells attach to cell surface carbohydrates through its lectin domain and confer immune privilege within the tumor microenvironment. LGALS1expression in Classical Hodgkin lymphoma (HL) is mediated either by constitutive activation or EBV mediated enhancement of AP-1 driven pathway. The EBV positivity in our HL population is higher than reported in the Western data. The aim of this study was to assess the expression of the LGALS1in HL and correlate its expression with EBV status and other clinicopathological parameters. LGALS1expression was analyzed by using immunohistochemistry on paraffin blocks of 60 cases of HL. An expression in &gt; 50% cells was taken as positive. Clinical parameters including age, gender, histological subtype, clinical stage, bulky disease, clinical response, B- symptoms, bone marrow infiltration, relapse, follow up, survival, outcome along with histological parameters and EBV expression were recorded and analysed for any correlation with LGALS1expression. Nearly two-third (78%, <i>n</i> = 47) cases showed LGALS1expression. A significantly higher expression of LGALS1 (82%, <i>n</i> = 41) was seen in EBV high expressing cases. The other clinical and histological parameters did not show any significant differences when compared with LGALS1expression. LGALS1 expression was seen in major proportion of HL cases. LGALS1 and EBV might have a pathogenetic link in HL.</p>

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Immunohistochemical Detection of Galectin-1 in Classical Hodgkin Lymphoma and its Correlation with Epstein-Barr Virus LMP-1 Expression and Other Clinicopathological Features

  • 期刊论文

  • 发表日期：

    2025年8月6日

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  • Shalini Rawat,
  • Mili Jain,
  • Rashmi Kushwaha,
  • Shailendra Prasad Verma,
  • Nishant Verma

摘要

Galectin-1 (LGALS1) secreted by tumor cells attach to cell surface carbohydrates through its lectin domain and confer immune privilege within the tumor microenvironment. LGALS1expression in Classical Hodgkin lymphoma (HL) is mediated either by constitutive activation or EBV mediated enhancement of AP-1 driven pathway. The EBV positivity in our HL population is higher than reported in the Western data. The aim of this study was to assess the expression of the LGALS1in HL and correlate its expression with EBV status and other clinicopathological parameters. LGALS1expression was analyzed by using immunohistochemistry on paraffin blocks of 60 cases of HL. An expression in > 50% cells was taken as positive. Clinical parameters including age, gender, histological subtype, clinical stage, bulky disease, clinical response, B- symptoms, bone marrow infiltration, relapse, follow up, survival, outcome along with histological parameters and EBV expression were recorded and analysed for any correlation with LGALS1expression. Nearly two-third (78%, n = 47) cases showed LGALS1expression. A significantly higher expression of LGALS1 (82%, n = 41) was seen in EBV high expressing cases. The other clinical and histological parameters did not show any significant differences when compared with LGALS1expression. LGALS1 expression was seen in major proportion of HL cases. LGALS1 and EBV might have a pathogenetic link in HL.