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Related Experiment Videos

GD2 expression in breast cancer.

Giulia Orsi1, Monica Barbolini1, Guido Ficarra2,3

  • 1Department of Medical and Surgical Sciences for Children and Adults, University-Hospital of Modena and Reggio Emilia, 71-41124 Modena, Italy.

Oncotarget
|April 19, 2017
PubMed
Summary

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This summary is machine-generated.

Disialoganglioside GD2 is prevalent in aggressive breast cancer (BC) subtypes, including triple-negative and metaplastic variants. This finding highlights GD2

Area of Science:

  • Oncology
  • Cancer Biology
  • Immunohistochemistry

Background:

  • Breast cancer (BC) is a heterogeneous disease with varying prognoses among subtypes.
  • Claudin-low and basal-like BC subtypes exhibit mesenchymal features and poor outcomes.
  • Disialoganglioside GD2, a neuroectodermal antigen, has potential but underexplored roles in BC.

Purpose of the Study:

  • To investigate the expression of Disialoganglioside GD2 in breast cancer (BC) patient specimens.
  • To correlate GD2 expression with clinical-pathological features of BC.
  • To determine the prevalence of GD2 in aggressive BC subtypes.

Main Methods:

  • Analysis of 63 BC patient surgical specimens (2001-2014) without prior neoadjuvant therapy.
  • Immunohistochemistry was used to assess GD2 staining intensity and percentage of positive cells.
Keywords:
BCGD2TNBCdisialogangliosidemetaplastic

Related Experiment Videos

  • Semi-quantitative scoring system and logistic regression analysis were employed.
  • Main Results:

    • GD2 staining was positive in 59% of the evaluated breast cancer (BC) cohort.
    • Significant associations were found between GD2 expression and triple-receptor negative phenotype.
    • Metaplastic carcinoma specimens showed a high prevalence of GD2 positivity.

    Conclusions:

    • Disialoganglioside GD2 is highly prevalent in aggressive breast cancer (BC) subtypes.
    • GD2 expression is linked to triple-negative and metaplastic BC variants.
    • These findings suggest GD2's potential role in aggressive BC biology.