Galectin-3 and CD44v6 positivity by RT-PCR method in fine needle aspirates of benign thyroid lesions

N Matesa1, I Samija, Z Kusić

  • 1Department of Oncology and Nuclear Medicine, Sisters of Mercy University Hospital, Zagreb, Croatia. nmatesa@kbsm.hr

Insights

Macrophages and Hürthle cells (HC) in benign thyroid lesions may cause false positives for galectin-3 and CD44v6 expression detected by reverse transcriptase-polymerase chain reaction (RT-PCR). This finding is significant for nodular goitre and Hashimoto thyroiditis diagnoses.

Area of Science:

  • Thyroid pathology
  • Immunohistochemistry
  • Molecular diagnostics

Background:

  • Galectin-3 and CD44v6 are potential biomarkers for thyroid lesions.
  • Reverse transcriptase-polymerase chain reaction (RT-PCR) is used to detect their expression.
  • Benign thyroid lesions can sometimes show false-positive results for these markers.

Purpose of the Study:

  • To determine if macrophages and Hürthle cells (HC) contribute to false-positive galectin-3 and CD44v6 expression in benign thyroid lesions.
  • To investigate the cellular basis of marker expression in specific benign thyroid conditions.

Main Methods:

  • Ultrasound-guided fine needle aspiration cytology (FNAC) was performed on 123 patients with benign thyroid lesions.
  • RNA was isolated from aspirates for galectin-3 and CD44v6 expression analysis using RT-PCR.
  • RT-PCR results were correlated with definitive FNAC diagnoses and cellular presence of macrophages and HC.

Main Results:

  • Galectin-3 positivity was linked to macrophages in nodular goitre (NG) and Hashimoto thyroiditis (HT).
  • Hürthle cells (HC) correlated with galectin-3 positivity in HT and showed a tendency in NG.
  • HC presence was significantly associated with CD44v6 positivity in NG and tended to be associated in HT.

Conclusions:

  • Macrophages and/or Hürthle cells (HC) likely explain false-positive galectin-3 and CD44v6 RT-PCR results in nodular goitre (NG) and Hashimoto thyroiditis (HT) cytological samples.
  • Understanding cellular contributions is crucial for accurate interpretation of molecular markers in thyroid diagnostics.
Abstract

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