[Usefulness of galectin-3 expression in the clinical behavior of differentiated thyroid carcinoma]. / Utilidad de la expresión de galectina-3 en el comportamiento clínico del cáncer diferenciado de tiroides.

BACKGROUND AND OBJECTIVE: Our objective was to quantify the galectin-3 (gal-3) expression in differentiated thyroid carcinoma and study its relation with the clinical behavior of these tumors. PATIENTS AND METHOD: We investigated the immunohistochemical reaction of gal-3 in patients with papillary thyroid carcinoma (PTC) and follicular thyroid carcinoma (FTC) and performed a retrospective study in order to find correlations with clinical features. Gal-3 expression was studied in 53 differentiated tyroid carcinomas (42 PTC and 11 FTC), and was related with clinical features: metastases, extrathyroid invasion and initial stage in the diagnosis and persistence disease and relapses in the follow up. RESULTS: Gal-3 expression positivity in PTC had a median of 60% (percentil 25 [p25], 17.5%; percentil 75 [p75], 100%), and was significantly higher (p < 0.0001) than in FTC (median, 0%; p25, 0%; p75, 15%). In PTC, gal-3 expression was significantly higher in advanced stages at the time of initial diagnosis (p = 0.014), persistent disease (p = 0.012) and relapses (p = 0.012) during the follow up. We did not find any significant association between gal-3 expression and clinical features of FTC. CONCLUSIONS: Gal-3 is a negative prognosis marker in PTC but not in FTC.

Analysis of HER2 by chromogenic in situ hybridization and immunohistochemistry in lymph node-negative breast carcinoma: Prognostic relevance.

In patients with lymph node-negative breast carcinoma (LNNBC), the prevalence of HER2 overexpression and gene amplification and their prognostic value have not been extensively evaluated. We examined 162 patients with LNNBC with complete follow-up. Immunohistochemistry (IHC) for HER2, Ki67, and p53 was performed. HER2 gene status was analyzed by chromogenic in situ hybridization (CISH) and discordant cases by fluorescence in situ hybridization. HER2 overexpression was seen in 24.7% of cases (40/162) and amplification by CISH in 17.6% (28/159). Agreement between IHC and CISH was achieved in 147 (92.5%) cases. Amplification was seen in 21 (100%) of 21 (3+), 6 (35.3%) of 17 (2+), and 1 (0.6%) of 121 (0-1+) tumors. Fluorescence in situ hybridization detected 3 (1.8%) additional cases. HER2 overexpression and amplification were present in tumors of high grade, with necrosis and lymph-vascular invasion (LVI) (all P < .027). In addition, amplified tumors showed Ki67 of more than 20% and p53 overexpression (P < .05). By univariate analysis, shorter disease-free survival (DFS) and overall survival (OS) were seen for patients with tumors showing HER2 amplification, LVI, and Ki67 of more than 20% (P < .05) (Kaplan-Meier). However, the multivariate analysis (Cox regression) demonstrated only Ki67 as an independent prognostic factor for both DFS (P = .017) and OS (P = .010), and as a trend for HER2 gene status (OS, P = .087) and LVI (DFS, P = .11; OS, P = .063). We conclude that IHC is a reliable method for detecting HER2 expression that can be complemented by CISH in nondefinitive cases (2+). Moreover, CISH is a valuable tool for the assessment of HER2 gene status with potential prognostic value and, therefore, in clinical decision making for treatment of high-risk LNNBC.