Prognostic Significance of CD68 And CD163 Tumor-Associated Macrophages in Hormone Receptor-Positive Vs Triple-Negative Invasive Breast Carcinoma: A Retrospective IHC Study
DOI:
https://doi.org/10.55489/njmr.160320261276Keywords:
Breast carcinoma, Densities, Invasive, Triple negative, Tumor Associated MacrophagesAbstract
Background: Tumor-associated macrophages (TAMs) influence tumor progression within the microenvironment. M1-like macrophages (CD68⁺) exhibit tumoricidal properties, whereas M2-like macrophages (CD68⁺/CD163⁺) promote tumor growth through hypoxia-driven angiogenesis. This study assessed the localization and density of CD68⁺ and CD163⁺ TAMs in hormone receptor-positive and triple-negative invasive breast carcinomas and evaluated their association with clinicopathological parameters.
Methods: A retrospective cross-sectional study was conducted on histopathologically confirmed invasive breast carcinoma cases. Formalin-fixed paraffin-embedded tissues underwent immunohistochemical staining for ER, PR, Her2/neu, CD68, and CD163. Descriptive statistics were calculated, and associations with clinicopathological variables were analyzed using the χ² test. Survival outcomes were assessed by Kaplan-Meier and log-rank tests, and prognostic significance was evaluated using univariate Cox regression analysis.
Results: The study showed association of CD68⁺ and CD163⁺ TAMs in ER, PR positive and Her2/neu negative cases in TS (tumor stroma) and TN (tumor nest) with higher histologic grades. High infiltration of both CD68⁺ and CD163⁺ TAMs were seen in triple negative invasive breast carcinomas (TNBC). There was significant correlation of increased CD163⁺ TAMs in TN and TS with relapse free survival and overall survival rates based on log rank tests.
Conclusion: Breast cancer remains the leading malignancy contributing to cancer-related mortality among women globally. Conventional treatment strategies have primarily focused on directly targeting tumor cells. However, increasing evidence highlights the importance of addressing the tumor microenvironment as a therapeutic approach to overcome treatment resistance and enhance clinical outcomes.
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