The prognostic impact of M‐CSF, CSF‐1 receptor, CD68 and CD3 in prostatic carcinoma
Résumé fourni par la source
AIMS: Macrophage colony-stimulating factor (M-CSF) binds to colony-stimulating factor-1 receptor (CSF-1R) and stimulates proliferation and differentiation of monocytes, macrophages and their bone marrow progenitors. M-CSF, CSF-1R, the macrophage marker CD68, and the pan T-lymphocyte marker CD3 are increased in many human cancers. Their prognostic importance in primary prostatic carcinoma has not been fully delineated. The aim was to compare the expression of M-CSF, CSF-1R, CD68 and CD3 in metastatic and non-metastatic prostatic cancer. METHODS AND RESULTS: Digital video analysis of tumour cell areas and tumour stromal areas was performed in 59 cancer specimens: 32 patients with metastases and 27 patients without metastases. Expression of M-CSF and CSF-1R was recorded as 0 (negative immunoreactivity), 1 (weak), 2 (moderate) or 3 (strong reactivity). Macrophages (CD68) and T lymphocytes (CD3) were detected as proportions of moderately or strongly immunoreactive cells. Patients with metastatic primary cancers showed higher expression of M-CSF (P < 0.0001, P = 0.005), CSF-1R (both P < 0.0001) and CD3 (P = 0.007, P < 0.0001) in both tumour cell areas and tumour stromal areas, compared with the non-metastatic cancers. CONCLUSION: This study suggests that expression of M-CSF, CSF-1R and CD3 is a significant prognostic factor in primary prostatic cancers by predicting the development of metastases.
Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.
Contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- The prognostic impact of M‐CSF, CSF‐1 receptor, CD68 and CD3 in prostatic carcinoma
- Date Crossref
- 28/06/2008
- Éditeur
- Wiley
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude et ne compte pas comme une seconde source scientifique indépendante.
Institutions déclarées
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