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JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Prognostic impact of CD68 and kallikrein 6 in human glioma.
Anticancer Research 2009 August
AIMS: To evaluate the expression of CD68 and kallikrein 6 in human gliomas, and investigate their prognostic significance for survival of brain cancer patients in comparison to some known prognostic markers.
PATIENTS AND METHODS: Histological sections of 51 primary astrocytic tumours (11 benign, 40 malignant) were immunohistochemically stained for CD68, cathepsin B, kallikrein 6 and Ki-67. CD68 and kallikrein 6 expressions were also analyzed by real-time PCR in nine brain tumour biopsies.
RESULTS: Both microglia and tumour cells expressed CD68. High CD68 and cathepsin B staining scores were significantly, more frequent in the malignant than in the benign tumours (p=0.036 and p=0.014, respectively). In contrast, the benign group presented a stronger immunoreactivity for kallikrein 6 compared with the malignant tumours (p=0.013). A CD68 staining score of tumour cells higher than 3 was a significant predictor of shorter overall survival (p<0.01) in all patients and of borderline significance in the malignant group (p=0.057). Strong CD68 staining was of greater predictive value in the subgroup of anaplastic astrocytomas (p=0.021). Furthermore, as expected on the basis of our previous studies, prognostic significance was confirmed for cathepsin B, but not for any of the other markers under evaluation.
CONCLUSION: Kallikrein 6 was down-regulated in malignant glioma, but this differential expression did not have an impact on patient prognosis. In contrast, immunostaining of glioma tissue for CD68 and for cathepsin B may be used for prognosis of survival in these patients. This finding suggests that besides the known role of cathepsin B in invasion and angiogenesis, CD68 may be also associated with glioma progression.
PATIENTS AND METHODS: Histological sections of 51 primary astrocytic tumours (11 benign, 40 malignant) were immunohistochemically stained for CD68, cathepsin B, kallikrein 6 and Ki-67. CD68 and kallikrein 6 expressions were also analyzed by real-time PCR in nine brain tumour biopsies.
RESULTS: Both microglia and tumour cells expressed CD68. High CD68 and cathepsin B staining scores were significantly, more frequent in the malignant than in the benign tumours (p=0.036 and p=0.014, respectively). In contrast, the benign group presented a stronger immunoreactivity for kallikrein 6 compared with the malignant tumours (p=0.013). A CD68 staining score of tumour cells higher than 3 was a significant predictor of shorter overall survival (p<0.01) in all patients and of borderline significance in the malignant group (p=0.057). Strong CD68 staining was of greater predictive value in the subgroup of anaplastic astrocytomas (p=0.021). Furthermore, as expected on the basis of our previous studies, prognostic significance was confirmed for cathepsin B, but not for any of the other markers under evaluation.
CONCLUSION: Kallikrein 6 was down-regulated in malignant glioma, but this differential expression did not have an impact on patient prognosis. In contrast, immunostaining of glioma tissue for CD68 and for cathepsin B may be used for prognosis of survival in these patients. This finding suggests that besides the known role of cathepsin B in invasion and angiogenesis, CD68 may be also associated with glioma progression.
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