Alteration of Serum Neural Cell Adhesion Molecule (NCAM) in Patients With Brain Tumors

TODARO, M. VARELA, M. G. PALLOTA, J. LASTIRI, M. E. LINCUEZ,E. BAL DE KIER JOFF´E, E. SACERDOTE DE LUSTIG, AND L. PURICELLI

CELLULAR AND MOLECULAR NEUROBIOLOGY.

Kluwer Academic/Plenum Publishers

Lugar: New York; Año: 2004 vol. 24 p. 178 - 179

0272-4340

NCAMis a membrane glycoprotein, expressed in neuroectodermis, mesenchyma and tumor cells derived from these tissues. N-CAM can also be found in sera, although little is known about its modulation in different pathological states. Objective: To study the expression of serum NCAM in patients with brain tumors [gliomas (n D 34), metastasis confined to brain (n D 27) and benign tumors (n D 22)] compared with non-tumoral controls (n D 69). NCAM was measured by Western blot and densitometric quantitative analysis, employing a monoclonal antibody which revealed bands of high (HMW, ¸130 kDa) and low (LMW, <130 kDa) molecular weight. We observed that the levels of HMW NCAM increased and the levels of LMW decreased in tumor patients respect to control subjects (p < 0:01). Therefore, the better parameter to discriminate patients from controls was the rate HMW/LMW, which was significantly increased in patients with brain tumors (p < 0:001). On basis of this ratio, the value of the percentile 80 of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. better parameter to discriminate patients from controls was the rate HMW/LMW, which was significantly increased in patients with brain tumors (p < 0:001). On basis of this ratio, the value of the percentile 80 of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. the levels of LMW decreased in tumor patients respect to control subjects (p < 0:01). Therefore, the better parameter to discriminate patients from controls was the rate HMW/LMW, which was significantly increased in patients with brain tumors (p < 0:001). On basis of this ratio, the value of the percentile 80 of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. better parameter to discriminate patients from controls was the rate HMW/LMW, which was significantly increased in patients with brain tumors (p < 0:001). On basis of this ratio, the value of the percentile 80 of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. low (LMW, <130 kDa) molecular weight. We observed that the levels of HMW NCAM increased and the levels of LMW decreased in tumor patients respect to control subjects (p < 0:01). Therefore, the better parameter to discriminate patients from controls was the rate HMW/LMW, which was significantly increased in patients with brain tumors (p < 0:001). On basis of this ratio, the value of the percentile 80 of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. better parameter to discriminate patients from controls was the rate HMW/LMW, which was significantly increased in patients with brain tumors (p < 0:001). On basis of this ratio, the value of the percentile 80 of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. the levels of LMW decreased in tumor patients respect to control subjects (p < 0:01). Therefore, the better parameter to discriminate patients from controls was the rate HMW/LMW, which was significantly increased in patients with brain tumors (p < 0:001). On basis of this ratio, the value of the percentile 80 of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. better parameter to discriminate patients from controls was the rate HMW/LMW, which was significantly increased in patients with brain tumors (p < 0:001). On basis of this ratio, the value of the percentile 80 of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. analysis, employing a monoclonal antibody which revealed bands of high (HMW, ¸130 kDa) and low (LMW, <130 kDa) molecular weight. We observed that the levels of HMW NCAM increased and the levels of LMW decreased in tumor patients respect to control subjects (p < 0:01). Therefore, the better parameter to discriminate patients from controls was the rate HMW/LMW, which was significantly increased in patients with brain tumors (p < 0:001). On basis of this ratio, the value of the percentile 80 of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. better parameter to discriminate patients from controls was the rate HMW/LMW, which was significantly increased in patients with brain tumors (p < 0:001). On basis of this ratio, the value of the percentile 80 of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. the levels of LMW decreased in tumor patients respect to control subjects (p < 0:01). Therefore, the better parameter to discriminate patients from controls was the rate HMW/LMW, which was significantly increased in patients with brain tumors (p < 0:001). On basis of this ratio, the value of the percentile 80 of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. better parameter to discriminate patients from controls was the rate HMW/LMW, which was significantly increased in patients with brain tumors (p < 0:001). On basis of this ratio, the value of the percentile 80 of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. low (LMW, <130 kDa) molecular weight. We observed that the levels of HMW NCAM increased and the levels of LMW decreased in tumor patients respect to control subjects (p < 0:01). Therefore, the better parameter to discriminate patients from controls was the rate HMW/LMW, which was significantly increased in patients with brain tumors (p < 0:001). On basis of this ratio, the value of the percentile 80 of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain tumors. On the other hand, Cox hazard analysis indicated that survival was not associated with serum HMW/LMW NCAM in patients with malignant brain tumors. In conclusion, our results indicated that although alterations in serum NCAM are associated with brain tumor pathology, this molecule was not useful to discriminate between benign and malignant disease. Besides, serum NCAM did not behave as prognostic marker for survival. of the control population was chosen as cutoff point. It was found that 17/33 (52%) patients with glioma, 16/27 (59%) with brain metastasis and 15/22 (68%) with benign brain tumors presented elevated values of HMW/LMW compared with controls (14/69, 20%) (p < 0:01). However, no significant differences were observed among the groups of patients with different brain pathologies. Serum NCAM, measured as HMW/LMW rate, showed a specificity of 80% and a sensitivity of 60% to identify patients with brain