Despite significant research on the role of inflammation and immunosurveillance in the immunologic microenvironment of tumors, little attention has been given to the oncogenic capabilities of the complement cascade. The recent finding that complement may contribute to tumor growth suggests an insidious relationship between complement and cancer, especially in light of evidence that complement facilitates cellular proliferation and regeneration. We address the hypothesis that complement proteins promote carcinogenesis and suggest mechanisms by which complement can drive the fundamental features of cancer. Evidence shows that this diverse family of innate immune proteins facilitates dysregulation of mitogenic signaling pathways, sustained cellular proliferation, angiogenesis, insensitivity to apoptosis, invasion and migration, and escape from immunosurveillance. Given that the traditionally held functions for the complement system include innate immunity and cancer defense, our review suggests a new way of thinking about the role of complement proteins in neoplasia.

In this study of a cohort of patients undergoing surgery for WHO Grade I meningiomas, the authors demonstrate that the benefit of more aggressive attempts to resect the tumor with dura and underlying bone was negligible compared with simply removing the entire tumor, or even leaving small amounts of tumor attached to critical structures. The authors believe that these data reflect an evolution in the nature of meningioma surgery over the past 2 decades, and bring into question the relevance of using Simpson's grading system as the sole predictor of recurrence.

Treatment with gross-total resection provides the greatest survival advantage and should be pursued aggressively as an initial therapy. The addition of postoperative adjuvant radiation does not seem to confer a survival benefit.

The authors' analysis is limited by the quality and accuracy of these studies and may reflect source study biases, as it is impossible to control for the quality of the data reported in the literature. Finally, due to the diverse range of data presentation, the authors found that they were limited in their ability to study and control for certain variables. Some of these limitations should be minimized with their use of meta-analysis methods, which statistically evaluate and adjust for between-study heterogeneity. These results provide the impetus to initiate a prospective study, appropriately controlling for variables that can confound the retrospective analyses that largely comprise the existing literature.

Background Grade II and III meningiomas have higher rates of tumor recurrence than grade I meningiomas after surgery and/or external irradiation. As the utility of non-invasive treatments for brain tumors increases, it is becoming increasingly important to assess the likelihood that a tumor is not benign before treatment initiation. Hence, we have reviewed a large-series of our patients to determine risk-factors for higher-grade pathology with particular interest paid towards tumor location. Methods We reviewed 378 patients presenting to our institution from 2000 to 2007 with: histologically confirmed meningioma, central pathology grading according to the WHO 2000 guidelines, and tumor location confirmed with preoperative imaging. We performed univariate and multivariate logistic regression on potential risk-factors for high-grade pathology. Results Risk-factors for grade II/III pathology included non-skull base location (twofold) and male gender (two-fold). Patients with prior surgery had a three-fold increased incidence of higher-grade meningiomas at presentation to our center. We controlled for this referral bias by performing a multivariate regression, and analysis without patients receiving prior treatment. 97% of operations were performed for tumor size and clinical symptoms, while less than 3% for interval growth or features concerning of higher-grade pathology. Conclusion Non-skull-base meningiomas, male gender, and prior surgery impart increased risk for grade II or III pathology. This increased risk translates to probable poorer prognosis and increased likelihood of recurrence after treatment. Thus, it is prudent to take these specific variables into consideration in conjunction with the complete clinical presentation when advising patients regarding their prognosis.