Meningiomas are tumours that arise from meninges of the brain and the spinal cord. They represent approximately 20% of all primary intracranial tumours, and these tumours have been divided into benign, atypical and malignant subtypes based on histopathologic criteria 1. Benign meningiomas are typically slow growing tumours with 5 year survival reported to range from 90% to 100% in the era of modern imaging and treatment modalities 2. Malignant meningiomas display a more aggressive clinical course with 5 year survival rates ranging between 50 and 60% 3. The 2000 and 2007 WHO classifications defined the most frequent subtypes as grade I meningioma ,atypical and anaplastic neoplasms as grades II and III meningiomas, respectively 4,5. Atypical meningioma,which represented only 5-7% of meningiomas before the 2007 WHO classification, now accounts for more than 20% of all meningiomas 5-7. Because of their aggressive behavior, grades II and III meningiomas have an unpredictable outcome 6,8,9 and reported series have consisted of only a few patients 10-15. As a consequence, prognostic factors and therapeutic strategy are not clear and considerable controversy remains. AIm of work This retrospective study aims to analyze the prognostic factors, the effect of different treatments and the behavior of atypical meningioma. PAtIEntS And mEtHodS Patients populations: This retrospective study included 44 patients with atypical meningioma (after revision of 186 pathological slides of meningiomas) presented to the departments of
Bone metastases are a frequent complication of cancer, occurring in up to 70 percent of patients with advanced breast or prostate cancer 1 and in approximately 15 to 30 percent of patients with carcinoma of the lung, colon, stomach, bladder, uterus, rectum, thyroid, or kidney. Furthermore, once tumors metastasize to bone, they are usually incurable: only 20 percent of patients with breast cancer are still alive five years after the discovery of bone metastasis 2 .
Background: There is an increasing interest for Notch signalling pathway and particularly Delta-like ligand 4 (DLL4), a Notch ligand as potential therapeutic target to improve outcome for patients with pancreatic ductal adenocarcinoma (PDAC). Aim: characterize the expression of DLL4 in PDAC and ampullary adenocarcinoma (AA), evaluate their correlation with clinicopathologic features and patients' survival. Materials and Methods: In a retrospective study, using immunohistochemistry, we assessed the expression of DLL4 in 62 cases composed of 39 cases of PDAC and 23 cases of AA undergone Whipple and received adjuvant chemotherapy and radiotherapy. We assessed the expression level of DLL4 both in tumor cells and stromal vascular endothelial cells. The relationships of DLL4 expression with clinico-pathologic parameters and clinical outcome were evaluated.Results: There was no statistically significant relation between clinico-pathological parameters and DLL4 score expression in tumor cells of PDAC cases. However, there was statistically significant relation between DLL4 score expression in tumor cells of AA cases and tumor stage (p= 0.041). Also, there was no statistical significance regarding DLL4 expression in stromal cells in PDAC and AA cases and clinico-pathological parameters. Regarding survival functions for pancreatic & ampullary tumor cases; the median overall survival (OS) was 10 and 22 months for pancreatic (95% CI: 1-45) and ampullary tumors (95% CI: 1-69) respectively. OS for pancreatic and ampullary tumors was higher in cases with low DLL4 expression versus cases with high expressions with no statistically significance (P=0.48 & 0.09 respectively). The median Progression free survival (PFS) was 7 and 17.5 months for pancreatic (95% CI: 0-43) and ampullary tumors (95% CI: 0-96) respectively. PFS was higher in cases with low DLL4 expression rather than cases with high expressions with no statistically significant differences (P=0.52 and 0.19 respectively). Conclusions: High DLL4 expression in cancer cells was associated with worse OS and DFS than low DLL4 expression.
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