Background Medulloblastoma (MB) is a heterogeneous disease, displaying distinct genetic profiles with specific molecular subgroups. This study aimed to validate MB molecular subgrouping using surrogate immunohistochemistry and associate molecular subgroups, histopathological types, and available clinicopathological parameters with overall survival (OS) and progression-free survival (PFS) of MB patients. This study included 40 MBs; immunohistochemical staining, using β-catenin and GRB2-Associated Binding Protein 1 (GAB1) antibodies, was used to classify MB cases into wingless signaling activated (WNT), sonic hedgehog (SHH), and non-WNT/SHH molecular subgroups. Nuclear morphometric analysis (for assessment of degree of anaplasia) and Kaplan-Meier survival curves were done. Results MB cases were classified into WNT (10%), SHH (30%), and non-WNT/SHH (60%) subgroups. Histopathological types differed significantly according to tumor location (p< 0.001), degree of anaplasia (p = 0.014), molecular subgroups (p < 0.001), and risk stratification (p = 0.008). Molecular subgroups differed significantly in age distribution (p = 0.031), tumor location (p< 0.001), histopathological variants (p < 0.001), and risk stratification (p < 0.001). OS was 77.5% and 50% after 1 and 2 years, while PFS was 65% and 27.5% after 1 and 2 years, respectively. OS and PFS were associated significantly with histopathological variants (p < 0.001 and 0.001), molecular subgroups (p = 0.012 and 0.005), and risk stratification (p < 0.001 and < 0.001), respectively. Conclusions Medulloblastoma classification based on molecular subgroups, together with clinicopathological indicators, mainly histopathological types; accurately risk stratifies MB patients and predicts their survival.

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Introduction: Endometrial carcinoma [EC], particularly the most predominant endometrioid type [EEC] is a major contributor to cancer burden globally, and its molecular classification has gained much importance recently. Aim: This study aimed to determine the immunohistochemical expression of mismatch repair proteins 'MLH1 and MSH2' in relation to clinicopathologic parameters in EEC and to characterize clinicopathologic features of mismatch repair protein (MMRP) deficient EEC. Material and Methods: The current work was carried out on 80 cases of EEC retrieved [with clinical data] from the Department of Pathology, Faculty of Medicine, Tanta University in the period from June 2018 to December 2019. H&E staining and immunohistochemical staining with MLH and MSH2 were done for each case. Results: 29 (36.3%) carcinomas showed abnormal MMRP expression (11 cases showed isolated MLH1 deficiency (37.93%), 10 cases showed isolated MSH2 deficiency (34.48%), and 8 cases (27.59) showed a combined loss of both proteins), whereas the remaining 51 (63.7%) of cases demonstrated normal MLH1/MSH2 immunoreactivity (MMRP intact). MLH1, MSH2 expression, and MMRP status were closely related to some clinicopathologic features (patient's age, histopathological tumor grade, and tumor stage) with a statistically significant relation. Conclusions: A subset of endometrioid type EC demonstrates MMRP defect; the MMRP deficient EEC often displays adverse clinicopathological parameters as poorly differentiated or undifferentiated histology, an advanced stage with young age at presentation.

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