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BACKGROUND:Bladder cancer represents the fifth most common malignancy worldwide and a major cause of cancer-related morbidity and death. Incidence and mortality rates have remained relatively constant over the past four decades. Urothelial bladder cancers have identified multiple risk factors.AIM:We aimed at evaluating the expression of the FGFR3 protein and gene amplification in the urothelial cells of neoplastic and non-neoplastic urothelial lesions of the urinary bladder, and correlation with tumour grade, stage and associated bilharziasis.MATERIAL AND METHODS:One hundred and five different urinary bladder lesions were studied, including 15 cystitis cases (9 bilharzial and 6 non-bilharzial cystitides), 75 urothelial carcinoma cases (18 bilharzial associated and 57 non-bilharzial associated) and 15 squamous cell carcinoma associated with bilharziasis, beside 5 control cases. Data concerning age, sex, tumour grade, stage, and associated bilharziasis were obtained. Each case was studied for FGFR3 expression, and FISH technique was applied on forty malignant cases that show high protein expression.RESULTS:The highest incidence of cystitis was in the fourth decade while of bladder cancer was in the seventh decade. Tumour grade was correlated significantly with tumour stage. FGFR3 correlates significantly with tumour grade, stage and with a bilharzial infestation. FGFR3 gene amplification was reported mainly in low grade and NNMBIC tumours.CONCLUSIONS:FGFR3 overexpression in malignant cases was significantly higher than in chronic cystitis. FGFR3 gene amplification was reported mainly in low grade and NNMBIC tumours. FGFR3 may be further studied as a subject for target therapy of bladder cancer.

Background and aim: Imaging guided microwave ablation (MWA) for hepatocellular carcinoma (HCC) has become a widely used method over recent years. Tumors close to the diaphragm, gastrointestinal tract, gallbladder, pancreas, hepatic hilum and major bile duct or vessels are generally considered relative contraindications for microwave ablation. This study was conducted to assess the effectiveness and safety of ultrasonography-guided MWA in treating patients with HCC in difficult anatomical sites in comparison to those in conventional sites. Patients and methods: Eighty-eight patients were included and divided into two groups: the study group of 44 with 46 lesions lying <5mm from the diaphragm, hepatic capsule, gall bladder (GB) or large vessel; and the control group of 44 patients with 50 lesions in non-risky sites. Each lesion was ablated using an ultrasound guided microwave probe using a detailed protocol. Results: Most of the patients were males, with a mean age of 57.8 years. In the study group, two patients had lesions adjacent to the GB, twelve were perivascular and 32 were subcapsular. The overall successful ablation rates were 84.8% and 92% in the study and control groups, respectively. Within the study group, ablation rates were 100%, 75% and 87.5% for lesions close to the GB, perivascular lesions and subcapsular lesions, respectively. One patient developed a subcutaneous abscess, with good outcome after proper treatment. Fever, pain and asymptomatic pleural effusion were reported after ablation without statistically significant difference between the groups or among subgroups. In conclusion: MWA for HCC in difficult anatomical sites is as effective and safe as for ordinary sites.

Despite all of the progress in understanding its molecular biology and pathogenesis, glioblastoma (GBM) is one of the most aggressive types of cancers, and without an efficient treatment modality at the moment, it remains largely incurable. Nowadays, one of the most frequently studied molecules with important implications in the pathogenesis of the classical subtype of GBM is the epidermal growth factor receptor (EGFR). Although many clinical trials aiming to study EGFR targeted therapies have been performed, none of them have reported promising clinical results when used in glioma patients. The resistance of GBM to these therapies was proven to be both acquired and innate, and it seems to be influenced by a cumulus of factors such as ineffective blood–brain barrier penetration, mutations, heterogeneity and compensatory signaling pathways. Recently, it was shown that EGFR possesses kinase-independent (KID) pro-survival functions in cancer cells. It seems imperative to understand how the EGFR signaling pathways function and how they interconnect with other pathways. Furthermore, it is important to identify the mechanisms of drug resistance and to develop better tailored therapeutic agents.

Introduction: Overexpression of epidermal growth factor receptor (EGFR) has been described in several solid tumors including bladder cancer. Transforming growth factor alpha (TGFα) is frequently deregulated in neoplastic cells and plays a role in the development of bladder cancer. TGFα-EGFR ligand-receptor combination constitutes an important event in multistep tumorigenesis. Methods: This study was done on 30 bladder biopsies from patients with urothelial carcinoma, 15 with squamous cell carcinoma, 10 with cystitis and 5 normal control bladder specimens. All were immuohistochemically stained with EGFR and TGFα antibodies. Results: EGFR and TGFα were over-expressed in higher grades and late stages of bladder cancer. Moreover, they show higher expression in squamous cell carcinoma compared to urothelial carcinoma and in schistosomal associated lesions than in non-schistosomal associated lesions. Conclusion: EGFR and TGFα could be used as prognostic predictors in early stage and grade of bladder cancer cases, especially those with schistosomal association. In addition they can help in selecting patients who can get benefit from anti-EGFR molecular targeted therapy.

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BACKGROUND AND AIM: Gastric cancer (GC) is one of the top causes of cancer-related deaths worldwide. According to the Cancer Genome Atlas, there are four subtypes of GC, with the Epstein-Barr virus (EBV) subtype accounting for about 10% of cases. EBV infection causes EBV-associated GC (EBVaGC). The previous research suggested that the presence of the EBV viral genome in gastric carcinomas could be used as a surrogate marker for targeted therapy and optimal GC treatment. AIM: We aimed to explore the rate of EBV involvement in gastric carcinogenesis from molecular perspective view and to evaluate the role of the tumor-suppressor protein p16 as a marker for diagnosis in GC Egyptian patients in relation to EBV infection. METHODS: One hundred-four surgically resected GC cases were analyzed. Two methods including quantitative real-time polymerase chain reaction (qPCR) for detecting EBV-derived latent membrane protein-1 (LMP-1) and Epstein-Barr nuclear antigen-1 (EBNA-1) genes as well as immunohistochemistry (IHC) detection of LMP-1 protein and p16 protein on paraffinized tissue blocks were applied. RESULTS: Using IHC, p16 protein was presented in 90/104 (86.5%) of the GC cases, and EBV LMP-1 was detected in 4 cases (3.84%). qPCR detected 14 cases positive for EBV (13.46%). In EBV positive cases detected using qPCR, no expression of p16 was detected. CONCLUSION: EBVaGC has a low incidence in Egypt; loss of p16 expression was recognized in EBVaGC and could be considered as a promising biomarker of EBVaGC. The combination of the two methods IHC and qPCR in addition to p16 is recommended for improving the accuracy of identification of infected cancer.

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