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Ashraf Omar,1 Ahmed Kaseb,2 Tamer Elbaz,1 Mohamed El-Kassas,3 Amr El Fouly,3 Abdel Fatah Hanno,4 Ahmed El Dorry,5 Ahmed Hosni,6 Amr Helmy,7 Amr S Saad,8 Ashwaq Alolayan,9 Basem Elsayed Eysa,10 Emad Hamada,11 Hamdy Azim,11 Hany Khattab,12 Hesham Elghazaly,8 Hesham Tawfik,13 Hisham Ayoub,14 Hussein Khaled,11 Ibtessam Saadeldin,11 Imam Waked,15 Eman MF Barakat,16 Mahmoud El Meteini,17 Mohamed Hamed Shaaban,6 Mohamed EzzElarab,10 Mohamed Fathy,17 Mohamed Shaker,5 Mohamed Sobhi,5 Mohamed Kamal Shaker,16 Mohamed ElGharib,5 Mohammed Abdullah,11 Mohesn Mokhtar,11 Mostafa Elshazli,18 Omar Mohamed Khaleil Heikal,14 Osama Hetta,5 Reda Mahmoud ElWakil,16 Sameh Abdel Wahab,5 Samir Shehata Eid,19 Yousri Rostom20 On behalf of the Egyptian Liver Cancer Committee Study Group1Department of Gastroenterology, Faculty of Medicine, Cairo University, Cairo, Egypt; 2Department of Gastrointestinal Medical Oncology, the University of Texas MD Anderson Cancer Center, Houston, TX, USA; 3Department of Endemic Medicine, Faculty of Medicine, Helwan University, Cairo, Egypt; 4Department of Gastroenterology, Faculty of Medicine, Alexandria University, Alexandria, Egypt; 5Department of Interventional Radiology, Faculty of Medicine, Ain Shams University, Cairo, Egypt; 6Department of Interventional Radiology, Faculty of Medicine, Cairo University, Cairo, Egypt; 7Department of Surgery, National Liver Institute Menoufia University, Menoufia, Egypt; 8Department of Oncology, Faculty of Medicine, Ain Shams University, Cairo, Egypt; 9Department of Oncology, National Guard Hospital, Riyadh, Saudi Arabia; 10Department of Gastroenterology, National Hepatology and Tropical Medicine Research Institute, Cairo, Egypt; 11Department of Oncology, Faculty of Medicine, Cairo University, Cairo, Egypt; 12Department of Pathology, Faculty of Medicine, Cairo University, Cairo, Egypt; 13Department of Oncology, Faculty of Medicine, Tanta University, Tanta Egypt; 14Department of Gastroenterology, Military Medical Academy, Cairo, Egypt; 15Department of Gastroenterology, Menoufia Liver Institute, Menoufia, Egypt; 16Department of Gastroenterology, Faculty of Medicine, Ain Shams University, Cairo, Egypt; 17Department of Surgery, Faculty of Medicine, Ain Shams University, Cairo, Egypt; 18Department of Surgery, Faculty of Medicine, Cairo University, Cairo, Egypt; 19Department of Oncology, Faculty of Medicine, Assiut University, Assiut, Egypt; 20Department of Oncology, Faculty of Medicine, Alexandria University, Alexandria, EgyptCorrespondence: Ashraf Omar, Department of Gastroenterology, Faculty of Medicine, Cairo University, Cairo, Egypt, Email abdelazizashraf@hotmail.comAbstract: Globally, hepatocellular carcinoma (HCC) is the fourth most common cause of death from cancer. The prevalence of this pathology, which has been on the rise in the last 30 years, has been predicted to continue increasing. HCC is the most common cause of cancer-related morbidity and mortality in Egypt and is also the most common cancer in males. Chronic liver diseases, including chronic hepatitis C, which is a primary health concern in Egypt, are considered major risk factors for HCC. However, HCC surveillance is recommended for patients with chronic hepatitis B virus (HBV) and liver cirrhosis; those above 40 with HBV but without cirrhosis; individuals with hepatitis D co-infection or a family history of HCC; and Nonalcoholic fatty liver disease (NAFLD) patients exhibiting significant fibrosis or cirrhosis. Several international guidelines aid physicians in the management of HCC. However, the availability and cost of diagnostic modalities and treatment options vary from one country to another. Therefore, the current guidelines aim to standardize the management of HCC in Egypt. The recommendations presented in this report represent the current management strategy at HCC treatment centers in Egypt. Recommendations were developed by an expert panel consisting of hepatologists, oncologists, gastroenterologists, surgeons, pathologists, and radiologists working under the umbrella of the Egyptian Society of Liver Cancer. The recommendations, which are based on the currently available local diagnostic aids and treatments in the country, include recommendations for future prospects.Keywords: hepatocellular carcinoma, clinical recommendations, Egyptian society of liver cancer, hepatitis c virus, Egypt, guidelines

Background: Dedicator of cytokinesis 8 (DOCK8)-deficient patients have severe eczema, elevated IgE, and eosinophilia, features of atopic dermatitis (AD)., Objective: We sought to understand the mechanisms of eczema in DOCK8 deficiency., Methods: Skin biopsy samples were characterized by histology, immunofluorescence microscopy, and gene expression. Skin barrier function was measured by transepidermal water loss. Allergic skin inflammation was elicited in mice by epicutaneous sensitization with ovalbumin (OVA) or cutaneous application of Staphylococcus aureus., Results: Skin lesions of DOCK8-deficient patients exhibited type 2 inflammation, and the patients' skin was colonized by Saureus, as in AD. Unlike in AD, DOCK8-deficient patients had a reduced FOXP3:CD4 ratio in their skin lesions, and their skin barrier function was intrinsically intact. Dock8 -/- mice exhibited reduced numbers of cutaneous T regulatory (Treg) cells and a normal skin barrier. Dock8 -/- and mice with an inducible Dock8 deletion in Treg cells exhibited increased allergic skin inflammation after epicutaneous sensitization with OVA. DOCK8 was shown to be important for Treg cell stability at sites of allergic inflammation and for the generation, survival, and suppressive activity of inducible Treg cells. Adoptive transfer of wild-type, but not DOCK8-deficient, OVA-specific, inducible Treg cells suppressed allergic inflammation in OVA-sensitized skin of Dock8 -/- mice. These mice developed severe allergic skin inflammation and elevated serum IgE levels after topical exposure to Saureus. Both were attenuated after adoptive transfer of WT but not DOCK8-deficient Treg cells., Conclusion: Treg cell dysfunction increases susceptibility to allergic skin inflammation in DOCK8 deficiency and synergizes with cutaneous exposure to Saureus to drive eczema in DOCK8 deficiency., (Copyright © 2024 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)