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Maher Kurdi,1,2 Nasser Mulla,3 Yousef Katib,4 Taghreed Alsinani,5 Sahar Hakamy,2 Bassam MJ Addas,6 Husam Malibary,7 Taher F Halawa,8 Marwa S Farhan,9 Eyad Faizo,10 Saleh Baeesa6 1Department of Pathology, Faculty of Medicine, King Abdulaziz University, Rabigh, Saudi Arabia; 2Brain Tumour Unit, KFMRC, King Abdulaziz University, Jeddah, Saudi Arabia; 3Department of Internal Medicine, Faculty of Medicine, Taibah University, Medina, Saudi Arabia; 4Department of Radiology, Faculty of Medicine, Taibah University, Madinah, Saudi Arabia; 5Department of Surgery, King Fahad General Hospital, Jeddah, Saudi Arabia; 6Department of Surgery, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia; 7Department of Internal Medicine, Faculty of Medicine, King Abdul Aziz University, Jeddah, Saudi Arabia; 8Pediatric Hematology and Oncology Consultant, Faculty of Medicine, King Abdulaziz University, Rabigh, Saudi Arabia; 9Clinical Pathology Department, Cairo University, Cairo, Egypt; 10Division of Neurosurgery, Department of Surgery, Faculty of Medicine, Tabuk University, Tabuk, Saudi ArabiaCorrespondence: Maher Kurdi, Department of Pathology, Faculty of Medicine, King Abdulaziz University, Rabigh, Saudi Arabia, Tel +966 556655467, Email Ahkurdi@kau.edu.saPurpose: IDH1 and IDH2 are hotspot mutations commonly identified in WHO-grade 4 astrocytomas. Their association with TAMs has never been investigated. We aim to explore the crosstalk between the IDH1/2 mutation metabolic effect and TAMs in tumour microenvironment and how this relationship affects the tumour recurrence.Patients and Methods: The study included 20 samples of patients with WHO-grade 4 astrocytoma. The alteration hotspot in codon IDH1R132 and IDH2R172 was examined using direct sequencing. The protein expression of CD204 on TAM was detected through immunohistochemistry.Results: IDH1R132 and IDH2R172 were symmetrically identified as wildtype in 18/20 tumours (90%) and the remaining 2 tumours (10%) showed synonymou

Background: Sudden infant death syndrome (SIDS) is a tragic incident which remains a mystery even after post-mortem investigation and thorough researches. Methods: This comprehensive review is based on the genes reported in the molecular autopsy studies conducted on SIDS so far. A total of 20 original studies and 7 case reports were identified and included in this analysis. The genes identified in children or adults were not included. Most of the genes reported in these studies belonged to cardiac channel and cardiomyopathy. Cardiac channel genes in SIDS were scrutinized for further analysis. Results: After screening and removing the duplicates, 42 unique genes were extracted. When the location of these genes was assessed, it was observed that most of these belonged to Chromosomes 11, 1 and 3 in sequential manner. The pathway analysis shows that these genes are involved in the regulation of heart rate, action potential, cardiac muscle cell contraction and heart contraction. The protein-protein interaction network was also very big and highly interactive. SCN5A, CAV3, ALG10B, AKAP9 and many more were mainly found in these cases and were regulated by many transcription factors such as MYOG C2C1 and CBX3 HCT11. Micro RNA, hsa-miR-133a-3p was found to be prevalent in the targeted genes. Conclusions: Molecular and computational approaches are a step forward toward exploration of these sad demises. It is so far a new arena but seems promising to dig out the genetic cause of SIDS in the years to come.