Publications by authors named "Gek Bee Ong"

Introduction: Advancements in genomic profiling led to the discovery of four major molecular subgroups in medulloblastoma (MB), which have now been incorporated into the World Health Organization classification of central nervous system tumors. The current study aimed to determine the prognostic significance of the MB molecular subgroups among children in Malaysia.

Methods: We assembled MB samples from children <18 years between January 2003 and June 2017 from four pediatric oncology centers in Malaysia.

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Objective: Thalassaemia is the most common inherited blood disorder in Malaysia. This study aims to report the current status of thalassaemia in Malaysia and provide a comprehensive understanding of the disease through data obtained from the Malaysian Thalassaemia Registry.

Design: Data were extracted from the Malaysian Thalassaemia Registry, a web-based system accessible to enrolled users through www.

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Background: Although thalassemia is a genetic hemoglobinopathy in Malaysia, there is limited data on thalassemia mutations in the indigenous groups. This study aims to identify the types of globin gene mutations in transfusion-dependent patients in Northern Sarawak.

Methods: Blood was collected from 32 patients from the Malay, Chinese, Kedayan, Bisayah, Kadazandusun, Tagal, and Bugis populations.

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Background: Tumor prostheses currently give the best short- and medium-term results for limb-salvage reconstruction procedures in the treatment of bone tumors. However, in developing countries, the cost of a tumor prosthesis is beyond the reach of much of the population. We report the use of autoclaved tumor-bearing bone in 10 patients, as an affordable alternative to the use of prostheses.

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Children with Down syndrome and acute megakaryoblastic leukemia (DS-AMKL) have been shown to have increased sensitivity to cytarabine based chemotherapy. The excellent prognosis in patients with DS-AMKL may be due to mutations in the GATA1 gene leading to reduced expression of the enzyme cytidine deaminase. This leads to a decreased ability to convert cytarabine into its inactive metabolite, resulting in high intracellular concentration of this cytotoxic agent.

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