Beta Thalassemia represents a major public health problem in Egypt. The carrier rate varies between 
5.5% to > 9%. It is estimated that there are 1000/1.5 million per year live births born with beta 
thalassemia.(1) β thalassemia occurs when there is a quantitative reduction of β globin chains that are 
usually structurally normal.(2) They are caused by mutations that nearly all affect the β globin locus 
and are extremely heterogeneous. Almost every possible defect affecting gene expression at 
transcription or post-transcriptional level, including translation, have been identified in β 
thalassemia.(3) These genetic defects lead to a variable reduction in β globin output ranging from a 
minimal deficit (mild β+ thalassemia alleles) to complete absence (β° thalassemia). Aim of the work:
We aimed in this study to assess the molecular changes in transfusion dependent Beta thalassemia 
patients and the correlation of these molecular changes with their clinical outcomes. Patients & 
methods: This study will include 40 transfusion dependent β thalassemia patients with age range of 2 
-18 years, recruiting the Pediatric Hematology unit in Minia University children hospital. Study 
procedure: β-Thalassemia mutation identification of samples will be performed by the reverse dot 
blot hybridization technique (RDB). For RDB, a panel of primers and probes using the beta globin 
strip assay well be used (β-Globin Strip Assay MED kit, VIENNA lab