الفهرس 
Childhood MalignancyOnly 14 pages are availabe for public view
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Abstract
Children suffering from malignancies represent a growing cohort of our society. Fortunately, we are witnessing great improvements in the management of patients suffering from childhood cancer, including early diagnosis, multimodal therapy and hospital supportive care. These improvements eventually lead to increasing the survival rate and treatment outcome of patients suffering of cancer. However, childhood cancer survivors are at increased risk of facing chronic health problems, some of which appear during or soon after treatment whereas others manifest years after therapy.
Cardiovascular disease is one of the leading causes of morbidity and mortality in long-term cancer survivors. Cardiovascular complications related to cancer treatment may arise after long time of end of therapy. Therefore, it is very important to regularly follow up survivors for early detection and management of such conditions.
Cardiac dysfunction, in childhood cancer survivors, related to anthracycline treatment is initially subclinical and unfortunately passes unnoticed in regular cardiac assessment by conventional echocardiographic methods. Early detection of cardiac dysfunction plays a crucial role in management of the condition before developing a life threatening health issue. Therefore, it is becoming a priority for cardiologists and oncologists to develop new modalities and techniques directed for early detection of subclinical cardiac dysfunction.
Speckle tracking echocardiography (STE) and cardiac magnetic resonance (CMR) imaging and Genotyping of the CELF4( rs 1786814) gene polymorphism are giving impressing results regarding cardiac assessment in childhood cancer survivors.
Layer-specific myocardial deformation may be of relevance in childhood cancer survivors as the subendocardial layer of the ventricle has been shown to be particularly sensitive to doxorubicin damage. The recently introduced speckle tracking echocardiographic technology has allowed noninvasive bedside assessment of layer-specific myocardial deformation.
Interindividual variability in the dose-dependent association between anthracycline exposure and cardiac complication cardiotoxicity risk suggests that genetic variants possibly modify this association.
The CELF protein family belongs to a group of splicing regulators that controls developmentally regulated, tissue-specific splicing event. One of the classic targets of CELF family members is TNNT2, the gene encoding for cardiac troponin T (cTnT) which has an essential role in Ca signaling in cardiac muscle and is an established biochemical marker of myocardial injury; serum cTnT levels are increased after anthracycline treatment.
The objective of this study was:
To detect the modifying effect of CELF4 rs (1786814) polymorphism on anthracycline-related cardiotoxicity and traditional risk factors for atherosclerosis in Childhood Cancer Survivors.
This study was held on 106 children 53 of them complete their anticancer therapy and attending for regular follow up (32 of them were males and 21 were females) and 53 were healthy children of matched age and sex as control. The age of our survivors ranged from 5.5 to 20 years.
Patients were subjected to the followings:
1. Full history taking.
2. Thorough clinical examination.
3. Laboratory evaluation in the form of (CBC, liver and kidney function tests, lipid profile, and HbA1c).
4. Cardiac imaging assessment by conventional 2D echocardiography and 2D speckle tracking echocardiography.
5. Molecular genetic study and Genotyping of the CELF4 rs (1786814) gene polymorphism by allelic discrimination assay using real time PCR technique.