الفهرس 
ContentsOnly 14 pages are availabe for public view
 |  | from | 177 |  |  |
| | | from | 177 | | |
Abstract
Conventional childhood ALL stratification is based on prognostic factors related to characteristics of the patient (age at diagnosis) and the disease itself white blood cei] (WBC) count at diagnosis, immunophenotype of the leukemic cells, presence of known genetic fusions, numerical abnormalities or abnormal gene expression, and early response to therapy (evaluated by morphological methods or using a more accurate measurement such as minimal residual disease (MRD) analysis) tPui et al, 201SI. promotes B cell survival and proliferation, and is involved in inflammation, CRLF2 allergic responses and malignant transfomtation. Approximately 40% of children with B cell ALL have CRLF2 cryptic genetic alterations, which induce abnomial signaling during B cell development. About 5-7% of Caucasian non-selected B cell ALL patients present CRLF2 rearrangements and overexpression. This frequency increased to 1 6- 1 9% in high risk B cell ALL patients; for this reason CRLF2 abnormalities have been associated with adverse prognosis tChiaretti et al., 20161. In the current study of 54 patients with B-ALL, patients were categorized according to NCI into the standard risk group (55%) and high-risk group (45%) tMaloney et al, 20001. We observed that CRLF2 expression was found in 48% of our patients. High CRLF2 expression was more prevalent in patients with HR B-ALL than in the patients with SR B-ALL. In the present study, only two individuals had JAK2 mutations, and both were MRI) positive with CRLF2 0verexpression. MRD monitoring based on a specific marker can help us predict leukemia relapse and detemiine the best-individualized treatment. In the present work, we measured MRD at the end of induction therapy and relate their value to CRLF2 gene expression. We found that the patients’ higher CRLF2 gene expression at diagnosis was associated with significantly higher MRD. In the present work, patients were followed for the treatment response up to 24 months, and the influence of CRLF2 gene expression was detemiined using Kaplan-Meier analysis. There was no significance between CRLF2 gene expression and overall survival. IJnlike overall survival, the influence of CRLF2 overexpression on 2 year relapse- free survival was significant. This highlights the prognostic significance of CRLF2 evidenced by significantly higher relapse rate among patients with overexpression of CRLF2. In summary, we report that; CRLF2 overexpression was found to be unfavorable prognostic factor for childhood ALL patients evidenced by overexpression in high risk patients and in patients with lower relapse free survival. This emphasizes its role in prediction of treatment response encouraging its involvement in risk stratification based therapy. Preceding MRD detection at the end of induction chemotherapy, CRLF2 expression can be endorsed for tailoring the initial treatment plan for patients according to its level of expression.