In:
Blood, American Society of Hematology, Vol. 128, No. 22 ( 2016-12-02), p. 5157-5157
Abstract:
Abstract Background: Chemokine (C-C Motif) Ligand 17 is a protein coding gene. This chemokine plays important roles in T cell development in thymus as well as in trafficking and activation of mature T cells. Diseases associated with CCL17 include mycosis fungoides, paragonimiasis and some hematologic malignancies such as Hodgkin¡¯s lymphoma, B cell lymphoma, and Nasal natural killer/T cell lymphoma (NNKTL). However, our knowledge of the expression levels of CCL17 in B-cell acute lymphoblastic leukemia (ALL) remains limited. Aims: The purpose of this study was to investigate the expression levels of human CCL17 messenger RNA in adult B-cell ALL. Methods: A real-time quantitative reverse transcription-polymerase chain reaction assay based on TaqMan fluorescence methodology was used to quantify the CCL17 mRNA copy number in the bone marrow cells from patients with adult leukemia and in 16 human hematologic malignant cell lines. Normal marrow samples from the allogeneic stem cell transplantation donors were served as control. Informed consent was obtained for every marrow sample. Results: Expression levels of the CCL17 gene in leukemic cell lines, leukemia patients and normal donor marrow are shown in Figure 1. These results showed that the relative levels of CCL17 gene expression in marrow from 189 newly diagnosed B-cell ALL(median 0.23%; range 0%¡«69000%) was significantly higher than those of bone marrow from the 43 healthy donors (median 0.05%; range 0%¡«6.87%;P =0.0007). Significant CCL17 mRNA overexpression was found in the de novo B-cell ALL patients compared with 102 treated B-cell ALL patients(median 0.02%; range 0%¡«3339%) who achieved complete remission or 70 de novo AML (median 0.02%; range 0%¡«9.132%;P¡¯s 〈 0.0001). The expression levels of CCL17 was higher in 21 refractory/relapsed B-cell ALL patients (median 0.68%; range 0.003%¡«13490%) than that newly diagnosed B-cell ALL, but no statistical significant difference was observed (P=0.34). Besides, no statistical significant difference was observed in 16 newly diagnosed T-cell ALL(median 0.06%, range 0%¡«9.947%), 70 AML and 43 healthy donors (P¡¯s 〉 0.05), but it was higher in SupB15 and Nalm-6 cells from B-cell ALL cell lines than in other cells from AML or T-cell ALL cell lines. Conclusion: These results suggest that abnormal expression of CCL17 in leukemia may be involved in the pathomechanism of B-cell ALL. Figure 1 A: CCL17 expression levels in B-cell ALL and healthy donors( ** represent P 〈 0.01). B: CCL17 expression levels in human hematologic malignant cell lines. Figure 1. A: CCL17 expression levels in B-cell ALL and healthy donors( ** represent P 〈 0.01). / B: CCL17 expression levels in human hematologic malignant cell lines. Disclosures No relevant conflicts of interest to declare.
Type of Medium:
Online Resource
ISSN:
0006-4971
,
1528-0020
DOI:
10.1182/blood.V128.22.5157.5157
Language:
English
Publisher:
American Society of Hematology
Publication Date:
2016
detail.hit.zdb_id:
1468538-3
detail.hit.zdb_id:
80069-7
