CXCL12 rs1801157 polymorphism in patients with breast cancer, hodgkin's lymphoma, and non-hodgkin's lymphoma
Chemokines and their receptors regulate the trafficking of immune cells during their development, inflammation, and tissue repair. The single‐nucleotide polymorphism (SNP) rs1801157 (previously known as CXCL12‐A/ stromal cell‐derived factor‐1 (SDF1)‐3′A) in CXCL12/SDF1 gene was assessed in breast ca...
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Veröffentlicht in: | Journal of clinical laboratory analysis 2009, Vol.23 (6), p.387-393 |
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Zusammenfassung: | Chemokines and their receptors regulate the trafficking of immune cells during their development, inflammation, and tissue repair. The single‐nucleotide polymorphism (SNP) rs1801157 (previously known as CXCL12‐A/ stromal cell‐derived factor‐1 (SDF1)‐3′A) in CXCL12/SDF1 gene was assessed in breast cancer, Hodgkin's lymphoma (HL), and non‐Hodgkin's lymphoma (NHL), since the chemokine CXCL12, previously known as SDF1, and its receptor CXCR4 regulate leukocyte trafficking and many essential biological processes, including tumor growth, angiogenesis, and metastasis of different types of tumors. Genotyping was performed by PCR‐RFLP (polymerase chain reaction followed by restriction fragment length polymorphism) using a restriction enzyme HpaII cleavage. No significant difference was observed in genotype distribution between breast cancer patients (GG: 57.3%; GA: 39.8%; AA: 2.9%) and healthy female controls (GG: 62.9%; GA: 33%; AA: 4.1%) nor between HL patients (GG: 61.1%; GA:27.8%; AA: 11.1%) and healthy controls (GG: 65.6%; GA: 28.9%; AA: 5.5%), whereas a significant difference was observed in genotype distribution between NHL patients (GG: 51.4%; GA: 47.1%; AA: 1.5%) and healthy controls (GG: 65.6%; GA: 28.9%; AA: 5.5%). Further studies will be necessary to elucidate the cancer chemokine network. However, this study suggests that CXCL12 rs1801157 polymorphism may have important implications in the pathogenesis of NHL. J. Clin. Lab. Anal. 23:387–393, 2009. © 2009 Wiley‐Liss, Inc. |
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ISSN: | 0887-8013 1098-2825 1098-2825 |
DOI: | 10.1002/jcla.20346 |