Interleukin-10 gene promoter polymorphisms influence the clinical outcome of diffuse large B-cell lymphoma

Lech-Maranda, Ewa; Baseggio, Lucile; Bienvenu, Jacques; Charlot, Carole; Berger, Françoise; Rigal, Dominique; Warzocha, Krzysztof; Coiffier, Bertrand; Salles, Gilles

doi:10.1182/blood-2003-06-1850

Cited by 161 publications

(143 citation statements)

References 38 publications

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“…In NHL, SNPs of several genes have been previously related to lymphoma susceptibility, such as genes coding for xenobiotic proteins (GSTT1, PON1, Methionine synthase), 26,27 inflammation regulator cytokines (IL1, IL10, TNFa), [28][29][30] mismatch repairing elements (hMSH2), 31 or oncoproteins (H-ras 1). 32 Since BCL6 plays a crucial role during both normal B-cell maturation and lymphomagenesis, it has been hypothesized that constitutional or acquired mutations of putative functional elements may impact on lymphoma predisposition or lymphoma outcome.…”

Section: Discussionmentioning

confidence: 99%

Clinical and biological relevance of single-nucleotide polymorphisms and acquired somatic mutations of the BCL6 first intron in follicular lymphoma

et al. 2005

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Genetic modifications of the BCL6 gene in lymphoma include translocations, deletions, and somatic mutations (SM) of the 5 0 noncoding region. Three single-nucleotide polymorphisms (SNPs) of the major mutation cluster region (MMC) have been reported, including two substitutions (397G/C, 502G/A) and one deletion (520DT). Clinical and biological relevance of these SNPs are unknown. Based on a case-control study, BCL6 SNPs frequencies were assessed in 97 t(14;18) follicular lymphomas (FL) and in 54 lymphomas with 3q27 rearrangement. Allele frequencies were similar in the FL and controls groups. The 397 G/C genotype was correlated to a higher-grade transformation risk (P ¼ 0.02). SM were observed in 39.1% of FL and were characterized by a clustering distribution (hot spots spanning position 420-435, 106-127, and 590-600). No correlation between genotypes or acquired mutational status and BCL6 expression was demonstrated. However, gel mobility-shift assays, using SNPs containing probes show results representative for protein/DNA complexes. This study demonstrates that the first BCL6 intron is a highly variable region as a consequence of both SNP and SM, which may contribute to biology and outcome of FL.

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Section: Discussionmentioning

confidence: 99%

Clinical and biological relevance of single-nucleotide polymorphisms and acquired somatic mutations of the BCL6 first intron in follicular lymphoma

et al. 2005

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“…[16][17][18][19][20][21] Increased IL-10 plasma levels and poor outcome of some lymphoma entities have been shown, suggesting an role for IL-10 in lymphoma development. 3,4,9,22 Recently Lech-Maranda and co-workers reported that homozygocity for À1087A (rs1800896 A/G) of the IL-10 promoter is associated with lower rates of complete remission and lower overall survival (OS) in patients with diffuse large B-cell lymphoma (DLBCL), whereas Berglund and co-workers showed an absence of such an association. 22,23 In a recent epidemiological multicenter study, evidence was provided that for carriers of the IL-10 À3538A allele (rs1800890 A/T) the risk of NHL is doubled, but this was not verified by a follow-up study.…”

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confidence: 98%

The interleukin-10 gene promoter polymorphism −1087AG does not correlate with clinical outcome in non-Hodgkin's lymphoma

Kube

Klöss

et al. 2007

Genes Immun

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“…26,27 In fact, increased serum levels of IL-10 in diffuse large B cell lymphoma was detected in 20% of NHL patients 26,28 and was correlated with poor prognosis including significantly shortened overall survival (OS) and disease-free survival (DFS). 26,29,30 It was shown that IL-10 is also produced by MDSCs.…”

Section: Introductionmentioning

confidence: 99%

Characterization of the myeloid-derived suppressor cell subset regulated by NK cells in malignant lymphoma

et al. 2015

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TNFa, tumor necrosis factor a; VEGF, vascular endothelial growth factor.Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population with the ability to suppress immune responses and are currently classified into three distinct MDSC subsets: monocytic, granulocytic and non-monocytic, and non-granulocytic MDSCs. Although NK cells provide an important first-line defense against newly transformed cancer cells, it is unknown whether NK cells can regulate MDSC populations in the context of cancer. In this study, we initially found that the frequency of MDSCs in non-Hodgkin lymphoma (NHL) patients was increased and inversely correlated with that of NK cells, but not that of T cells. To investigate the regulation of MDSC subsets by NK cells, we used an EL4 murine lymphoma model and found the non-monocytic and non-granulocytic MDSC subset, i.e., Gr1 C CD11b C Ly6G med Ly6C med MDSC, is increased after NK cell depletion. The MDSC population that expresses MHC class II, CD80, CD124, and CCR2 is regulated mainly by CD27 C CD11b C NK cells. In addition, this MDSC subset produces some immunosuppressive cytokines, including IL-10 but not nitric oxide (NO) or arginase. We also examined two subsets of MDSCs (CD14 C HLA-DR ¡ and CD14 ¡ HLA-DR ¡ MDSC) in NHL patients and found that higher IL-10-producing CD14 C HLA-DR ¡ MDSC subset can be seen in lymphoma patients with reduced NK cell frequency in peripheral blood. Our analyses of MDSCs in this study may enable a better understanding of how MDSCs manipulate the tumor microenvironment and are regulated by NK cells in patients with lymphoma.

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Interleukin-10 gene promoter polymorphisms influence the clinical outcome of diffuse large B-cell lymphoma

Cited by 161 publications

References 38 publications

Clinical and biological relevance of single-nucleotide polymorphisms and acquired somatic mutations of the BCL6 first intron in follicular lymphoma

Clinical and biological relevance of single-nucleotide polymorphisms and acquired somatic mutations of the BCL6 first intron in follicular lymphoma

The interleukin-10 gene promoter polymorphism −1087AG does not correlate with clinical outcome in non-Hodgkin's lymphoma

Characterization of the myeloid-derived suppressor cell subset regulated by NK cells in malignant lymphoma

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