Stromal cell-derived factor-1 (SDF-1) gene and susceptibility of Iranian patients with lung cancer

Razmkhah, Mahboobeh; Doroudchi, Mehrnoosh; Ghayumi, Mohammad Ali; Erfani, Nasrollah; Ghaderi, Abbas

doi:10.1016/j.lungcan.2005.04.014

Cited by 53 publications

(44 citation statements)

References 28 publications

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“…Of note, the CXCL12-801A allelic variant has been associated with a higher incidence of breast and lung cancer, acute myeloid leukemia, lymphoma and chronic myeloproliferative disease, and with a slower progression to AIDS. 31,[34][35][36][37][38] An interaction between CXCL12 and CXCR4 is critical for the trafficking of hematopoietic progenitor cells in the BM, and an interruption of this interaction can affect…”

Section: Discussionmentioning

confidence: 99%

Impact of constitutional polymorphisms in VCAM1 and CD44 on CD34+ cell collection yield after administration of granulocyte colony-stimulating factor to healthy donors

Martín-Antonio¹,

Carmona²,

Falantes³

et al. 2010

Haematologica

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The online version of this article has a Supplementary Appendix. BackgroundThe number of CD34 + cells mobilized from bone marrow to peripheral blood after administration of granulocyte colony-stimulating factor varies greatly among healthy donors. This fact might be explained, at least in part, by constitutional differences in genes involved in the interactions tethering CD34 + cells to the bone marrow. Design and MethodsWe analyzed genetic characteristics associated with CD34 + cell mobilization in 112 healthy individuals receiving granulocyte colony-stimulating factor (filgrastim; 10 μg/kg; 5 days). ResultsGenetic variants in VCAM1 and in CD44 were associated with the number of CD34 + cells in peripheral blood after granulocyte colony-stimulating factor administration (P=0.02 and P=0.04, respectively), with the quantity of CD34 + cells ¥10 6 /kg of donor (4.6 versus 6.3; P<0.001 and 7 versus 5.6; P=0.025, respectively), and with total CD34 + cells ¥10 6 (355 versus 495; P=0.002 and 522 versus 422; P=0.012, respectively) in the first apheresis. Of note, granulocyte colonystimulating factor administration was associated with complete disappearance of VCAM1 mRNA expression in peripheral blood. Moreover, genetic variants in granulocyte colony-stimulating factor receptor (CSF3R) and in CXCL12 were associated with a lower and higher number of granulocyte colony-stimulating factor-mobilized CD34 + cells/μL in peripheral blood (81 versus 106; P=0.002 and 165 versus 98; P=0.02, respectively) and a genetic variant in CXCR4 was associated with a lower quantity of CD34 + cells ¥10 6 /kg of donor and total CD34 + cells ¥10 6 (5.3 versus 6.7; P=0.02 and 399 versus 533; P=0.01, respectively). ConclusionsIn conclusion, genetic variability in molecules involved in migration and homing of CD34 + cells influences the degree of mobilization of these cells.

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Section: Discussionmentioning

confidence: 99%

Impact of constitutional polymorphisms in VCAM1 and CD44 on CD34+ cell collection yield after administration of granulocyte colony-stimulating factor to healthy donors

Martín-Antonio¹,

Carmona²,

Falantes³

et al. 2010

Haematologica

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“…For example, mice completely deficient in either SDF-1 or CXCR4 die perinatally from multiple developmental defects in the brain, gut, and bone marrow (10). Humans bearing a relatively common human SDF-1 polymorphism (801A) that is thought to decrease SDF-1 expression (57) are at higher risk for certain conditions that might theoretically be exacerbated by low IL-10 levels, including transmitting HIV-1 maternally (58), developing early onset type I diabetes after a shorter lag time (59), and developing lung cancer (60). In addition, rare mutations in CXCR4 that truncate CXCR4 and enhance some SDF-1-dependent signals are linked to WHIM syndrome, which is characterized by extensive human papillomavirus infection in addition to other pathologies (61).…”

Section: Discussionmentioning

confidence: 99%

Haplotype-Independent Costimulation of IL-10 Secretion by SDF-1/CXCL12 Proceeds via AP-1 Binding to the Human IL-10 Promoter

Kremer

Kumar

Hedin

2007

The Journal of Immunology

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Costimulation by the chemokine, stromal cell-derived factor-1 (SDF-1)/CXCL12, has been shown to increase the amount of IL-10 secreted by TCR-stimulated human T cells; however, the molecular mechanisms of this response are unknown. Knowledge of this signaling pathway may be useful because extensive evidence indicates that deficient IL-10 secretion promotes autoimmunity. The human IL-10 locus is highly polymorphic. We report in this study that SDF-1 costimulates IL-10 secretion from T cells containing all three of the most common human IL-10 promoter haplotypes that are identified by single-nucleotide polymorphisms at −1082, −819, and −592 bp (numbering is relative to the transcription start site). We further show that SDF-1 primarily costimulates IL-10 secretion by a diverse population of CD45RA− (“memory”) phenotype T cells that includes cells expressing the presumed regulatory T cell marker, Foxp3. To address the molecular mechanisms of this response, we showed that SDF-1 costimulates the transcriptional activities in normal human T cells of reporter plasmids containing 1.1 kb of all three of the common IL-10 promoter haplotypes. IL-10 promoter activity was ablated by mutating two nonpolymorphic binding sites for the AP-1 transcription factor, and chromatin immunoprecipitation assays of primary human T cells revealed that SDF-1 costimulation enhances AP-1 binding to both of these sites. Together, these results delineate the molecular mechanisms responsible for SDF-1 costimulation of T cell IL-10 secretion. Because it is preserved among several human haplotypes and in diverse T cell populations including Foxp3+ T cells, this pathway of IL-10 regulation may represent a key mechanism for modulating expression of this important immunoregulatory cytokine.

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“…The most compelling evidence for the role of the SdF-1 G→a polymorphism in malignancy is provided by previous genotype and allele-frequency studies showing that this specific polymorphism is associated with a susceptibility to breast, lung and prostate cancer (36,38,(40)(41)(42). in the current study, we attempted to determine whether an association exists between this SdF-1 gene variant and pancreatic cancer.…”

Section: Discussionmentioning

confidence: 92%

“…on the other hand, current studies on colorectal cancer have failed to suggest a serious impact of the SdF-1 polymorphism on the risk of colorectal cancer development (43,44). Hypothetically, different mechanisms involved in the pathogenesis of colorectal carcinogenesis, along with a host of modifying molecular events, may account for this lack of association, in contrast to the documented role of the SdF-1 polymorphism in breast, lung, prostate and pancreatic cancer (36,38,(40)(41)(42). in other words, based on tissue origin, the influence of the sDF-1 gene polymorphism may contribute differentially between malignancies in mediating tumor progression, angiogenesis, metastasis and leukocyte migration.…”

Section: Discussionmentioning

confidence: 97%

“…This single nucleotide polymorphism of the SdF-1 gene has been investigated in type 1 diabetes and HiV-1 infection, and has been reported to be associated with an increased risk of non-Hodgkin's lymphoma in HiV-1 infected individuals (30,34,35). The SdF-1 G→a polymorphism has been investigated in various cancers, but no information is currently available regarding its role in pancreatic cancer (36)(37)(38)(39)(40)(41)(42)(43)(44).…”

Section: Introductionmentioning

confidence: 99%

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Analysis of the stromal cell-derived factor 1-3'A gene polymorphism in pancreatic cancer

Theodoropoulos

Panoussopoulos²,

Michalopoulos³

et al. 2010

Mol Med Rep

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Abstract.Stromal cell derived factor-1 (SdF-1), a cXc chemokine that plays an important role in the tumor growth, angiogenesis and metastasis of tumor cells, has a polymorphism at position 801 of its 3'-untranslated region, known as SdF1-3' a. The SdF1-3' a polymorphism has been investigated in various types of cancer, but no information is currently available on its role in pancreatic cancer. in this study, 80 pancreatic cancer patients and 160 normal healthy control subjects were investigated for the genotype and allelic frequencies of the SdF-1 gene using Pcr-rFlP. The genotype frequencies for GG, Ga and aa were 21.25, 77.5 and 1.25% in patients, and 42.5, 55 and 2.5% in healthy subjects, respectively. The a carrier group (Ga+aa genotype) and the a allele were overrepresented among the patients with pancreatic cancer (p=0.015 and p=0.031, respectively). The Ga+aa genotype was statistically correlated with an advanced T stage and the presence of lymph node metastasis, and displayed a clear trend towards significance in relation to the presence of distant metastatic disease (p=0.061). Only T stage was significantly related to a allele frequency (p=0.004). SdF1-3' a allele carriers were more prevalent among cancer patients than among normal subjects. SdF1-3' a allele carrier status may imply a higher risk of pancreatic cancer, while the presence of the a allele in pancreatic cancer patients may be related to aggressive features of this malignancy.

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Stromal cell-derived factor-1 (SDF-1) gene and susceptibility of Iranian patients with lung cancer

Cited by 53 publications

References 28 publications

Impact of constitutional polymorphisms in VCAM1 and CD44 on CD34+ cell collection yield after administration of granulocyte colony-stimulating factor to healthy donors

Impact of constitutional polymorphisms in VCAM1 and CD44 on CD34+ cell collection yield after administration of granulocyte colony-stimulating factor to healthy donors

Haplotype-Independent Costimulation of IL-10 Secretion by SDF-1/CXCL12 Proceeds via AP-1 Binding to the Human IL-10 Promoter

Analysis of the stromal cell-derived factor 1-3'A gene polymorphism in pancreatic cancer

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