High incidence of CTLA-4 AA (CT60) polymorphism in renal cell cancer

Cózar, J.M.; Romero, José María; Aptsiauri, Natalia; Vázquez, Fernando; Vilchez, Jose R.; Tallada, M; Garrido, Federico; Ruiz‐Cabello, Francisco

doi:10.1016/j.humimm.2007.05.002

Cited by 78 publications

(59 citation statements)

References 25 publications

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“…Moreover, it was found by us and others that the same allele confers susceptibility to female-related cancers: sporadic breast cancer [31,48], and cervical cancer [29,32] as well as non-small cell lung cancer in women [24]. In contrast to our results CTLA-4g.319C>T polymorphism was not associated with lung cancer (without stratification by gender) [41] or other cancers, such as colon cancer [42], colorectal cancer [52] or multiple myeloma [44]. The meta-analysis performed by Zhang et al [49] indicated this polymorphism as related to cancer risk in the Europeans.…”

Section: Discussioncontrasting

confidence: 99%

“…It has also been postulated that the CTLA-4c.49A>G polymorphism in the leader sequence may influence rates of endocytosis or surface trafficking [39], the glycosylation of CTLA-4, and intracellular/surface partitioning, and in that way alter inhibitory function of that molecule [40]. The role of the CTLA-4c.49A>G[A] allele as a risk factor for cancer development was shown in many types of cancers, such as esophageal cancer, gastric cardia cancer [41], nonHodgkin's lymphoma [28], breast cancer [27,41], and renal cancer [42].…”

Section: Discussionmentioning

confidence: 99%

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Is the Genetic Background of Co-Stimulatory CD28/CTLA-4 Pathway the Risk Factor for Prostate Cancer?

Karabon

Tupikowski

Tomkiewicz

et al. 2017

Pathol. Oncol. Res.

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The impairment of immunological surveillance caused by aberrant T cell activation can lead to an inadequate anti-tumor response. Therefore, deregulation in co-stimulatory pathway might be associated with cancer susceptibility. Here we undertook a prospective study to investigate whether genetic variations in gene encoding molecule CD28 and CTLA-4 playing pivotal role in regulating adoptive immune response can influence susceptibility to prostate cancer. Single nucleotide polymorphisms (SNPs) in CTLA-4 and CD28 genes were genotyped in 301 prostate cancer (PCa) patients and 301 controls. The distributions of the genotypes and haplotypes in the CTLA-4/CD28 SNPs were similar in both studied groups. However, the overrepresentation of carriers of CTLA4c.49A>G[A] allele and carriers of CTLA-4g.319C>T[T] allele in PCa as compared to controls was observed (p = 0.082 and p = 0.13, respectively). The risk of disease was higher (OR 1.78) for carriers of both susceptibility alleles as compared to carriers of protective genotypes (p = 0.03). The CTLA4c.49A>G and CTLA-4g.319C>T SNPs might be considered as low risk susceptibility locus for PCa.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Is the Genetic Background of Co-Stimulatory CD28/CTLA-4 Pathway the Risk Factor for Prostate Cancer?

Karabon

Tupikowski

Tomkiewicz

et al. 2017

Pathol. Oncol. Res.

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“…None of the described ICOS SNPs leads to changes in amino acid, while a few have been demonstrated to be functional variants [17][18][19][20]. The chromosomal region of 2q33 harboring the CD28, CTLA-4, and ICOS gene family has been described as carrying predisposing genes for several autoimmune diseases [19,[21][22][23] and, recently, for cancer [24][25][26]. Our recent results indicate that the ICOS microsatellite polymorphism c.1554+4GT(8_15) is associated with susceptibility to B-CLL [24].…”

Section: Introductionmentioning

confidence: 79%

<i>ICOS</i> gene polymorphisms in B-cell chronic lymphocytic leukemia in the Polish population

Karabon¹,

Jedynak²,

Tomkiewicz³

et al. 2011

Folia Histochem Cytobiol.

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Abstract:There is strong evidence that altered immunological function entails an increased risk of B-cell chronic lymphocytic leukemia (B-CLL). The main mechanism of an anti-tumor response depends on T-cell activation. Unlike the constitutively expressed CD28, inducible costimulatory molecule (ICOS) is expressed on the T-cell surface after activation. ICOS enhances all the basic T-cell responses to a foreign antigen, namely proliferation, secretion of lymphokines, the upregulation of molecules that mediate cell-cell interaction, and effective help for antibody secretion by B cells. ICOS is essential for both efficient interaction between T and B cells and normal antibody responses to T cell-dependent antigens. It does not upregulate the production of interleukin-2, but superinduces the synthesis of interleukin-10. Our previous results indicated the ICOS gene has a role as a susceptibility locus to B-CLL. Therefore an extended study was undertaken to evaluate the association between four ICOS polymorphisms (which were recently described as functional ones) and susceptibility to B-CLL in the Polish population. A case-control study of 296 individuals, including 146 B-CLL patients, was conducted on four polymorphisms in the ICOS gene. Genotyping of the polymorphisms ICOS ISV1+173T>C (rs10932029), ICOSc.1624C>T (rs10932037), ICOSc.2373G>C (rs4675379), and ICOSc.602A>C (rs10183087) was carried out using allelic discrimination methods with the TaqMan ® SNP Genotyping Assay. There were no statistically significant differences in the allele, genotype, or haplotype distributions between B-CLL patients and healthy controls for any of the investigated polymorphic markers in the ICOS gene.

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“…CTLA-4 genotype and AML relapse A Pérez-García et al Moreover, a high incidence of CTLA-4 CT60 AA and þ 49 AA genotypes has been reported in patients with renal cell cancer, suggesting a role for the CTLA4 gene in tumor development. 13 In other words, the presence of a more tolerogenic CTLA4 genotype could represent a potential form of tumor immune evasion. However, little is known regarding the impact of the CTLA-4 genotype on the maintenance of cancer remission once the treatment with chemotherapy has been successful.…”

Section: -12mentioning

confidence: 99%

CTLA-4 genotype and relapse incidence in patients with acute myeloid leukemia in first complete remission after induction chemotherapy

et al. 2008

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High incidence of CTLA-4 AA (CT60) polymorphism in renal cell cancer

Cited by 78 publications

References 25 publications

Is the Genetic Background of Co-Stimulatory CD28/CTLA-4 Pathway the Risk Factor for Prostate Cancer?

Is the Genetic Background of Co-Stimulatory CD28/CTLA-4 Pathway the Risk Factor for Prostate Cancer?

<i>ICOS</i> gene polymorphisms in B-cell chronic lymphocytic leukemia in the Polish population

CTLA-4 genotype and relapse incidence in patients with acute myeloid leukemia in first complete remission after induction chemotherapy

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