Association studies of CTLA-4, CD28, and ICOS gene polymorphisms with B-cell chronic lymphocytic leukemia in the Polish population

Suwalska, Katarzyna; Pawlak, Edyta; Karabon, Lidia; Tomkiewicz, Anna; Dobosz, Tadeusz; Urbaniak-Kujda, Donata; Kuliczkowski, Kazimierz; Wołowiec, Dariusz; Jedynak, Anna; Frydecka, Irena

doi:10.1016/j.humimm.2008.01.014

Cited by 53 publications

(66 citation statements)

References 43 publications

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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: 77%

<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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Section: Introductionmentioning

confidence: 77%

<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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“…Therefore the [T] allele may contribute to the upregulation of the expression of the down-regulatory CTLA-4 molecule, inhibition of the activation of T lymphocytes, and eventually limitation of the potency of antitumor immunity, and in that way susceptibility to cancer. Previously we have shown an association between this promoter polymorphism and B-cell chronic lymphocytic leukemia [30]. 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].…”

Section: Discussionmentioning

confidence: 80%

“…Interestingly, the opposite results for this SNP were shown for mucosa-associated lymphoid tissue lymphoma [43] and multiple myeloma [44], while no associations with cancer risk were observed for colorectal cancer [45], chronic lymphocytic leukemia [30], cervical squamous cell carcinoma [29], malignant melanoma [46], or non-malignant melanoma [47].…”

Section: Discussionmentioning

confidence: 87%

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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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“…CTLA-4 has also been implicated to serve functions in neoplastic cells, including B cell chronic lymphocytic leukaemia (10), non-Hodgkin's lymphoma (11), breast cancer (12), lung cancer (13), melanoma (14), gastric cancer (15), colorectal cancer (15), cervical cancer (16) and oesophageal carcinoma (17). Prior studies indicated that CTLA-4 expression in tumour cells is associated with poor prognosis (12,17).…”

Section: Introductionmentioning

confidence: 99%

Potential function of CTLA‑4 in the tumourigenic capacity of melanoma stem cells

Zhang

Dang

et al. 2018

Oncol Lett

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Abstract. Extensive clinical evidence supports that cytotoxic T lymphocyte antigen-4 (CTLA-4) is expressed in a variety of human malignant tumour cells in addition to T cells. In certain types of cancer, the overexpression of CTLA-4 is associated with poor patient prognosis. However, few studies have demonstrated the effects of tumour-intrinsic CTLA-4 in cancer stem cells, including melanoma stem cells (MSCs). In the present study, it was demonstrated that melanoma cell-intrinsic CTLA-4 induced tumour cell proliferation in vitro and suppressed tumour cell apoptosis. Furthermore, CTLA-4 was expressed in aldehyde dehydrogenase (ALDH) + MSCs. CTLA-4 inhibited MSCs proliferation in vitro by blocking antibodies and significantly downregulated ALDH1A1, ALDH1A3 and ALDH2 mRNA expression (P<0.01). Functionally, blocking CTLA-4 in melanoma cell lines suppressed the properties of stem-like cells, including ALDH activity and significantly suppressed the ability of these cells to form spheres in vitro (P<0.05). In addition, the blocking of CTLA-4 in melanoma cells suppressed the properties of stem-like cells in vivo, including the capacity for tumourigenesis. The presence of residual ALDH + MSCs within the tumour was observed, and the blocking CTLA-4 significantly decreased the number of residual ALDH + MSCs in vivo (P<0.01). Altogether, these results indicate the identification of a novel mechanism underlying melanoma progression in the present study and that CTLA-4-targeted therapy may benefit candidate CTLA-4-targeted therapy by improving the long-term outcome for patients with advanced stages of melanoma.

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Association studies of CTLA-4, CD28, and ICOS gene polymorphisms with B-cell chronic lymphocytic leukemia in the Polish population

Cited by 53 publications

References 43 publications

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

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

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

Potential function of CTLA‑4 in the tumourigenic capacity of melanoma stem cells

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