The ATP-binding cassette transporter ABCG2 (BCRP) and ABCB1 (MDR1) variants are not associated with disease susceptibility and disease phenotype in Hungarian patients with inflammatory bowel diseases

Fischer, Stephan; Lakatos, Lajos; Kovacs, A.; Molnár, Tünde; Altorjay, I; Papp, Mária; Tulassay, Z; Osztovits, Janos; Demeter, Pál; Tordai, Attila; Andrikovics, Hajnalka; Papp, Julius Gy.; Lakatos, P

doi:10.1055/s-2007-982655

Cited by 4 publications

(6 citation statements)

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“…Reduced expression of transporter protein is seen in several tissues as a result of the ABCG2 c.421 C/A polymorphism, which makes ABCG2 protein unstable, especially in the endoplasmic reticulum, thus increasing the vulnerability to denaturation (Furukawa et al, 2009;Kobayashi et al, 2005;Prasad et al, 2013;Tanaka et al, 2015). Our investigation found that the prevalence of the ABCG2 34G/A polymorphism in our healthy control group differed when compared with studies done by Bäckström et al (2003), Bosch et al (2005), however, it is comparable with studies conducted by Fischer et al (2007), Lee, Jeong, et al (2007), Słomka et al (2020), Wang et al (2004), Wang et al (2007). ABCG2 421AA and 34AA genotypes showed an elevated risk for advancement of HIV disease when patients with HIV infection were compared with healthy subjects (p = 0.49, OR: 2.49; p = 0.38, OR = 2.35).…”

Section: Discussionsupporting

confidence: 77%

ABCG2 polymorphisms and susceptibility to ARV‐associated hepatotoxicity

Singh,

Dhotre,

Shyamveer

et al. 2024

Molec Gen & Gen Med

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BackgroundThe ABCG2 421C/A polymorphism contributes significantly to the distribution and absorption of antiretroviral (ARV) regimens and is associated with the undesirable side effects of efavirenz.MethodsTo investigate this, we examined ABCG2 34G/A (rs2231137) and 421C/A (rs2231142) genetic variations in 149 HIV‐infected patients (116 without hepatotoxicity, 33 with ARV‐induced hepatotoxicity) and 151 healthy controls through the PCR‐restriction fragment length polymorphism (PCR‐RFLP) technique.Results and DiscussionThe ABCG2 34GA genotype and 34A allele indicated a risk for antiretroviral therapy‐associated hepatotoxicity development (p = 0.09, OR = 1.58, 95% CI: 0.93–2.69; p = 0.06, OR = 1.50, 95% CI: 0.98–2.30). The haplotype GA was associated with hepatotoxicity (p = 0.042, OR = 2.37, 95% CI: 1.04–5.43; p = 0.042, OR = 2.49, 95% CI: 1.04–5.96). Moreover, when comparing HIV patients with hepatotoxicity to healthy controls, the haplotype GA had an association with an elevated risk for the development of hepatotoxicity (p = 0.041, OR = 1.73, 95% CI: 1.02–2.93). Additionally, the association of the ABCG2 34GA genotype with the progression of HIV (p = 0.02, OR = 1.97, 95% CI: 1.07–3.63) indicated a risk for advanced HIV infection. Furthermore, the ABCG2 421AA genotype was linked to tobacco users and featured as a risk factor for the progression of HIV disease (p = 0.03, OR = 11.07, 95% CI: 1.09–270.89).ConclusionThe haplotype GA may enhance the risk of hepatotoxicity development and its severity. Individuals with the ABCG2 34A allele may also be at risk for the development of hepatotoxicity. Additionally, individuals with an advanced stage of HIV and the ABCG2 34GA genotype may be at risk for disease progression.

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Section: Discussionsupporting

confidence: 77%

ABCG2 polymorphisms and susceptibility to ARV‐associated hepatotoxicity

Singh,

Dhotre,

Shyamveer

et al. 2024

Molec Gen & Gen Med

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“…Few studies have evaluated the involvement of ABCB1 in anti-TNF agent response. No correlation between ABCB1 gene variants and response to infliximab was observed in Italian IBD patients (Palmieri et al, 2005) or in Hungarian patients (Fischer et al, 2007).…”

Section: Discussionmentioning

confidence: 87%

“…Few studies have evaluated the involvement of ABCB1 in anti‐TNF agent response. No correlation between ABCB1 gene variants and response to infliximab was observed in Italian IBD patients (Palmieri et al, ) or in Hungarian patients (Fischer et al, ). In our study, we found that the low levels of ABCB1 in patients are significantly restored by anti‐TNF treatment, reaching, in treated patients, levels similar to those of non‐IBD controls.…”

Section: Discussionmentioning

confidence: 99%

Mucosal gene expression changes induced by anti‐TNF treatment in inflammatory bowel disease patients

Milanesi

Dobre

Manuc

et al. 2019

Drug Development Research

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In the last two decades anti‐tumor necrosis factor (anti‐TNF) therapy for inflammatory bowel disease (IBD) has been widely used to induce and maintain clinical and endoscopical remission, completely changing management of the disease. In this study, we aimed to identify gene expression changes in inflamed mucosa from Crohn's disease and ulcerative colitis patients treated with 5‐aminosalicylic acid (5‐ASA) (N = 25) or anti‐TNF agents (N = 12) compared to drug‐free IBD patients (N = 12) and non‐IBD control subjects (N = 18). The mucosal expression of 84 genes previously associated with IBD was evaluated by qPCR. We found that both therapeutic regimens induce a decrease in LCN2, NOS2, and TFF1, the levels of which are overexpressed in drug‐free patients compared to non‐IBD control subjects. Interestingly, a stronger effect of anti‐TNF drugs was observed on LCN2 and TFF1 levels. However, 5‐ASA seems to induce a more robust reduction of NOS2 expression. Moreover, we found that anti‐TNF treatment significantly increased ABCB1, leading to levels similar to those found in non‐IBD control subjects.

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“…Nevertheless, in a meta-analysis including nine studies the association between C3435T and UC was confirmed [102]. Also studies on the G2677T SNP and IBD have yielded contradictory results [99,103]. However, a combined C3435T and G2677T haplotype was shown to be associated with UC.…”

Section: Mdr1mentioning

confidence: 95%