Placental isoform glutathione S-transferase and P-glycoprotein expression in advanced nonsmall cell lung cancer

Vlachogeorgos, George S.; Manali, Effrosini D.; Blana, Ekaterini; Legaki, Stella; Karagiannidis, Napoleon; Polychronopoulos, Vlasis; Roussos, Charis

doi:10.1002/cncr.23981

Cited by 14 publications

(11 citation statements)

References 28 publications

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“…Recent cell line studies [30] report a positive correlation between GST-PI expression and resistance to cisplatin which would underline the previous findings of Arai et al [30]. Later clinical studies also report a prognostic role of GST-PI expression in NSCLC patients treated with cisplatinum-based chemoradiation [31]. Interestingly we found a difference in the GST-PI mRNA expression and NSCLC histology.…”

Section: Discussionsupporting

confidence: 75%

Glutathione S-transferase PI (GST-PI) mRNA expression and DNA methylation is involved in the pathogenesis and prognosis of NSCLC

et al. 2012

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Section: Discussionsupporting

confidence: 75%

Glutathione S-transferase PI (GST-PI) mRNA expression and DNA methylation is involved in the pathogenesis and prognosis of NSCLC

et al. 2012

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“…Some clinical studies showed a correlation between lack of response187, 249–251 or increased risk of relapse or shortened survival187 and high tumor187, 249–251 or serum252 GST-pi expression in NSCLC patients treated with platinum-vindesine249, platinum-etoposide250, cisplatin, ifosfamide, vinblastine and radiation187 or various platinum-based regimens251, 252 for advanced disease249–252, for locally advanced disease187, or with adjuvant cisplatin-based chemotherapy for resected disease246. NSCLC patients treated with platinum-based regimens who had the GST-pi exon 6 wild type host genotype (Ala/Ala) had significantly worse survival than did patients with the variant genotype (Ala/Val or Val/Val), while GSTpi exon 5 genotype was not associated with survival253.…”

Section: 0 Drug Detoxificationmentioning

confidence: 99%

“…In NSCLC, there was a significant correlation of tumor P-gp IHC expression with response in 2 studies using paclitaxel and a platinum185, 186 and in one study using cisplatin, ifosfamide, vinblastine and radiation187, and P-gp expression also correlated inversely with survival in this latter study187. The MDR1 3435 CC host genotype was associated with a significantly better response to cisplatin-vinorelbine compared with the combined 3435 CT and TT genotypes, and patients with the 2677G-3435C haplotype also had significantly better responses to chemotherapy compared to patients with other haplotypes combined 188.…”

Section: 0 Drug Effluxmentioning

confidence: 99%

Tumor and host factors that may limit efficacy of chemotherapy in non-small cell and small cell lung cancer

Stewart

2010

Critical Reviews in Oncology/Hematology

161

157

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While chemotherapy provides useful palliation, advanced lung cancer remains incurable since those tumors that are initially sensitive to therapy rapidly develop acquired resistance. Resistance may arise from impaired drug delivery, extracellular factors, decreased drug uptake into tumor cells, increased drug efflux, drug inactivation by detoxifying factors, decreased drug activation or binding to target, altered target, increased damage repair, tolerance of damage, decreased proapoptotic factors, increased antiapoptotic factors, or altered cell cycling or transcription factors. Factors for which there is now substantial clinical evidence of a link to small cell lung cancer (SCLC) resistance to chemotherapy include MRP (for platinum-based combination chemotherapy) and MDR1/P-gp (for non-platinum agents). SPECT MIBI and Tc-TF scanning appears to predict chemotherapy benefit in SCLC. In non-small cell lung cancer (NSCLC), the strongest clinical evidence is for taxane resistance with elevated expression or mutation of class III β-tubulin (and possibly α tubulin), platinum resistance and expression of ERCC1 or BCRP, gemcitabine resistance and RRM1 expression, and resistance to several agents and COX-2 expression (although COX-2 inhibitors have had minimal impact on drug efficacy clinically). Tumors expressing high BRCA1 may have increased resistance to platinums but increased sensitivity to taxanes. Limited early clinical data suggest that chemotherapy resistance in NSCLC may also be increased with decreased expression of cyclin B1 or of Eg5, or with increased expression of ICAM, matrilysin, osteopontin, DDH, survivin, PCDGF, caveolin-1, p21WAF1/CIP1, or 14-3-3sigma, and that IGF-1R inhibitors may increase efficacy of chemotherapy, particularly in squamous cell carcinomas. Equivocal data (with some positive studies but other negative studies) suggest that NSCLC tumors with some EGFR mutations may have increased sensitivity to chemotherapy, while K-ras mutations and expression of GST-pi, RB or p27kip1 may possibly confer resistance. While limited clinical data suggest that p53 mutations are associated with resistance to platinum-based therapies in NSCLC, data on p53 IHC positivity are equivocal. To date, resistance-modulating strategies have generally not proven clinically useful in lung cancer, although small randomized trials suggest a modest benefit of verapamil and related agents in NSCLC.

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“…Many studies have reported the relationship between GSTP1 polymorphisms and prognosis of advanced NSCLC, but the results are inconclusive (Booton et al, 2006;Lu et al, 2006;Vlachogeorgos et al, 2008;Kalikaki et al, 2009;Sun et al, 2010;Lv et al, 2014;Han et al, 2015). Sun et al (2010), Han et al (2015) and Lv et al, (2014) conducted studies in Chinese populations and reported that GSTP1 genetic variations might be the predictive markers for the treatment outcome of advanced NSCLC.…”

Section: Discussionmentioning

confidence: 99%

“…Sun et al (2010), Han et al (2015) and Lv et al, (2014) conducted studies in Chinese populations and reported that GSTP1 genetic variations might be the predictive markers for the treatment outcome of advanced NSCLC. Booton et al (2006), Vlachogeorgos et al (2008) and Lu et al (2006) carried out studies in Caucasians and they reported that GSTP1 polymorphisms may predict response to treatment and survival in patients with advanced NSCLC. However, Kalikaki et al (2009) did not revealed a significant correlation between GSTP1 genetic polymorphisms and treatment outcomes in advanced NSCLC.…”

Section: Discussionmentioning

confidence: 99%

Glutathione S-transferase pi polymorphism contributes to the treatment outcomes of advanced non-small cell lung cancer patients in a Chinese population

et al. 2016

Genet. Mol. Res.

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ABSTRACT. We analyzed the association between polymorphisms in three glutathione S-transferase genes (GSTP1, GSTM1, and GSTT1) and the treatment outcome for advanced non-small cell lung cancer (NSCLC). We recruited 284 NSCLC patients at advanced significantly decreased risk of death from all causes in patients with NSCLC, and the HRs (95%CIs) were 0.52 (0.29-0.92) and 0.37 (0.17-0.79), respectively No significant association was observed between GSTM1 and GSTT1 polymorphisms and progression-free survival and overall survival in the NSCLC patients. In summary, we suggest that GSTP1 polymorphisms might influence the treatment outcome of advanced NSCLC patients, and our results could help improve individualized therapy.

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Placental isoform glutathione S-transferase and P-glycoprotein expression in advanced nonsmall cell lung cancer

Cited by 14 publications

References 28 publications

Glutathione S-transferase PI (GST-PI) mRNA expression and DNA methylation is involved in the pathogenesis and prognosis of NSCLC

Glutathione S-transferase PI (GST-PI) mRNA expression and DNA methylation is involved in the pathogenesis and prognosis of NSCLC

Tumor and host factors that may limit efficacy of chemotherapy in non-small cell and small cell lung cancer

Glutathione S-transferase pi polymorphism contributes to the treatment outcomes of advanced non-small cell lung cancer patients in a Chinese population

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