The polymorphism XRCC1 Arg194Trp and 8-hydroxydeoxyguanosine increased susceptibility to arsenic-related renal cell carcinoma

Hsueh, Yu Mei; Lin, Ying; Chen, Wei-Jen; Huang, Chao Yuan; Shiue, Horng Sheng; Pu, Yeong-Shiau; Chen, Chi-Hung; Su, Chien Tien

doi:10.1016/j.taap.2017.07.012

Cited by 10 publications

(13 citation statements)

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“…However, the underlying mechanism of follicular activation remains unclear. It has been demonstrated that the inhibitors of the Akt and mammalian target of rapamycin (mTOR) signaling pathway play a pivotal role in retaining follicular dormancy while the activators initiate the transition of primordial follicles into growing follicles (Hsueh, Kawamura, Cheng, & Fauser, 2017; Kallen, Polotsky, & Johnson, 2018). Therefore, the primordial follicle stockpile represents the “ovarian reserve” of potential fertility available to each individual, and interventions designed to keep primordial follicles in a dormant state would be expected to reduce the ovarian toxicity of cancer treatment and lengthen the reproductive lifespan of patients.…”

Section: Introductionmentioning

confidence: 99%

Rapamycin preserves the primordial follicle pool during cisplatin treatment in vitro and in vivo

Xie

Zhou

et al. 2020

Molecular Reproduction Devel

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Rapamycin has been proven to effectively inhibit the activation of primordial follicles while cisplatin-induced the loss of primordial follicles due to the overactivation of the primordial follicle stockpile. Whether rapamycin could inhibit the loss of primordial follicles induced by cisplatin is still unknown. The ovaries of neonatal Sprague Dawley rats were cultured in vitro in different doses of rapamycin (0.08, 0.16, and 0.32 μg/ml) and cisplatin (0.1, 0.4, and 0.8 μg/ml). The immature BALB/c mice were administered cisplatin with or without rapamycin by intraperitoneal injection. Ovaries were collected to analyze the histomorphology, the messenger RNA (mRNA) expression of anti-Mullerian hormone (AMH), growth differentiation factor 9 (GDF9), and bone morphogenetic protein 15 (BMP15) and the expression of key proteins of mammalian target of rapamycin (mTOR) pathway.Growing follicle counts of ovaries cultured in vitro in the R0.16 and R0.32 groups were decreased and the ratio of growing to primordial follicles was also decreased in a dose-dependent manner. In the C0.8 group, growing follicles were decreased compared with the other groups while the ratio was substantially increased in the C0.4 and C0.8 group. Co-treatment attenuated primordial follicle loss and reduced the upregulated ratio induced by cisplatin. Ovarian follicle dynamics in vivo was consistent with the in vitro results. Primordial follicles counts were statistically increased and the ratio was reduced in the rapamycin group compared with the control group. Primordial follicle counts were dramatically reduced in the cisplatin group whereas co-treatment with rapamycin slightly recovered its counts. There was no obvious difference in the number of growing follicles between the cisplatin group and other groups. The ratio was significantly increased in cisplatin-treated mice whereas decreased in the co-treatment group. The apoptosis rate of antral follicles in cisplatin-treated mice was higher than the other groups while the apoptosis rate was decreased in the co-treatment group in vivo. Compared with the control and rapamycin group, the mRNA expression of AMH, GDF9, and BMP15 were Abbreviations: AMH, anti-Mullerian hormone; BMP15, bone morphogenetic protein 15; CCK-8, cell counting kit-8; con, control group; FBS, fetal bovine serum; GDF9, growth differentiation factor 9; HE, hematoxylin and eosin; mTOR, mammalian target of rapamycin; mTORC1, mammalian target of rapamycin complex 1; PBS, phosphate-buffered solution; PFA, paraformaldehyde; POI, premature ovarian insufficiency; PTEN, phosphate and tension homology deleted on chromosome ten; qPCR, quantitative polymerase chain reaction; TSC1/TSC2, tuberous sclerosis complex; TUNEL, terminal deoxynucleotidyl transferase-mediated nick end labeling assay. downregulated in the cisplatin group. The co-treatment group recovered the mRNA expression of BMP15. In addition, the expression of key protein of mTOR pathway rpS6 and its phosphorylated forms were increased in the cisplatin-treated group while co-treatme...

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Section: Introductionmentioning

confidence: 99%

Rapamycin preserves the primordial follicle pool during cisplatin treatment in vitro and in vivo

Xie

Zhou

et al. 2020

Molecular Reproduction Devel

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“…A total of 22 studies describing 39 models that predict the risk of kidney cancer using genetic risk factors were identified and included in the narrative synthesis [ 15 , 17 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 ].…”

Section: Resultsmentioning

confidence: 99%

“…In all, 90 genetic variants (SNPs) are used in the 39 models. The number of SNPs included in each of the models ranges from one (combined with other risk factors in a mixed genetic‐phenotypic models [ 21 , 27 , 28 , 30 ]) to 19 [ 15 , 26 ]. Details of the variables (including SNPs) used in each model are given in Table 1 .…”

Section: Resultsmentioning

confidence: 99%

The current state of genetic risk models for the development of kidney cancer: a review and validation

Harrison

Saunders

et al. 2022

BJU International

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To review the current state of genetic risk models for predicting the development of kidney cancer, by identifying and comparing the performance of published models. MethodsRisk models were identified from a recent systematic review and the Cancer-PRS web directory. A narrative synthesis of the models, previous validation studies and related genome-wide association studies (GWAS) was carried out. The discrimination and calibration of the identified models was then assessed and compared in the UK Biobank (UKB) cohort (cases, 452; controls, 487 925). ResultsA total of 39 genetic models predicting the development of kidney cancer were identified and 31 were validated in the UKB. Several of the genetic-only models (seven of 25) and most of the mixed genetic-phenotypic models (five of six) had some discriminatory ability (area under the receiver operating characteristic curve >0.5) in this cohort. In general, models containing a larger number of genetic variants identified in GWAS performed better than models containing a small number of variants associated with known causal pathways. However, the performance of the included models was consistently poorer than genetic risk models for other cancers. ConclusionsAlthough there is potential for genetic models to identify those at highest risk of developing kidney cancer, their performance is poorer than the best genetic risk models for other cancers. This may be due to the comparatively small number of genetic variants associated with kidney cancer identified in GWAS to date. The development of improved genetic risk models for kidney cancer is dependent on the identification of more variants associated with this disease. Whether these will have utility within future kidney cancer screening pathways is yet to determined.

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“…The defects include oxidized and N-alkylated nitrogen bases, uracil and apurinic/pyrimidine sites (36). According to the latest literature data, OGG1 Ser326Cys and XRCC1 Arg399Gln polymorphisms may be associated with many neoplastic diseases (37)(38)(39)(40)(41)(42)(43)(44). In our study, OGG1 Ser326Cys and XRCC1 Arg399Gln polymorphisms were associated with an increased risk of endometrial cancer and influenced the histological malignancy grading.…”

Section: Discussionmentioning

confidence: 99%

Studies of Correlations Between Single Nucleotide Polymorphisms of DNA Repair Genes and Endometrial Cancer in Polish Women

et al. 2018

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The polymorphism XRCC1 Arg194Trp and 8-hydroxydeoxyguanosine increased susceptibility to arsenic-related renal cell carcinoma

Cited by 10 publications

References 44 publications

Rapamycin preserves the primordial follicle pool during cisplatin treatment in vitro and in vivo

Rapamycin preserves the primordial follicle pool during cisplatin treatment in vitro and in vivo

The current state of genetic risk models for the development of kidney cancer: a review and validation

Studies of Correlations Between Single Nucleotide Polymorphisms of DNA Repair Genes and Endometrial Cancer in Polish Women

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