CYP2W1, CYP4F11 and CYP8A1 Polymorphisms and Interaction of CYP2W1 Genotypes with Risk Factors in Mexican Women with Breast Cancer

Cárdenas-Rodríguez, Noemi; Lara‐Padilla, Eleazar; Bandala, Cindy; Lopez-Cruz, J.; Uscanga-Carmona, C; Pf, Lucio-Monter; Floriano-Sánchez, Esaú

doi:10.7314/apjcp.2012.13.3.837

Cited by 13 publications

(7 citation statements)

References 54 publications

(19 reference statements)

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“…Enriched genes such as SGMS2 [Zheng et al 2019], ACAT1 [Ye et al 2016], UGP2 [Zeng et al 2019], GOT1 [Wang et al 2019], CDA (cytidinedeaminase) [Ye et al 2015] and FOS (Fos proto-oncogene, AP-1 transcription factor subunit) [Liu et al 2018] were important for proliferation of various cancer cells types, but these genes may be involved in proliferation of hepatoblastoma cells. SNP in enriched genes such as MAT1A [Mumbrekar et al 2017], ADH1C [Hidaka et al 2015], UGT2B7 [Sutiman et al 2016], HSD11B1 [Wang et al 2013], CYP2B6 [Kuo et al 2017], CHST9 [Yuan et al 2017], CYP39A1 [Melchardt et al 2015], FMO3 [Bae et al 2006], CYP3A43 [Han et al 2015], CYP4F3 [Yin et al 2017], CYP4F11 [Cardenas-Rodriguez et al 2012], SULT2A1 [Wilborn et al 2006], GSTA2 [Maekawa et al 2011] and GSTA3 [Duan et al 2018] were involved in progression of various cancer types, but these polymorphic genes may be linked with development of hepatoblastoma. Enriched genes such as MGLL (monoglyceride lipase) [Yang et al 2018], DMGDH (dimethylglycine dehydrogenase) [Liu et al 2016], SHMT1 [Dou et al 2019], ARG1 [You et al 2018], CXCL8 [Li et al 2015] and FGG (fibrinogen gamma chain) [Zhang et al 2019] were involved in invasion of hepatocellular carcinoma cells, but these genes may be responsible for invasion of hepatoblastoma cells.…”

Section: Discussionmentioning

confidence: 99%

Identification of potential core genes in hepatoblastoma via bioinformatics analysis

Vastrad¹,

Vastrad²,

Kotturshetti³

2020

Preprint

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Hepatoblastoma is the childhood liver cancer. Profound efforts have been made to illuminate the pathology, but the molecular mechanisms of hepatoblastoma are still not well understood. To identify the candidate genes in the carcinogenesis and progression of hepatoblastoma, microarray dataset GSE131329 was downloaded from Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) were identified, and pathway and Gene Ontology (GO) enrichment analysis were performed. The protein-protein interaction network (PPI), module analysis, target gene - miRNA regulatory network and target gene - TF regulatory network were constructed and analyzed. A total of 996 DEGs were identified, consisting of 499 up regulated genes and 497 down regulated genes. The pathway and Gene Ontology (GO) enrichment analysis of the DEGs include proline biosynthesis, superpathway of tryptophan utilization, chromosome organization and organic acid metabolic process. Twenty-four hub genes were identified and biological process analysis revealed that these genes were mainly enriched in cell cycle, chromosome organization, lipid metabolic process and oxidation-reduction process. Validation of hub genes showed that TP53, PLK1, AURKA, CDK1, ANLN, ESR1, FGB, ACAT1, GOT1 and ALAS1 may be involved in the carcinogenesis, invasion or recurrence of hepatoblastoma. In conclusion, DEGs and hub genes identified in the present study help us understand the molecular mechanisms underlying the carcinogenesis and progression of hepatoblastoma, and provide candidate targets for diagnosis and treatment of hepatoblastoma.

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Section: Discussionmentioning

confidence: 99%

Identification of potential core genes in hepatoblastoma via bioinformatics analysis

Vastrad¹,

Vastrad²,

Kotturshetti³

2020

Preprint

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“…Inter-individual genetic variation in the metabolism of carcinogens is a determinant factor of susceptibility to various types of cancer (96). CYPs serve a profound role in the metabolism of carcinogens (97).…”

Section: Effect Of Cyps On Carcinogen Metabolismmentioning

confidence: 99%

“…CYPs serve a profound role in the metabolism of carcinogens (97). The difference in the enzyme activity of CYPs determines the susceptibility to chemical carcinogens (96). Numerous CYPs are involved in catalyzing the metabolism of potential breast cancer-related carcinogens (96).…”

Section: Effect Of Cyps On Carcinogen Metabolismmentioning

confidence: 99%

“…The difference in the enzyme activity of CYPs determines the susceptibility to chemical carcinogens (96). Numerous CYPs are involved in catalyzing the metabolism of potential breast cancer-related carcinogens (96). Polycyclic aromatic hydrocarbons (PAHs) are common environmental carcinogens that induce tumorigenesis when they are activated by CYPs (98).…”

Section: Effect Of Cyps On Carcinogen Metabolismmentioning

confidence: 99%

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Cytochrome P450: Implications for human breast cancer (Review)

Luo

Yan

et al. 2021

Oncol Lett

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The treatment options for breast cancer include endocrine therapy, targeted therapy and chemotherapy. However, some patients with triple-negative breast cancer cannot benefit from these methods. Therefore, novel therapeutic targets should be developed. The cytochrome P450 enzyme (CYP) is a crucial metabolic oxidase, which is involved in the metabolism of endogenous and exogenous substances in the human body. Some products undergoing the metabolic pathway of the CYP enzyme, such as hydroxylated polychlorinated biphenyls and 4-chlorobiphenyl, are toxic to humans and are considered to be potential carcinogens. As a class of multi-gene superfamily enzymes, the subtypes of CYPs are selectively expressed in breast cancer tissues, especially in the basal-like type. In addition, CYPs are essential for the activation or inactivation of anticancer drugs. The association between CYP expression and cancer risk, tumorigenesis, progression, metastasis and prognosis has been widely reported in basic and clinical studies. The present review describes the current findings regarding the importance of exploring metabolic pathways of CYPs and gene polymorphisms for the development of vital therapeutic targets for breast cancer.

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“…One study tested the association between SNPs in different selenoprotein-related genes ( GPX1, GPX2, GPX3, GPX4, SELS, SEP15, SEPN1, SEPP1, SEPW1, TXNRD1 , and TXNRD2 ) and breast cancer risk in US Latinas, finding mostly negative results except when analyses were stratified by genetic ancestry and by tumor subtype [173]. Other studies were conducted in Mexico and Brazil and investigated multiple genes: CYP2W1, CYP4F11 , CYP8A1 , and CYP1B1 [174], which are important in the activation of carcinogenic compounds; ABCB1 , which encodes the MDR1 protein, [105,106] and is involved in the elimination of xenotoxic agents; GSTM1 and GSTP1 , members of the glutathione S -transferase ( GST ) gene family [91,108,109,113]; and eNOS , which can react with other free radicals and damage DNA [114]. Results for the CYP genes were mostly negative, except for CYP1B1 [107], while positive associations were reported for the GSTM1 deletion (tagged by rs366631), and ABCB1 c.3435C>T (rs1045642), GSTP1 c.313A>G (rs1695), and eNOS polymorphisms [91,105,106,108,109,113,114,174].…”

Section: Breast Cancer Candidate Gene Studies In Latin Americamentioning

confidence: 99%

Genetic Epidemiology of Breast Cancer in Latin America

Zavala

Serrano-Gómez

Dutil

et al. 2019

Genes

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The last 10 years witnessed an acceleration of our understanding of what genetic factors underpin the risk of breast cancer. Rare high- and moderate-penetrance variants such as those in the BRCA genes account for a small proportion of the familial risk of breast cancer. Low-penetrance alleles are expected to underlie the remaining heritability. By now, there are about 180 genetic polymorphisms that are associated with risk, most of them of modest effect. In combination, they can be used to identify women at the lowest or highest ends of the risk spectrum, which might lead to more efficient cancer prevention strategies. Most of these variants were discovered in populations of European descent. As a result, we might be failing to discover additional polymorphisms that could explain risk in other groups. This review highlights breast cancer genetic epidemiology studies conducted in Latin America, and summarizes the information that they provide, with special attention to similarities and differences with studies in other populations. It includes studies of common variants, as well as moderate- and high-penetrance variants. In addition, it addresses the gaps that need to be bridged in order to better understand breast cancer genetic risk in Latin America.

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CYP2W1, CYP4F11 and CYP8A1 Polymorphisms and Interaction of CYP2W1 Genotypes with Risk Factors in Mexican Women with Breast Cancer

Cited by 13 publications

References 54 publications

Identification of potential core genes in hepatoblastoma via bioinformatics analysis

Identification of potential core genes in hepatoblastoma via bioinformatics analysis

Cytochrome P450: Implications for human breast cancer (Review)

Genetic Epidemiology of Breast Cancer in Latin America

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