Log in

Relevant bibliographies by topics / NQO1*2 genetic polymorphism / Journal articles

To see the other types of publications on this topic, follow the link: NQO1*2 genetic polymorphism.

Journal articles on the topic 'NQO1*2 genetic polymorphism'

Author: Grafiati

Published: 4 June 2021

Last updated: 19 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'NQO1*2 genetic polymorphism.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Sharma, Mohini, Mohit Mehndiratta, Stuti Gupta, Om P. Kalra, Rimi Shukla, and Jasvinder K. Gambhir. "Genetic association of NAD(P)H quinone oxidoreductase (NQO1*2) polymorphism with NQO1 levels and risk of diabetic nephropathy." Biological Chemistry 397, no. 8 (2016): 725–30. http://dx.doi.org/10.1515/hsz-2016-0135.

Full text

Abstract:

Abstract NAD(P)H quinone oxidoreductase 1 (NQO1) catalyzes reactions having a cyto-protective effect against redox cycling and oxidative stress. A single base polymorphism (C/T) at nucleotide 609 of the NQO1 gene impairs the stability and function of its protein. Its role in the development of diabetic nephropathy (DN) has not been deciphered. Therefore, this study aimed to evaluate the association of NQO1*2 (rs1800566) polymorphism with plasma NQO1 levels and DN. This study screened 600 participants including healthy controls (HC), type 2 diabetes mellitus without complications (T2DM) and dia

APA, Harvard, Vancouver, ISO, and other styles

2

Koldehoff, Michael, Dietrich W. Beelen, and Ahmet H. Elmaagacli. "Genetic Polymorphism of NAD(P)H:Quinine Oxidoreductase 1 Is Associated with An Increased Treatment-Related Mortality in Patients Undergoing Allogeneic Transplantation." Blood 114, no. 22 (2009): 3342. http://dx.doi.org/10.1182/blood.v114.22.3342.3342.

Full text

Abstract:

Abstract Abstract 3342 Poster Board III-230 Introduction: The widely expressed detoxification enzyme NAD(P)H:quinine oxidoreductase 1 (NQO1) is involved in the cellular response to oxidative stress and irradiation and protects cells against the mutagenicity from free radicals and toxic oxygen metabolities. NQO1 is subject to a genetic polymorphism (C609T) leading to a change in its amino acid sequence. Heterozygous individuals C/T have intermediate activity and homozygotes T/T are NQO1 deficient. Never before the influence of genetic polymorphisms of NQO1 on patients who underwent allogeneic t

APA, Harvard, Vancouver, ISO, and other styles

3

Okoturo, Eyituoyo, Anslem Osasuyi, and Taofiq Opaleye. "Genetic Polymorphism of Head and Neck Cancers in African Populations: A Systematic Review." OTO Open 4, no. 3 (2020): 2473974X2094220. http://dx.doi.org/10.1177/2473974x20942202.

Full text

Abstract:

Objective Head and neck cancers are mostly composed of head and neck squamous cell carcinoma (HNSCC). The incidence and mortality of HNSCC are higher in countries with emerging health care systems, particularly Africa. Given that they are more genetically diverse, characterization of polymorphism in African HNSCC may result in the identification of distinct molecular targets as compared with the known HNSCC candidate genes. This study objective is to review the current evidence of genetic data on HNSCC among African populations as well as to demonstrate any distinctions as compared with known

APA, Harvard, Vancouver, ISO, and other styles

4

Malik, Elad, Sara B. Cohen, and Deborah Rund. "The NAD(P)H:Quinone Oxidoreductase (NQO1) C609T Polymorphism Is Found at Variable Frequency in Different Ethnic Groups but Does Not Predispose to De Novo AML in Israel." Blood 104, no. 11 (2004): 4381. http://dx.doi.org/10.1182/blood.v104.11.4381.4381.

Full text

Abstract:

Abstract Background: The NQO1 gene is located on chromosome 16q22.1. This gene encodes a cytosolic enzyme which is expressed in many tissues including the hematopoietic system. NQO1 has an important role in detoxifying quinones, which are widespread compounds that are present thoughout the body (vitamin K), the diet (proteins, fruits and vegetables) and the environment (solvents, cosmetics, cigarette smoke). A single nucleotide polymorphism (C to T) at position 609 (NQO1*2) produces a proline to serine substitution at codon 187 and results in very reduced enzyme activity (null allele). Wild ty

APA, Harvard, Vancouver, ISO, and other styles

5

Tanaviyutpakdee, Pharrunrat, Krongtong Yoovathaworn, Jintana Sirivarasai, et al. "Role of CYP2E1 and NQO1 polymorphisms in oxidative stress derived cancer in Thais with and without dyslipidemia." Asian Biomedicine 9, no. 5 (2017): 601–11. http://dx.doi.org/10.5372/1905-7415.0904.430.

Full text

Abstract:

Abstract Background Hyperlipidemia can induce the endogenous production of reactive oxygen species (ROS), which may cause carcinogenesis. Cytochrome P450 (CYP) 2E1 activity, induced by various factors including polyunsaturated fatty acids, effects the incidence of cancers, whereas NQO1, a flavoprotein, may protect against ROS. Objectives To investigate the effect of CYP2E1 and NQO1 polymorphism on oxidative stress status in Thais with and without dyslipidemia. Methods We included 1380 apparently healthy employees of the Electricity Generating Authority of Thailand in this study. We determined

APA, Harvard, Vancouver, ISO, and other styles

6

Megías, Juan Eduardo, Pau Montesinos, María José Herrero, et al. "Prognostic Impact of Anthracycline Metabolism Gene Polymorphisms in Newly Diagnosed Acute Myeloid Leukemia Adults." Blood 124, no. 21 (2014): 2237. http://dx.doi.org/10.1182/blood.v124.21.2237.2237.

Full text

Abstract:

Abstract Background: The genetic variability related with single nucleotide polymorphisms (SNPs) within the genes involving drug transport or metabolism, DNA repair and oxidative stress, could lead to interindividual differences in treatment outcome. Several studies suggested, in different kinds of cancer, that SNPs of genes coding for drug detoxification enzymes of anthracyclines may influence their effectiveness or toxicity. However the association of these polymorphisms in adult acute myeloid leukemia (AML) patients treated with the combination of cytarabine and anthracyclines for induction

APA, Harvard, Vancouver, ISO, and other styles

7

Vinayagamoorthy, Nadimuthu, Kannan Krishnamurthi, Sivanesan Saravana Devi, et al. "Genetic polymorphism of CYP2D6∗2 C→T 2850, GSTM1, NQO1 genes and their correlation with biomarkers in manganese miners of Central India." Chemosphere 81, no. 10 (2010): 1286–91. http://dx.doi.org/10.1016/j.chemosphere.2010.08.047.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Carta, Angela, Sofia Pavanello, Giuseppe Mastrangelo, Ugo Fedeli, Cecilia Arici, and Stefano Porru. "Impact of Occupational Exposures and Genetic Polymorphisms on Recurrence and Progression of Non-Muscle-Invasive Bladder Cancer." International Journal of Environmental Research and Public Health 15, no. 8 (2018): 1563. http://dx.doi.org/10.3390/ijerph15081563.

Full text

Abstract:

Introduction: Additional or better markers are needed to guide the clinical monitoring of patients with non-muscle-invasive bladder cancer (NMIBC). Aim: To investigate the influence of occupational exposures and genetic polymorphisms on recurrence and progression of NMIBC. Methods: The study includes 160 NMIBC patients. We collected on questionnaire information on demographic variables, lifetime smoking history, lifetime history of occupational exposure to aromatic amines and polycyclic aromatic hydrocarbons. Genetic polymorphism (glutathione S-transferase M1; T1; P1 (GSTM1; GSTT1; GSTP1); N-a

APA, Harvard, Vancouver, ISO, and other styles

9

Siraj, Abdul K., Rong Bu, Mona Ibrahim, et al. "Polymorphisms in Xenobiotic Genes and Risk of Developing Diffuse Large B-Cell Lymphoma in Saudi Population." Blood 106, no. 11 (2005): 4424. http://dx.doi.org/10.1182/blood.v106.11.4424.4424.

Full text

Abstract:

Abstract Diffuse large B-Cell Lymphoma (DLBCL) is one of the most common types of non-Hodgkin lymphoma (NHL) and an increased incidence has been reported during the past 30 years. The cause of this remains unknown but population-based studies suggest a relationship with exposure to certain environment carcinogens. Particularly, exposure to asbestos, benzene, industrial and agricultural toxins has been implicated as possible cause of the disease. The xenobiotic enzyme system that enables us to detoxify these types of carcinogens exhibits identifiable genetic polymorphisms that are associated wi

APA, Harvard, Vancouver, ISO, and other styles

10

Siraj, Abdul K., Rong Bu, Maha Al-Rasheed, et al. "Association between Drug-Metabolizing Enzymes Polymorphisms and Diffuse Large B-Cell Lymphoma Risk in the Middle Eastern Population." Blood 108, no. 11 (2006): 2043. http://dx.doi.org/10.1182/blood.v108.11.2043.2043.

Full text

Abstract:

Abstract The last four decades have seen significant increase in the incidence of non-Hodgkin’s lymphoma (NHL) as a possible result of increasing environmental carcinogens exposure. Based on the increasing evidence for the association between carcinogens exposure related cancer risk and xenobiotic gene polymorphisms. We have undertaken a case control study on xenobiotic gene polymorphisms in Saudi individuals with a diagnosis of diffuse large B-cell lymphoma (DLBCL). Polymorphisms in five genes (CYP1A1, GSTT1, GSTP1, GSTM1 and NQO1) were characterized in 187 individuals with DLBCL and 513 norm

APA, Harvard, Vancouver, ISO, and other styles

11

Kristiansen, Ole P., Zenia M. Larsen, Jesper Johannesen, J�rn Nerup, Thomas Mandrup-Poulsen, and Flemming Pociot. "No linkage of P187S polymorphism in NAD(P)H: Quinone oxidoreductase (NQO1/DIA4) and type 1 diabetes in the Danish population." Human Mutation 14, no. 1 (1999): 67–70. http://dx.doi.org/10.1002/(sici)1098-1004(1999)14:1<67::aid-humu8>3.0.co;2-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Szpurka, Hadrian, Abdo Haddad, Soumit Basu, Mikkael Sekeres, and Jaroslaw P. Maciejewski. "Increased Frequency of Polymorphisms in XRCC3 and OGG1 Genes in Patients with MDS." Blood 106, no. 11 (2005): 3445. http://dx.doi.org/10.1182/blood.v106.11.3445.3445.

Full text

Abstract:

Abstract The effects of genetic factors on susceptibility to MDS are not well understood. The predisposition may be a result of complex genetic traits, various theories can explain how inherited genic sequence alterations could result in a higher susceptibility to this disease. In theory, genes involved in the metabolism of genotoxic chemicals, DNA repair genes and immunogenetic factors could all play a role. Possibly, the predisposition can be multifactorial and overall risk for MDS modified by acute or cumulative effects of environmental exposures. Alterations/variants of genes involved in M

APA, Harvard, Vancouver, ISO, and other styles

13

Rigacci, Luigi, Gabriele Perrone, Stefania Nobili, et al. "Role of Genetic Polymorphisms on Response to R-Chopregimen in Diffuse Large B-Cell Lymphoma Patients: An Interim Analysis of a Multicenter Prospective Pharmacogenetic Study." Blood 126, no. 23 (2015): 2483. http://dx.doi.org/10.1182/blood.v126.23.2483.2483.

Full text

Abstract:

Abstract Introduction: Standard chemotherapy represented by the R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) regimen is successful in about 60% of patients (pts) with diffuse large B-cell lymphoma (DLBCL). Pts who do not benefit from this treatment, due to the development of tumor drug resistance, have a very poor prognosis. Currently, knowledge on reasons of treatment related failures in DLBCL are scanty and predictive biomarker of response are largely unknown. We hypothesized that polymorphisms of gene involved in the pharmacokinetics and pharmacodynamics of dru

APA, Harvard, Vancouver, ISO, and other styles

14

Urtishak, Karen A., Blaine W. Robinson, Jaclyn A. Biegel, Kim E. Nichols, Julie W. Stern, and Carolyn A. Felix. "Unique Familial MLL-rearranged Precursor B Cell Infant Acute Lymphoblastic Leukemia (ALL) in Non-Twin Siblings." Blood 118, no. 21 (2011): 2417. http://dx.doi.org/10.1182/blood.v118.21.2417.2417.

Full text

Abstract:

Abstract Abstract 2417 Leukemia is the commonest malignancy in infants, the most frequently occurring form of which is infant ALL. When ALL occurs in infants the disease is clinically aggressive and associated with poor outcome. MLL gene rearrangements producing transforming fusion oncoproteins are found in 75% of infant ALL and they are adverse prognostic factors. Infant ALL has never occurred in families except in monozygous twins, where concordance in leukemia occurrence is nearly 100%. Identical but non-germline genomic breakpoint junction sequences have pointed to an in utero origin of ML

APA, Harvard, Vancouver, ISO, and other styles

15

Glorieux and Buc Calderon. "Cancer Cell Sensitivity to Redox-Cycling Quinones is Influenced by NAD(P)H: Quinone Oxidoreductase 1 Polymorphism." Antioxidants 8, no. 9 (2019): 369. http://dx.doi.org/10.3390/antiox8090369.

Full text

Abstract:

Background: Cancer cell sensitivity to drugs may be associated with disturbed antioxidant enzymes expression. We investigated mechanisms of resistance by using oxidative stress-resistant MCF-7 breast cancer cells (Resox cells). Since nicotinamide adenine dinucleotide phosphate (NAD(P)H): quinone oxidoreductase-1 (NQO1) is modified in tumors and oxidative stress-resistant cells, we studied its role in cells exposed to β-lapachone, menadione, and doxorubicin. Methods: Normal mammary epithelial 250MK, MCF-7, and Resox cells were employed. NQO1 expression and enzyme activity were determined by qua

APA, Harvard, Vancouver, ISO, and other styles

16

Filipenko, M. L., E. V. Pechkovsky, O. V. Mishukova, et al. "No association between NQO1 polymorphism and breast cancer risk in Siberian population." Journal of Clinical Oncology 25, no. 18_suppl (2007): 21185. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.21185.

Full text

Abstract:

21185 Background: NQO1 is a two-electron reductase, which metabolizes a variety of xenobiotics. This FAD-binding protein forms homodimers and reduces quinones to hydroquinones. This protein's enzymatic activity prevents the one electron reduction of quinones that results in the production of radical species. Mutations in this gene have been associated with tardive dyskinesia (TD), an increased risk of hematotoxicity after exposure to benzene, and susceptibility to various forms of cancer. Genetic polymorphism of NQO1 is a C to T point mutation at base pair 609 of exon 6, which codes for a prol

APA, Harvard, Vancouver, ISO, and other styles

17

Gorący, Jarosław, Anna Bogacz, Izabela Uzar, et al. "The Analysis of NADPH Quinone Reductase 1 (NQO1) Polymorphism in Polish Patients with Colorectal Cancer." Biomolecules 11, no. 7 (2021): 1024. http://dx.doi.org/10.3390/biom11071024.

Full text

Abstract:

Colorectal cancer (CRC) is one of the most common malignancies in Poland. Based on the findings of clinical trials, it is safe to conclude that genetic predisposition and environmental factors are the main factors responsible for the formation of colorectal cancer.The NQO1 gene plays an important role in reducing endogenous and exogenous quinones as well as quinone compounds to hydroquinones. It is an enzyme which is a part of the body’s antioxidant defense system. The aim of the study was to evaluate the correlation between the 609C > T polymorphism of the NQO1 gene and colorectal cancer r

APA, Harvard, Vancouver, ISO, and other styles

18

Park, Seun-Ja, Hua Zhao, Margaret R. Spitz, H. Barton Grossman, and Xifeng Wu. "An association between NQO1 genetic polymorphism and risk of bladder cancer." Mutation Research/Genetic Toxicology and Environmental Mutagenesis 536, no. 1-2 (2003): 131–37. http://dx.doi.org/10.1016/s1383-5718(03)00041-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Lu, Yi, Shirley Kow Yin Kham, Hany Ariffin, et al. "Integrated Molecular and Pharmacogenetic Profiles in Prediction of Early Response to Therapy in Children with Acute Lymphoblastic Leukemia (ALL): A Report From Malaysia-Singapore ALL Study Group." Blood 114, no. 22 (2009): 2624. http://dx.doi.org/10.1182/blood.v114.22.2624.2624.

Full text

Abstract:

Abstract Abstract 2624 Poster Board II-600 Although childhood ALL is the prototype for a drug-responsive malignancy, some patients relapse or develop severe toxicity due to significant inter-individual variability. Leukemic factors like the molecular subtype account for the majority of the variation in prognosis; some studies have suggested that polymorphisms in key genes involved in drug transport, uptake, metabolism or targeting are responsible for smaller magnitude of variance in terms of therapeutic efficacy. Thus far, genetic characteristics are not widely applied in modern risk-stratifyi

APA, Harvard, Vancouver, ISO, and other styles

20

Moudra, A., L. Minarik, M. Vančurová, Z. Hodný, J. Bartek, and A. Jonášová. "NQO1 * 2 Polymorphism Predicts Overall Survival in Primary MDS Patients." Leukemia Research 55 (April 2017): S146. http://dx.doi.org/10.1016/s0145-2126(17)30367-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Saldivar, Salvador J., Yunfei Wang, Hua Zhao, et al. "An association between a NQO1 genetic polymorphism and risk of lung cancer." Mutation Research/Genetic Toxicology and Environmental Mutagenesis 582, no. 1-2 (2005): 71–78. http://dx.doi.org/10.1016/j.mrgentox.2004.12.010.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Nagata, Misato, Tatsuo Kimura, Tomohiro Suzumura, et al. "C609T polymorphism of NADPH Quinone Oxidoreductase 1 Correlates Clinical Hematological Toxicities in Lung Cancer Patients Treated with Amrubicin." Clinical Medicine Insights: Oncology 7 (January 2013): CMO.S10839. http://dx.doi.org/10.4137/cmo.s10839.

Full text

Abstract:

Background Amrubicin hydrochloride (AMR) is a key agent for lung cancer. NADPH quinone oxidoreductase 1 (NQO1) metabolizes the quinone structures contained in both amrubicin (AMR) and amrubicinol (AMR-OH). We hypothesized that NQO1 C609T polymorphism may affect AMR-related pharmacokinetics and clinical outcomes. Methods Patients received AMR doses of 30 or 40 mg/m2/day on days 1–3. Plasma sampling was performed 24 hours after the first and third AMR injections. Concentrations of AMR and AMR-OH were determined by HPLC and the NQO1 C609T polymorphism was assayed by RT-PCR. Results A total of 35

APA, Harvard, Vancouver, ISO, and other styles

23

Marjani, H. A., F. Biramijamal, N. Rakhshani, A. Hossein-Nezhad, and R. Malekzadeh. "Investigation of NQO1 genetic polymorphism, NQO1 gene expression and PAH-DNA adducts in ESCC. A case-control study from Iran." Genetics and Molecular Research 9, no. 1 (2010): 239–49. http://dx.doi.org/10.4238/vol9-1gmr693.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Liu, Kai, Hui Tian, Kai-Zhong Yu, et al. "Association between NQO1 Pro187Ser polymorphism and esophageal cancer: a meta-analysis." Tumor Biology 35, no. 3 (2013): 2063–68. http://dx.doi.org/10.1007/s13277-013-1273-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Buda, Gabriele, Valentina Maggini, Sara Galimberti, Roberto Barale, Anna Maria Rossi, and Mario Petrini. "NQO1*2 polymorphism and response to treatment in patients with multiple myeloma." Leukemia Research 31, no. 8 (2007): 1029–30. http://dx.doi.org/10.1016/j.leukres.2007.01.011.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Milković, Lidija, Marko Tomljanović, Ana Čipak Gašparović, et al. "Nutritional Stress in Head and Neck Cancer Originating Cell Lines: The Sensitivity of the NRF2-NQO1 Axis." Cells 8, no. 9 (2019): 1001. http://dx.doi.org/10.3390/cells8091001.

Full text

Abstract:

Nutritional stress disturbs the cellular redox-status, which is characterized by the increased generation of reactive oxygen species (ROS). The NRF2-NQO1 axis represents a protective mechanism against ROS. Its strength is cell type-specific. FaDu, Cal 27 and Detroit 562 cells differ with respect to basal NQO1 activity. These cells were grown for 48 hours in nutritional conditions (NC): (a) Low glucose–NC2, (b) no glucose, no glutamine–NC3, (c) no glucose with glutamine–NC4. After determining the viability, proliferation and ROS generation, NC2 and NC3 were chosen for further exploration. These

APA, Harvard, Vancouver, ISO, and other styles

27

MA, Qiang, Krista KINNEER, Yongyi BI, Jefferson Y. CHAN, and Yuet Wai KAN. "Induction of murine NAD(P)H:quinone oxidoreductase by 2,3,7,8-tetrachlorodibenzo-p-dioxin requires the CNC (cap n collar) basic leucine zipper transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2): cross-interaction between AhR (aryl hydrocarbon receptor) and Nrf2 signal transduction." Biochemical Journal 377, no. 1 (2004): 205–13. http://dx.doi.org/10.1042/bj20031123.

Full text

Abstract:

TCDD (2,3,7,8-tetrachlorodibenzo-p-dixoin) induces phase II drug-metabolizing enzyme NQO1 [NAD(P)H:quinone oxidoreductase; EC 1.6.99.2; DT-diaphorase] in a wide range of mammalian tissues and cells. Here, we analysed the molecular pathway mediating NQO1 induction by TCDD in mouse hepatoma cells. Inhibition of protein synthesis with CHX (cycloheximide) completely blocks induction of NQO1 by TCDD as well as the basal expression and induction by phenolic antioxidant tBHQ (2-t-butylbenzene-1,4-diol), implicating a labile factor in NQO1 mRNA expression. The inhibition is both time- and concentratio

APA, Harvard, Vancouver, ISO, and other styles

28

Franko, Alenka, Nika Kotnik, Katja Goricar, Viljem Kovac, Metoda Dodic-Fikfak, and Vita Dolzan. "The influence of genetic variability on the risk of developing malignant mesothelioma." Radiology and Oncology 52, no. 1 (2018): 105–11. http://dx.doi.org/10.2478/raon-2018-0004.

Full text

Abstract:

Abstract Background Malignant mesothelioma is a rare cancer with poor outcome, associated with asbestos exposure. Reactive oxygen species may play an important role in the mechanism of carcinogenesis; therefore, genetic variability in antioxidative defence may modify an individual’s susceptibility to this cancer. This study investigated the influence of functional polymorphisms of NQO1, CAT, SOD2 and hOGG1 genes, gene-gene interactions and gene-environment interactions on malignant mesothelioma risk. Patients and methods In total, 150 cases with malignant mesothelioma and 122 controls with no

APA, Harvard, Vancouver, ISO, and other styles

29

Lou, Yuqing, Rong Li, Liwen Xiong, and Baohui Han. "NAD(P)H: Quinone oxidoreductase 1 (NQO1) C609T polymorphism and lung cancer risk: A meta-analysis." Journal of Clinical Oncology 30, no. 15_suppl (2012): 1551. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.1551.

Full text

Abstract:

1551 Background: No clear consensus has been reached on the NAD(P)H: quinone oxidoreductase 1 (NQO1) gene C609T polymorphism and lung cancer risk. We performed a meta-analysis to summarize the possible association. Methods: We conducted a computer retrieval of PUBMED and EMBASE databases prior to January 2012. References of retrieved articles were also screened. According to the inclusion criteria, 24 articles (31 studies) were finally included. The fixed-effects model and the random-effects model were applied for dichotomous outcomes to combine the results of the individual studies. Results:

APA, Harvard, Vancouver, ISO, and other styles

30

Smith, Martyn T., Yunxia Wang, Christine F. Skibola, et al. "Low NAD(P)H:quinone oxidoreductase activity is associated with increased risk of leukemia with MLL translocations in infants and children." Blood 100, no. 13 (2002): 4590–93. http://dx.doi.org/10.1182/blood-2001-12-0264.

Full text

Abstract:

An inactivating polymorphism at position 609 in the NAD(P)H:quinone oxidoreductase 1 gene (NQO1 C609T) is associated with an increased risk of adult leukemia. A small British study suggested thatNQO1 C609T was associated with an increased risk of infant leukemias with MLL translocations, especially infant acute lymphoblastic leukemia (ALL) with t(4;11). We explored NQO1 C609Tas a genetic risk factor in 39 pediatric de novo and 18 pediatric treatment-related leukemias with MLL translocations in the United States. Children with de novo B-lineage ALL withoutMLL translocations and a calculation of

APA, Harvard, Vancouver, ISO, and other styles

31

Larson, Richard A., Yunxia Wang, Mekhala Banerjee, et al. "Prevalence of the Inactivating 609C→T Polymorphism in the NAD(P)H:Quinone Oxidoreductase (NQO1) Gene in Patients With Primary and Therapy-Related Myeloid Leukemia." Blood 94, no. 2 (1999): 803–7. http://dx.doi.org/10.1182/blood.v94.2.803.

Full text

Abstract:

Abstract NAD(P)H:quinone oxidoreductase (NQO1) converts benzene-derived quinones to less toxic hydroquinones and has been implicated in benzene-associated hematotoxicity. A point mutation in codon 187 (Pro to Ser) results in complete loss of enzyme activity in homozygous subjects, whereas those with 2 wild-type alleles have normal activity. The frequency of homozygosity for the mutant allele among Caucasians and African Americans is 4% to 5% but is higher in Hispanics and Asians. Using an unambiguous polymerase chain reaction (PCR) method, we assayed nonmalignant lymphoblastoid cell lines deri

APA, Harvard, Vancouver, ISO, and other styles

32

Larson, Richard A., Yunxia Wang, Mekhala Banerjee, et al. "Prevalence of the Inactivating 609C→T Polymorphism in the NAD(P)H:Quinone Oxidoreductase (NQO1) Gene in Patients With Primary and Therapy-Related Myeloid Leukemia." Blood 94, no. 2 (1999): 803–7. http://dx.doi.org/10.1182/blood.v94.2.803.414k44_803_807.

Full text

Abstract:

NAD(P)H:quinone oxidoreductase (NQO1) converts benzene-derived quinones to less toxic hydroquinones and has been implicated in benzene-associated hematotoxicity. A point mutation in codon 187 (Pro to Ser) results in complete loss of enzyme activity in homozygous subjects, whereas those with 2 wild-type alleles have normal activity. The frequency of homozygosity for the mutant allele among Caucasians and African Americans is 4% to 5% but is higher in Hispanics and Asians. Using an unambiguous polymerase chain reaction (PCR) method, we assayed nonmalignant lymphoblastoid cell lines derived from

APA, Harvard, Vancouver, ISO, and other styles

33

Chang, H. Y., H. W. Li, Y. L. Guo, et al. "Genetic Polymorphism of CYP2E1, GSTT1/M1 and NQO1 on Biomarker of Urinary Spma Among Benzene-Exposed Workers." Epidemiology 17, Suppl (2006): S342. http://dx.doi.org/10.1097/00001648-200611001-00905.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Kim, Hee Nam, Li Yu, Nan Young Kim, et al. "GST T1 and GST M1 Polymorphisms Are Associated with the Risk of Acute Myeloid Leukemia." Blood 112, no. 11 (2008): 3978. http://dx.doi.org/10.1182/blood.v112.11.3978.3978.

Full text

Abstract:

Abstract Xenobiotic-metabolizing enzymes influence the susceptibility to malignancies as well as prognosis by causing chemotherapy resistance. We analyzed genetic polymorphisms of glutathione S-transferases T1 and M1 (del GSTT1 and del GSTM1) and NAD(P)H quinone-oxoreductase (NQO1 C609T) to evaluate the association and risk of acute myeloid leukemia (AML). A large-scale population-based, case-control study of 1700 controls and 663 cases was conducted in Chonnam National University Hwasun Hospital, Korea. GST T1 null genotype was associated with increased risk for AML [odds ratio (OR) = 1.20; 9

APA, Harvard, Vancouver, ISO, and other styles

35

Hori, Hiroko, Takahiro Shinkai, Chima Matsumoto, Osamu Ohmori, and Jun Nakamura. "Genetic association analysis between a functional NAD(P)H: quinone oxidoreductase (NQO1) gene polymorphism (Pro187Ser) and tardive dyskinesia." International Clinical Psychopharmacology 21, no. 4 (2006): A4—A5. http://dx.doi.org/10.1097/00004850-200607000-00019.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Chawla, Deepak. "Genetic Polymorphism and Preterm Birth." Indian Journal of Pediatrics 85, no. 2 (2017): 83–84. http://dx.doi.org/10.1007/s12098-017-2571-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

Shyu, H. Y., and C. W. Cheng. "PO01-MO-28 Genetic polymorphism of NQO1 associated with the severity of acute ischemic stroke and the carotid atherosclerosis." Journal of the Neurological Sciences 285 (October 2009): S162. http://dx.doi.org/10.1016/s0022-510x(09)70620-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Yang, Fei-Yun, Qing-Kai Guan, Yan-Hui Cui, Zhi-Qiang Zhao, Wang Rao, and Zan Xi. "NAD(P)H quinone oxidoreductase 1 (NQO1) genetic C609T polymorphism is associated with the risk of digestive tract cancer." European Journal of Cancer Prevention 21, no. 5 (2012): 432–41. http://dx.doi.org/10.1097/cej.0b013e32834f7514.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Moudra, A., M. Vancurová, V. Machalová, Z. Hodný, J. Bartek, and A. Jonáŝová. "272 NQO1*2 POLYMORPHISM DOES NOT PREDICT OVERALL SURVIVAL IN HIGHER RISK MDS PATIENTS TREATED WITH 5-AZACYTIDINE." Leukemia Research 39 (April 2015): S136—S137. http://dx.doi.org/10.1016/s0145-2126(15)30273-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Gupta, Dipti, Samuel Lessard, Nancy Moore, et al. "Genetic Activation of NRF2 By KEAP1 Inhibition Induces Fetal Hemoglobin Expression and Triggers Anti-Oxidant Stress Response in Erythroid Cells." Blood 134, Supplement_1 (2019): 210. http://dx.doi.org/10.1182/blood-2019-129479.

Full text

Abstract:

Nuclear factor (erythroid derived-2)-like 2 (NRF2), a basic leucine zipper transcription factor, is sequestered in the cell cytosol by Keap1, a kelch domain protein. Under steady state, this interaction results in ubiquitination and proteasomal degradation of the NRF2 protein. Modification of critical cysteine residues leads to conformational changes in KEAP1, resulting in nuclear translocation of newly synthesized NRF2 and modulation of downstream gene expression. NRF2 activation by compounds that modify KEAP1 such as dimethyl fumarate has been shown to induce γ-globin in erythroid cell syste

APA, Harvard, Vancouver, ISO, and other styles

41

Haimila, Katri E., Jukka A. Partanen, and Päivi M. Holopainen. "Genetic polymorphism of the human ICOS gene." Immunogenetics 53, no. 12 (2002): 1028–32. http://dx.doi.org/10.1007/s00251-002-0431-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Liou, Ying-Jay, Ying-Chieh Wang, Chao-Cheng Lin, et al. "Association analysis of NAD(P)H∶quinone oxidoreductase (NQO1) Pro187Ser genetic polymorphism and tardive dyskinesia in patients with schizophrenia in Taiwan." International Journal of Neuropsychopharmacology 8, no. 3 (2005): 483–86. http://dx.doi.org/10.1017/s1461145705005262.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Chen, Guo-zhong, Xiao-yun Shan, Gan-ping Cheng, and Hong-miao Tao. "Cyclooxygenase-2 Genetic Polymorphism and Stroke Subtypes in Chinese." Journal of Molecular Neuroscience 51, no. 2 (2013): 467–73. http://dx.doi.org/10.1007/s12031-013-0078-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Gloria-Bottini, F., N. Lucarini, R. Palmarino, et al. "Phosphoglucomutase genetic polymorphism of newborns." American Journal of Human Biology 13, no. 1 (2001): 9–14. http://dx.doi.org/10.1002/1520-6300(200101/02)13:1<9::aid-ajhb1001>3.0.co;2-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Goetz, Matthew P., David Toft, Joel Reid, et al. "Phase I Trial of 17-Allylamino-17-Demethoxygeldanamycin in Patients With Advanced Cancer." Journal of Clinical Oncology 23, no. 6 (2005): 1078–87. http://dx.doi.org/10.1200/jco.2005.09.119.

Full text

Abstract:

Purpose We determined the maximum-tolerated dose (MTD) and the dose-limiting toxicities (DLT) of 17-allylamino-17-demethoxygeldanamycin (17-AAG) when infused on days 1, 8, and 15 of a 28-day cycle in advanced solid tumor patients. We also characterized the pharmacokinetics of 17-AAG, its effect on chaperone and client proteins, and whether cytochrome P450 (CYP) 3A5 and NAD(P)H:quinone oxidoreductase 1 (NQO1) polymorphisms affected 17-AAG disposition or toxicity. Patients and Methods An accelerated titration design was used. Biomarkers were measured in peripheral-blood mononuclear cells (PBMCs)

APA, Harvard, Vancouver, ISO, and other styles

46

Thomas, Sally E., Anne E. Pheasant, Amanda J. Lee, et al. "Genetic polymorphisms and the development of cutaneous malignant melanoma: Association of the 609 C/T NAD(P)H: quinone oxidoreductase (NQO1) polymorphism." Toxicology 253, no. 1-3 (2008): 18. http://dx.doi.org/10.1016/j.tox.2008.07.021.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Gloria-Bottini, Fulvia, Elena Antonacci, Anna Neri, Andrea Magrini, and Egidio Bottini. "Adenylate kinase locus 1 genetic polymorphism and type 2 diabetes." Health 03, no. 02 (2011): 77–81. http://dx.doi.org/10.4236/health.2011.32014.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

Cerri, N., and F. De Ferrari. "Genetic polymorphism of Alpha-2-HS glycoprotein in Lombardy (Italy)." International Journal of Legal Medicine 104, no. 2 (1991): 77–79. http://dx.doi.org/10.1007/bf01626035.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Hsu, Ling-I., Meei-Maan Wu, Yuan-Hung Wang, et al. "Association of Environmental Arsenic Exposure, Genetic Polymorphisms of Susceptible Genes, and Skin Cancers in Taiwan." BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/892579.

Full text

Abstract:

Deficiency in the capability of xenobiotic detoxification and arsenic methylation may be correlated with individual susceptibility to arsenic-related skin cancers. We hypothesized that glutathione S-transferase (GST M1, T1, and P1), reactive oxygen species (ROS) related metabolic genes (NQO1, EPHX1, and HO-1), and DNA repair genes (XRCC1, XPD, hOGG1, and ATM) together may play a role in arsenic-induced skin carcinogenesis. We conducted a case-control study consisting of 70 pathologically confirmed skin cancer patients and 210 age and gender matched participants with genotyping of 12 selected p

APA, Harvard, Vancouver, ISO, and other styles

50

Barragan, Eva, Maria Collado, Jose Cervera, et al. "The GST deletions and NQO1*2 polymorphism confers interindividual variability of response to treatment in patients with acute myeloid leukemia." Leukemia Research 31, no. 7 (2007): 947–53. http://dx.doi.org/10.1016/j.leukres.2006.10.002.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!