Associations of common variants in genes involved in metabolism and response to exogenous chemicals with risk of multiple myeloma

Gold, Laura S.; Roos, Anneclaire J. De; Brown, Elizabeth E.; Lan, Qing; Milliken, Kevin; Davis, Scott; Chanock, Stephen J.; Zhang, Yawei; Severson, Richard K.; Zahm, Sheila Hoar; Zheng, Tongzhang; Rothman, Nat; Baris, Dalsu

doi:10.1016/j.canep.2009.08.005

Cited by 21 publications

(13 citation statements)

References 51 publications

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“…Additionally, the frequency of the G allele was found to be significantly higher in patients with lung cancer and non-Hodgkin lymphoma when compared to controls, according to Aksoy-Sagirli and coauthors [122] and Kerridge and coauthors [123]. Finally, studies by Gold and colleagues [124] and Van der Logt and associates [125] did not establish the rs662 polymorphism as a risk factor for multiple myeloma and colorectal carcinoma.…”

Section: Other Malignanciesmentioning

confidence: 80%

Common Genetic Variants in the Myeloperoxidase and Paraoxonase Genes and the Related Cancer Risk: A Review

Yuzhalin

Kutikhin

2012

Journal of Environmental Science and Health, Part C

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Modern approaches in health care are moving toward the model of "personalized medicine." Today, current research in molecular biology and medicine is focused on developing genomic markers with predictive, therapeutic, and prognostic significance. One of the most widespread and significant genomic markers is the single nucleotide polymorphism (SNP), which represents a variation in DNA sequence when a single nucleotide differs between members of a biological species or paired chromosomes in an individual. Antioxidant defense enzymes break down dangerous reactive compounds, called reactive oxygen species, and prevent DNA strand from carcinogen-specific mutations. It is well known that inherited variations in genes that encode antioxidant defense enzymes may modulate individual susceptibility to cancer. In our previous study we have determined the predictive significance of several SNPs of superoxide dismutase (SOD) and glutathione peroxidase gene families in the context of cancer risk. The present review includes a summary and discussion of the current findings evaluating the role of SNPs of the myeloperoxidase (MPO) and paraoxanase (PON) genes in cancer occurrence and development. We suggest that rs2333227 (MPO_ -463G/A) and rs854560 polymorphisms have a great predictive significance; they could probably be utilized as cancer predictors in the future. Also, we recommend further in-depth research for rs11079344 (MPO), rs8178406 (MPO), rs2243828 (MPO), rs662 (PON1), rs705379 (PON1), and PON1_304A/G polymorphisms. These SNPs may become significant cancer-associated biomarkers.

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Section: Other Malignanciesmentioning

confidence: 80%

Common Genetic Variants in the Myeloperoxidase and Paraoxonase Genes and the Related Cancer Risk: A Review

Yuzhalin

Kutikhin

2012

Journal of Environmental Science and Health, Part C

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“…Two of the CYP1B1 SNPs we assessed have previously been linked to cancer. This included the rare variant at rs1056836, a missense mutation, which has been linked to increased risk of lung cancer [56], [57], multiple myeloma [39] and head and neck cancer [58], [59], with a possible inverse association with pancreatic cancer [60]. Previous evaluations of the SNP's association with breast, colorectal, endometrial and prostate cancer have produced mostly null findings [61]–[65].…”

Section: Discussionmentioning

confidence: 99%

“…We included genes related to dioxin, phenoxyherbicide, insecticide, vinyl chloride, and radiation response, as well as variants in the previously identified AhR, MDM2 , and ERCC5 genes [32]–[38]. We also looked at polymorphisms in genes encoding proteins on the AhR/ARNT dioxin-response pathway ( CYP1A2 , CYP1B1 , HIF1A , NQO1 , and G6PC/G6PT ) [39]–[41], other related metabolizing pathways ( ADH1A , ADH1B , ADH1C , ALDH18A1 , ALDH1A1 , ALDH1A2 , ALDH1A3 , ALDH1B1 , ALDH1L1 , ALDH1L2 , ALDH2 , CYP2B6 , CYP2C8 , CYP2C9 , CYP2D6 , CYP2E1 , CYP3A4 , GSTM1 , GSTT1 , GSTP1 , HNF4A , NAT2 , NFE2L2, NOS2A , PTGS2/COX2 , and SULT1A1 ) [42]–[45] and TP53 , a tumor suppressor and cell cycle regulation gene closely related to MDM2 [26]. Additionally, we selected several DNA repair genes ( ERCC2 , RAD23B , XPA, and XPC ) in the same DNA repair pathway as ERCC5 , as polymorphisms in these nucleotide excision repair genes can affect individual sensitivity to carcinogen-induced DNA damage [46].…”

Section: Introductionmentioning

confidence: 99%

Gastrointestinal Stromal Tumors, Somatic Mutations and Candidate Genetic Risk Variants

et al. 2013

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Gastrointestinal stromal tumors (GISTs) are rare but treatable soft tissue sarcomas. Nearly all GISTs have somatic mutations in either the KIT or PDGFRA gene, but there are no known inherited genetic risk factors. We assessed the relationship between KIT/PDGFRA mutations and select deletions or single nucleotide polymorphisms (SNPs) in 279 participants from a clinical trial of adjuvant imatinib mesylate. Given previous evidence that certain susceptibility loci and carcinogens are associated with characteristic mutations, or “signatures” in other cancers, we hypothesized that the characteristic somatic mutations in the KIT and PDGFRA genes in GIST tumors may similarly be mutational signatures that are causally linked to specific mutagens or susceptibility loci. As previous epidemiologic studies suggest environmental risk factors such as dioxin and radiation exposure may be linked to sarcomas, we chose 208 variants in 39 candidate genes related to DNA repair and dioxin metabolism or response. We calculated adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for the association between each variant and 7 categories of tumor mutation using logistic regression. We also evaluated gene-level effects using the sequence kernel association test (SKAT). Although none of the association p-values were statistically significant after adjustment for multiple comparisons, SNPs in CYP1B1 were strongly associated with KIT exon 11 codon 557-8 deletions (OR = 1.9, 95% CI: 1.3-2.9 for rs2855658 and OR = 1.8, 95% CI: 1.2-2.7 for rs1056836) and wild type GISTs (OR = 2.7, 95% CI: 1.5-4.8 for rs1800440 and OR = 0.5, 95% CI: 0.3-0.9 for rs1056836). CYP1B1 was also associated with these mutations categories in the SKAT analysis (p = 0.002 and p = 0.003, respectively). Other potential risk variants included GSTM1, RAD23B and ERCC2. This preliminary analysis of inherited genetic risk factors for GIST offers some clues about the disease's genetic origins and provides a starting point for future candidate gene or gene-environment research.

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“…In a following study on polymorphisms in genes involved in benzene metabolism Lincz et al evidenced an increased susceptibility to MM for carriers of 'high-risk genotypes/phenotypes' of GSTT1 (null), NQO1 (187PS/SS, rs1800566) and mEH (high activity) genes as well as for the G/G homozygotes for the mEH H139R (rs2234922) polymorphism (106). Nevertheless, in another study investigating NQO1 P187S (rs1800566), PON-1 Q192R (rs622) and mEH H139R (rs2234922) SNPs no associations were found (107).…”

Section: Genetic Risk Factors In Multiple Myelomamentioning

confidence: 98%

Genetics and molecular epidemiology of multiple myeloma: The rationale for the IMMEnSE consortium (Review)

et al. 2011

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Abstract. There is strong evidence suggesting the presence of a genetic component in the aetiology of multiple myeloma (MM). However no genetic risk factors have been unequivocally established so far. To further our understanding of the genetic determinants of MM risk, a promising strategy is to collect a large set of patients in a consortium, as successfully done for other cancers. In this article, we review the main findings in the genetic susceptibility and pharmacogenetics of MM and present the strategy of the IMMEnSE (International Multiple Myeloma rESEarch) consortium in contributing to determine the role of genetic variation in pharmacogenetics and in MM risk.

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Associations of common variants in genes involved in metabolism and response to exogenous chemicals with risk of multiple myeloma

Cited by 21 publications

References 51 publications

Common Genetic Variants in the Myeloperoxidase and Paraoxonase Genes and the Related Cancer Risk: A Review

Common Genetic Variants in the Myeloperoxidase and Paraoxonase Genes and the Related Cancer Risk: A Review

Gastrointestinal Stromal Tumors, Somatic Mutations and Candidate Genetic Risk Variants

Genetics and molecular epidemiology of multiple myeloma: The rationale for the IMMEnSE consortium (Review)

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