Association of glutamate carboxypeptidase II (GCPII) haplotypes with breast and prostate cancer risk

Divyya, Shree; Naushad, Shaik Mohammad; Addlagatta, A.; Murthy, Pooja; Reddy, C. R. R. M.; Digumarti, Raghunadha Rao; Gottumukkala, Suryanarayana Raju; Subbarao, Sreedhar Amere; Kutala, Vijay Kumar

doi:10.1016/j.gene.2012.11.047

Cited by 9 publications

(6 citation statements)

References 29 publications

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“…Mannose‐6‐phosphate receptor binding protein 1 (M6PRBP1), which is also known as Tail‐Interacting Protein of 47 kDa (TIP47), is involved in transferring hydrolase enzymes by M6PR between golgi and endosomes. The relationship between glutamate carboxypeptidase II and BC and prostate cancer risk has been shown by dysregulation of the genes responsible for this protein . Gene screening of glutamate carboxypeptidase II was done for 61 BC samples compared to 75 controls and 58 prostate cancer samples compared to 76 controls by performing PCR analysis.…”

Section: Resultsmentioning

confidence: 99%

“…Gene screening of glutamate carboxypeptidase II was done for 61 BC samples compared to 75 controls and 58 prostate cancer samples compared to 76 controls by performing PCR analysis. Glutamate carboxypeptidase 2, also known as PSMA (prostate specific membrane antigen) and folate hydrolase (FOLH1) showed high plasma levels in prostate and BC respectively PSMA is considered as a prostate cancer biomarker and target for prostate cancer therapy . There was also one downregulated protein specific to the comparison of sample 5 (BC) versus 6 (control).…”

Section: Resultsmentioning

confidence: 99%

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Proteomics analysis of human breast milk to assess breast cancer risk

et al. 2018

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Detection of breast cancer (BC) in young women is challenging because mammography, the most common tool for detecting BC, is not effective on the dense breast tissue characteristic of young women. In addition to the limited means for detecting their BC, young women face a transient increased risk of pregnancy-associated BC. As a consequence, reproductively active women could benefit significantly from a tool that provides them with accurate risk assessment and early detection of BC. One potential method for detection of BC is biochemical monitoring of proteins and other molecules in bodily fluids such as serum, nipple aspirate, ductal lavage, tear, urine, saliva and breast milk. Of all these fluids, only breast milk provides access to a large volume of breast tissue, in the form of exfoliated epithelial cells, and to the local breast environment, in the form of molecules in the milk. Thus, analysis of breast milk is a non-invasive method with significant potential for assessing BC risk. Here we analyzed human breast milk by mass spectrometry (MS)-based proteomics to build a biomarker signature for early detection of BC. Ten milk samples from eight women provided five paired-groups (cancer versus control) for analysis of dysregulatedproteins: two within woman comparisons (milk from a diseased breast versus a healthy breast of the same woman) and three across women comparisons (milk from a woman with cancer versus a woman without cancer). Despite a wide range in the time between milk donation and cancer diagnosis (cancer diagnosis occurred from 1 month before to 24 months after milk donation), the levels of some proteins differed significantly between cancer and control in several of the five comparison groups. These pilot data are supportive of the idea that molecular analysis of breast milk will identify proteins informative for early detection and accurate assessment of BC risk, and warrant further research. Data are available via ProteomeXchange with identifier PXD007066.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Proteomics analysis of human breast milk to assess breast cancer risk

et al. 2018

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“…Limited studies are there on FOLH1 C1561T polymorphism in association with breast cancer (Mohammad et al 2011;Naushad et al 2011). Several other genetic variants of FOLH1 are also explored for their association with breast cancer (Divyya et al 2013). SLC19A1 G80A was shown to exert breast cancer risk in Indian and Brazilian populations (Carvalho Barbosa Rde et al 2011;Mohammad et al 2011;Naushad et al 2011), while no association was reported in the US population (Xu et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Population-level diversity in the association of genetic polymorphisms of one-carbon metabolism with breast cancer risk

et al. 2016

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Aberrations in one-carbon metabolism were reported to increase breast cancer risk by influencing the DNA synthesis and methylation of DNA and catecholamines. However, the results of these association studies remain inconclusive. We have explored the contribution of eight genetic polymorphisms in modulating the susceptibility to breast cancer by performing a meta-analysis of worldwide studies. In total, 62 case-control studies representing 17 different populations involving 18,117 breast cancer cases and 23,573 healthy controls were included in this meta-analysis. Out of the eight polymorphisms analyzed, methylenetetrahydrofolate reductase (MTHFR) C677T exhibited positive association with the breast cancer risk in both fixed effects (OR 1.14, 95 % CI 1.10-1.17) and random effects (OR 1.10, 95 % CI 1.02-1.18) models. Solute carrier family 19 (folate transporter), member 1 (SLC19A1) G80A exhibited positive association (OR 1.16, 95 % CI 1.03-1.31) while MTR A2756G exhibited an inverse association (OR 0.78, 95 % CI 0.75-0.82) with the breast in fixed effect model alone. Significant heterogeneity was observed in the association of MTHFR C677T with breast cancer even between studies from the same geographical area, specifically among Chinese, Indians, and Turks. Subgroup analysis revealed MTHFR C677T-mediated breast cancer risk in post-menopausal women and women with low dietary intake of folate. Geographical area wise segregation of data revealed MTHFR-mediated increased breast cancer risk in populations who consume methionine-rich diet. Altitude-level variations were observed in the association of SHMT1 C1420T with breast cancer. India and Brazil of same altitude showed an inverse association with this polymorphism, while USA and China that share similar altitude showed a null association. MTHFR C677T and SLC19A1 G80A are the two polymorphisms of one-carbon metabolic pathway that increase breast cancer in the worldwide population. Dietary patterns and altitudinal variations are the likely risk modulators that are contributing toward ethnic-and population-level variations in genetic associations.

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“…In prostate cancer, EcSOD expression correlates with mutations in GCPII [167]. The GCPII D191V mutation promotes SOD3 hypermethylation and is associated with an increased risk of breast cancer [167 177]. Additionally, the GCPII H475Y variant is associated with decreased SOD3 methylation and decreased risk of breast and prostate cancer [167 178].…”

Section: Deregulation Of Ecsod In Cancersmentioning

confidence: 99%

Extracellular superoxide dismutase and its role in cancer

Griess

Tom

Domann

et al. 2017

Free Radical Biology and Medicine

144

124

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Reactive oxygen species (ROS) are increasingly recognized as critical determinants of cellular signaling and a strict balance of ROS levels must be maintained to ensure proper cellular function and survival. Notably, ROS is increased in cancer cells. The superoxide dismutase family plays an essential physiological role in mitigating deleterious effects of ROS. Due to the compartmentalization of ROS signaling, EcSOD, the only superoxide dismutase in the extracellular space, has unique characteristics and functions in cellular signal transduction. In comparison to the other two intracellular SODs, EcSOD is a relatively new comer in terms of its tumor suppressive role in cancer and the mechanisms involved are less well understood. Nevertheless, the degree of differential expression of this extracellular antioxidant in cancer versus normal cells/tissues is more pronounced and prevalent than the other SODs. A significant association of low EcSOD expression with reduced cancer patient survival further suggests that loss of extracellular redox regulation promotes a conducive microenvironment that favors cancer progression. The vast array of mechanisms reported in mediating deregulation of EcSOD expression, function, and cellular distribution also supports that loss of this extracellular antioxidant provides a selective advantage to cancer cells. Moreover, overexpression of EcSOD inhibits tumor growth and metastasis, indicating a role as a tumor suppressor. This review focuses on the current understanding of the mechanisms of deregulation and tumor suppressive function of EcSOD in cancer.

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Association of glutamate carboxypeptidase II (GCPII) haplotypes with breast and prostate cancer risk

Cited by 9 publications

References 29 publications

Proteomics analysis of human breast milk to assess breast cancer risk

Proteomics analysis of human breast milk to assess breast cancer risk

Population-level diversity in the association of genetic polymorphisms of one-carbon metabolism with breast cancer risk

Extracellular superoxide dismutase and its role in cancer

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