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  • American Association for Cancer Research (AACR)  (110)
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  • 1
    Online Resource
    Online Resource
    Abstract 5183: The preclinical characterization of TST001, a novel humanized anti-claudin18.2 mAb with enhanced binding affinity and anti-tumor activity
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Research Vol. 80, No. 16_Supplement ( 2020-08-15), p. 5183-5183
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 16_Supplement ( 2020-08-15), p. 5183-5183
    Abstract: Claudin-18 isoform 2 (CLDN18.2) is a member of the human claudin family of tetraspan membrane proteins that are crucial structural and functional components of tight junctions. Unlike other family members, CLDN18.2 expression is strictly limited to differentiated epithelial cells of gastric mucosa. Interestingly CLDN18.2 was ectopically expressed at a significant level in multiple tumor types including gastric, esophageal, pancreatic and lung cancers, which makes it as an attractive anti-cancer target. TST001 is a novel humanized IgG1 monoclonal antibody, which specifically binds to cells expressing human CLDN18.2 with high affinity but not to the closely related Claudin 18.1. TST001 can compete with IMAB362, the clinical stage anti-CLDN18.2 mAb, for its binding to CLDN18.2 yet engages distinct epitope for binding. By reducing fucosylation during cell culture process, TST001 has further enhanced binding affinity to FcγRIIIa, which translates into more potent ADCC activity. Indeed, TST001 showed sub-nanomolar ADCC activity against gastric cancer cells expressing medium to low CLDN18.2 in the presence of human PBMC and NK cells, which is significantly more potent than IMAB362. TST001 also showed more potent CDC and ADCP activities against CLDN18.2 expressing cells than IMAB362. In both Sprague Dawley Rat and Cynomolgus Monkey, the systemic exposure of TST001 increased proportionally in a dose-dependent manner. In gastric cancer cell line and patient derived xenograft tumor models, TST001 showed more potent anti-tumor activity as compared with IMAB362. Furthermore, the combination of TST001 with chemo agents resulted in synergistic anti-tumor effect in these tumor models. In addition, we have also generated and characterized an antibody that is suitable for IHC based detection and is selective to CLDN18.2 over CLDN18.1. Altogether, these preclinical findings warrant further clinical evaluation of TST001 in patients with CLDN18.2 positive tumors. Citation Format: Fei Teng, Yi Gu, Hui Chai, Huanhuan Guo, Hongjun Li, Xiwen Wu, Xinlai Yao, Fei Xu, Lei Shi, Zhenzhi Yan, Xiaoli Zi, Zheng Dai, Timethy Liao, Lisa Zheng, Francis Fan, Zhen Li, Jerry Yang, Xueming Qian. The preclinical characterization of TST001, a novel humanized anti-claudin18.2 mAb with enhanced binding affinity and anti-tumor activity [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 5183.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2020-5183
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
    detail.hit.zdb_id: 2036785-5
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  • 2
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    Abstract 119: Urinary biomarkers of oxidative stress and breast cancer survival among Chinese breast cancer survivors.
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 8_Supplement ( 2013-04-15), p. 119-119
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. 119-119
    Abstract: Background: Systemic oxidative stress has been implicated in the pathogenesis and progression of many chronic diseases, including breast cancer. To our knowledge, no study has investigated the association of biomarkers of systemic oxidative stress after cancer treatment and breast cancer prognosis. Methods: We conducted a pilot study to investigate the association of systemic oxidative stress after primary cancer treatment with mortality in a nested case-control study in the Shanghai Breast Cancer Survival Study (SBCSS). Urinary levels of 15-F(2t)-isoprostane (15-F(2t)-IsoP) and one of its major metabolites (2,3-dinor-5,6-dihydro-15-F(2t)-IsoP (15-F(2t)-IsoP-M)), two well-studied biomarkers of systemic oxidative stress, were measured using gas chromatography/negative ion chemical ionization mass spectrometry for 57 deceased breast cancer patients (cases; 88% due to breast cancer) and 103 matched surviving breast cancer patients (controls) in the SBCSS with available post-cancer treatment urinary samples. Cases and controls were aged 26-70 years and were matched approximately 1:2 on age at diagnosis (+/- 1 year), stage (I-III), and year of diagnosis (2003-2004). Biomarkers were adjusted for creatinine concentrations and expressed as ng/mg of creatinine. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were derived from conditional logistic regression models, conditioned on age, stage, and year of diagnosis. Results: Elevated 15-F(2t)-IsoP levels, categorized based on the median level (≥1.73; & lt;1.73(reference)), were inversely associated with mortality (adjusted OR = 0.36, 95% CI: 0.14-0.96) after adjustment for known clinical prognostic factors (including cancer treatment and tumor characteristics), body mass index, vitamin supplement use, and weeks between breast cancer diagnosis and urine collection. The inverse association was marginally significant when 15-F(2t)-IsoP was categorized based on tertiles (p for trend = 0.08). In contrast, elevated 15-F(2t)-IsoPM levels, categorized based on the median level (≥0.91; & lt;0.91 (reference)), were associated with a statistically non-significant increased risk of mortality (adjusted OR = 1.39, 95% CI: 0.62-3.09). Conclusion: These preliminary results suggest differing associations for 15-F(2t)-IsoP and 15-F(2t)-IsoPM with mortality among breast cancer survivors. To our knowledge, this is the first study to investigate the association between 15-F(2t)-IsoP or 15-F(2t)-IsoP-M levels and breast cancer survival. Results from this pilot study require conformation in future larger studies. Citation Format: Sarah J. Nechuta, Qiuyin Cai, Ying Zheng, Ginger L. Milne, Hui Cai, Qi Dai, Gong Yang, Wei Zheng, Wei Lu, Xiao Ou Shu. Urinary biomarkers of oxidative stress and breast cancer survival among Chinese breast cancer survivors. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 119. doi:10.1158/1538-7445.AM2013-119
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2013-119
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
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    detail.hit.zdb_id: 410466-3
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  • 3
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    Molecular Subgroups of Intrahepatic Cholangiocarcinoma Discovered by Single-Cell RNA Sequencing–Assisted Multiomics Analysis
    American Association for Cancer Research (AACR) ; 2022
    In:  Cancer Immunology Research Vol. 10, No. 7 ( 2022-07-01), p. 811-828
    Details
    In: Cancer Immunology Research, American Association for Cancer Research (AACR), Vol. 10, No. 7 ( 2022-07-01), p. 811-828
    Abstract: Intrahepatic cholangiocarcinoma (ICC) is a relatively rare but highly aggressive tumor type that responds poorly to chemotherapy and immunotherapy. Comprehensive molecular characterization of ICC is essential for the development of novel therapeutics. Here, we constructed two independent cohorts from two clinic centers. A comprehensive multiomics analysis of ICC via proteomic, whole-exome sequencing (WES), and single-cell RNA sequencing (scRNA-seq) was performed. Novel ICC tumor subtypes were derived in the training cohort (n = 110) using proteomic signatures and their associated activated pathways, which were further validated in a validation cohort (n = 41). Three molecular subtypes, chromatin remodeling, metabolism, and chronic inflammation, with distinct prognoses in ICC were identified. The chronic inflammation subtype was associated with a poor prognosis. Our random forest algorithm revealed that mutation of lysine methyltransferase 2D (KMT2D) frequently occurred in the metabolism subtype and was associated with lower inflammatory activity. scRNA-seq further identified an APOE+C1QB+ macrophage subtype, which showed the capacity to reshape the chronic inflammation subtype and contribute to a poor prognosis in ICC. Altogether, with single-cell transcriptome-assisted multiomics analysis, we identified novel molecular subtypes of ICC and validated APOE+C1QB+ tumor-associated macrophages as potential immunotherapy targets against ICC.
    Type of Medium: Online Resource
    ISSN: 2326-6066 , 2326-6074
    URL: Article
    DOI: 10.1158/2326-6066.CIR-21-1101
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
    detail.hit.zdb_id: 2732517-9
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  • 4
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    Abstract B88: Plasma carotenoids, tocopherols, retinol and breast cancer risk: Results from the Shanghai Women's Health Study
    American Association for Cancer Research (AACR) ; 2008
    In:  Cancer Prevention Research Vol. 1, No. 7_Supplement ( 2008-11-01), p. B88-B88
    Details
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 1, No. 7_Supplement ( 2008-11-01), p. B88-B88
    Abstract: B88 Objective Studies conducted in Western countries have suggested that lipophilic antioxidants, particularly carotenoids, may have preventive effects on the risk of breast cancer. We prospectively investigated the associations of serum levels of tocopherols, total retinol, total and specific types of carotenoids with the risk of developing breast cancer among Chinese women; a population with low risk of breast cancer and low prevalence of vitamin supplement use. Methods A nested case-control study was conducted within the cohort of the Shanghai Women’s Health Study including 365 newly-diagnosed cases and 726 individually-matched controls 40-70 years of age who provided a blood sample at baseline. Multivariate conditional logistic regression analyses were used to assess associations between breast cancer risk and antioxidants. Results Overall, we did not observe significant associations between any of the tocopherols, retinol and most carotenoids, and breast cancer risk. Plasma levels of lycopene other than trans, 5-cis and 7-cis were associated with a reduced risk with an OR of 0.56 (95% CI: 0.32-0.97) for the highest quartile versus the lowest after adjusting for plasma levels of other antioxidants. This inverse association was seen predominantly among premenopausal women with a corresponding OR (95% CI) of 0.36 (0.16-0.80). We also found that trans α-cryptoxanthin was associated with a reduced risk of breast cancer in a dose-response manner, with a corresponding OR of 0.59 (95% CI: 0.34-1.01) (P trend, 0.02) and the inverse association for trans α-cryptoxanthin appeared in both pre- and post-menopausal women. Conclusions Our study did not show strong evidence for an overall protective effect of plasma lipophilic antioxidants on breast cancer risk. The few significant inverse associations for subtype carotenoids need to be confirmed in future studies. Citation Information: Cancer Prev Res 2008;1(7 Suppl):B88.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.PREV-08-B88
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2008
    detail.hit.zdb_id: 2422346-3
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  • 5
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    Abstract A1: An miR-502 binding site single-nucleotide polymorphism in the 3′-untranslated region of the SET8 gene is associated with early age of breast cancer onset
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Prevention Research Vol. 3, No. 1_Supplement ( 2010-01-07), p. A1-A1
    Details
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 3, No. 1_Supplement ( 2010-01-07), p. A1-A1
    Abstract: Purpose: MicroRNAs regulate gene expression by binding to the 3′-untranslated region (UTR) of target genes. Single-nucleotide polymorphisms of critical genes may affect their regulation by microRNAs. We have identified a single nucleotide polymorphism within the miR-502 seed binding region in the 3′-UTR of the SET8 gene. SET8 methylates TP53 and regulates genome stability. We investigated the role of this SET8 single nucleotide polymorphism and in concert with the TP53 codon72 single nucleotide polymorphism in the propensity for onset of breast cancer. Experimental Design: We measured the SET8 single nucleotide polymorphisms in a case-control study on 1110 breast cancer cases and 1097 controls. Results: The SET8 CC and TP53 GG genotypes were independently associated with an earlier age of breast cancer onset in an allele-dose-dependent manner (for SET8, 52.2 years for TT, 51.4 for TC, and 49.5 for CC; and for TP53, 53.1 years for CC, 51.5 for GC, 50.7 for GG). Individuals with combined SET8 CC and TP53 GG genotypes developed cancer at a median age of 47.7 years as compared with 54.6 years for individuals with combined SET8 TT and TP53 CC genotypes. In the 51 breast cancer tissue samples tested, the SET8 CC genotype was associated with reduced SET8, but not miR-502, transcript levels. Conclusions: These data suggest that the miR-502 binding site single nucleotide polymorphism in the 3′-UTR of SET8 modulates SET8 expression and contributes to the early development of breast cancer, either independently or together with the TP53 codon 72 single nucleotide polymorphism. Larger studies with multiethnic groups are warranted to validate our findings. Citation Information: Cancer Prev Res 2010;3(1 Suppl):A1.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.PREV-09-A1
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2422346-3
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  • 6
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    Abstract A92: Oxidative stress, obesity, and breast cancer risk: results from the Shanghai women health study (SWHS) .
    American Association for Cancer Research (AACR) ; 2008
    In:  Cancer Prevention Research Vol. 1, No. 7_Supplement ( 2008-11-01), p. A92-A92
    Details
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 1, No. 7_Supplement ( 2008-11-01), p. A92-A92
    Abstract: A92 Background Increased reactive oxygen species may exhaust the antioxidant capability of human defense systems, leading to oxidative stress and cancer development. Urinary F2-isoprostanes, secondary end products of lipid peroxidation, are more accurate markers of oxidative stress than other available biomarkers. No prospective study has investigated whether levels of 15-F2t-Isop and its metabolite (15-F2t-IsopM) are related to breast cancer risk. Methods We conducted a nested case-control study within the Shanghai Women’s Health Study, a population-based cohort study of 74,942 Chinese women between 40 and 70 years of age. Prediagnostic urinary 15-F2t-Isop and 15-F2t-IsopM were measured by gas chromatography-mass spectrometry for 436 breast cancer cases and 852 individually matched controls. Results Urinary excretion of isoprostanes was not significantly different between cases and controls. However, among overweight women, levels of isoprostanes were positively associated with breast cancer risk, which became stronger with increasing BMI. Among women with a BMI≥29, the odds ratio (OR) increased to10.27 (2.41-43.80) for the highest compared to the lowest tertile of 15-F2t-IsopM (p for trend, 0.003; p for interaction, 0.0004). In contrast, 15-F2t-Isop and 15-F2t-IsopM were inversely associated with breast cancer risk among non-overweight women. Among women with a BMI≤23, breast cancer risk was reduced with increasing 15-F2t-Isop levels in a dose-response manner (p for trend, 0.006), with an OR of 0.46 (95%CI: 0.26-0.80) for the highest tertile versus the lowest (p for interaction, 0.006). Conclusion Our results suggest that the role of oxidative stress in breast cancer development may depend on adiposity and menopausal status. Citation Information: Cancer Prev Res 2008;1(7 Suppl):A92.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.PREV-08-A92
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2008
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  • 7
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    Abstract 3763: Calcium intake, CABP1 polymorphisms, and the risk of colorectal adenoma: Results from Tennessee Colorectal Polyp Study
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 3763-3763
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 3763-3763
    Abstract: Background: High calcium consumption may confer a reduced risk of colorectal adenoma and cancer. This effect could differ by polymorphisms in the genes involved in calcium regulation. The calcium binding protein 1(CABP1) gene encodes a calbindin-D9k protein, an important component of calcium mediated cellular signal transduction. CABP1 express primarily in intestine, and increased levels of Calbindin-D9k in intestine were found to be correlated with calcium hyperabsorption. A recent study found that deletion of CABP1 and another gene had a significant effect on calcium processing under calcium-deficient conditions. These findings suggest the variations in CABP1 expression in intestine may explain some of the variability in calcium absorption. However, so far no study has evaluated genetic variations in CABP1 with the risk of colorectal adenoma. Objectives: In the current study, we first screened whether CABP1 variants or their interactions with calcium intake were associated with urinary calcium among 256 normal controls. Further, single-nucleotide polymorphisms (SNPs) were evaluated for their independent association and interactions with calcium intake in relation to colorectal adenoma risk. Methods: Included in the study were 958 adenoma cases and 909 controls from the Tennessee Colorectal Polyp Study (TCPS), an ongoing colonoscopy-based case-control study conducted in Nashville, TN. Genotyping was performed using the Affymetrix Human Mapping 500K array set. Seven tagging SNPs in CABP1 were analyzed. Linear regression models were used to estimate the association between genotypes and urinary calcium level. Multivariate unconditional logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals (CI). Multiplicative interactions for gene-diet interactions were evaluated in logistic regression models by using likelihood ratio tests. Results: Although no SNPs were observed to be associated with urinary calcium levels, one SNP (rs7956304) was found to be significantly associated with risk of adenoma. In comparison to participants with the GG genotype, participants with GA had higher risk of colorectal adenoma (OR=1.29, 95% CI 1.03-1.61, P=0.027), while participants with the AA genotype had no appreciable difference in risk (OR=0.82, 95% CI 0.50-1.35, P=0.428). This SNP was not observed to interact with calcium intake. Conclusions: These findings suggest that genetic variations in CABP1 may affect the risk of colorectal adenoma. To the best of our knowledge, this study is the first to evaluate CABP1 polymorphisms in relation to the risk of adenoma. Our finding of a significant association is promising; however, the finding should be confirmed in future studies. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3763. doi:10.1158/1538-7445.AM2011-3763
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-3763
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 8
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    Abstract LB-452: Genetic polymorphisms in the TRPM7 gene and colorectal adenoma risk
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. LB-452-LB-452
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. LB-452-LB-452
    Abstract: Background: Several epidemiologic studies suggest that high magnesium intake is associated with reduced risk of colorectal cancer or colorectal adenoma. Results, however, have been inconsistent. Ionized magnesium (Mg2+) counters the action of ionized calcium (Ca2+) in many physiologic activities. We previously reported that the associations between intakes of magnesium, calcium or calcium/magnesium ratio with risk of colorectal polyp were modified by the common Thr1482Ile polymorphism in the gene for the transient receptor potential melastatin 7 (TRPM7), which is a ubiquitously expressed constitutive ion channel with a higher affinity for Mg2+ than for Ca2+ and plays a central role in magnesium homeostasis and magnesium (re)absorption pathways. Except for our earlier study, no other study has investigated these possible gene-nutrient interactions in the etiology of colorectal adenoma or cancer. In the present study, we examined single nucleotide polymorphisms (SNPs) in the TRPM7 gene and their interaction with calcium and magnesium intake or calcium/magnesium ratio in relation to risk of colorectal adenoma using data from the Tennessee Colorectal Polyp Study. Methods: Included in the study were participants of the Tennessee Colorectal Polyp study, an ongoing colonoscopy-based case control study conducted in Nashville, TN. Genotyping was performed at Vanderbilt Microarray Shared Resource using the Affymetrix Genome-Wide Human SNP Array 5.0. Sixteen SNPs in the TRPM7 gene were genotyped for 958 colorectal adenoma cases and 909 controls. Hardy-Weinberg equilibrium was assessed for each SNP among controls. The associations of each genotype with colorectal adenoma risk were evaluated under dominant, recessive and additive models, respectively. Multivariate unconditional logistic regression models were used to estimate the odds ratio and 95% confidence intervals for each SNP. Multiplicative interactions were evaluated for gene-diet interactions using likelihood ratio tests. Results: All the genotype frequencies for the TRPM7 were in Hardy-Weinberg equilibrium. Of the sixteen SNPs, Four SNPs were significantly associated with risk of colorectal adenoma whereas six SNPs significantly interacted with dietary calcium intake or the ratio of dietary calcium to magnesium intake (five SNPs with calcium and six with the ratio) in relation to risk of colorectal adenoma. The two sets of SNPs were not in strong linkage disequilibrium (LD). However, either three of the four associated SNPs or all of the six interacting SNPs were in strong LD with one another respectively. No significant interactions with magnesium intake were observed. Conclusions: Our results suggest that genetic polymorphisms in the TRPM7 gene, particularly their interactions with calcium or calcium/magnesium ratio, contribute to risk of colorectal adenoma. Further replications in large-scale studies are ongoing. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-452. doi:10.1158/1538-7445.AM2011-LB-452
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-LB-452
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
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  • 9
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    Abstract 1674: Two phase study of KCNJ1 polymorphisms, calcium, magnesium and colorectal adenoma risk, results from the Tennessee Colorectal Polyp Study
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 1674-1674
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 1674-1674
    Abstract: Background: Previous studies generated inconsistent results on the associations between intakes of calcium and magnesium with risk of colorectal adenoma and cancer. It is possible that some of the inconsistency is due to a modifying effect by genetic polymorphisms involved in calcium and magnesium homeostasis. The KCNJ1 gene encodes the Inward-rectifier potassium channel (ROMK). ROMK plays an essential role in the homeostasis of potassium, which is critical for the reabsorption of calcium and magnesium. Objectives: We hypothesize that common variants in KCNJ1 may modify the associations between intakes of calcium and/or magnesium and risk of colorectal adenoma risk. Methods: Included were participants of the Tennessee Colorectal Polyp Study (TCPS), a colonoscopy-based case control study conducted in Nashville, TN. In the phase I study, genotyping was performed using the Affymetrix Human Mapping 500K array set in 958 colorectal adenoma cases and 909 controls and 13 tagging single-nucleotide polymorphisms (SNPs) in the KCNJ1 gene were evaluated. SNPs identified as significant in phase I were genotyped in phase II in an independent set (860 cases and 3083 controls). Results: In phase I, 1 tagging SNP was significantly associated with adenoma risk and 8 SNPs were interacted significantly with calcium or magnesium intake in risk of colorectal adenoma. In phase II, only 1 of the 9 SNPs significantly interacted with calcium and magnesium intakes in relation to colorectal adenoma although the genotype per se was not directly associated with the risk. In combined analysis, the p value for the interaction between the SNP and calcium intake was 0.00015 and it remained statistically significant after Bonferroni correction for multiple comparisons. In stratified analyses by levels of calcium and magnesium (above or below RDA levels), we found adenoma risk significantly increased for those who with at least 1 variant allele and whose intake levels of calcium and magnesium were below the RDA levels, with ORs (95% CI) of 1.35 (1.10, 1.67) and 1.43 (1.08, 1.89) respectively, compared to those who did not possess the variant allele. The corresponding ORs (95% CI) increased to 1.84 (1.33, 2.53) and 2.30 (1.53, 3.46), respectively, multiple adenomas versus controls. Conclusions: In this two-stage analysis, we found no overall association of adenoma with KCNJ1 genotype. However, common KCNJ1 variants significantly interacted with intakes of calcium and magnesium in risk of colorectal adenoma, particular for multiple adenomas. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1674. doi:1538-7445.AM2012-1674
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-1674
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036785-5
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  • 10
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    Abstract 865: Fat-1 gene suppression of breast cancer growth in mice
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 865-865
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 865-865
    Abstract: The high ratio of n-6/n-3 polyunsaturated fatty acids (PUFAs) content in Western diets (approximately 10 to 30) may be related to the high breast cancer rate in the United States compared to Japan (approximately 4). Numerous studies in literature report about the tumor suppression effect of n-3 PUFAs, a main component of fish or fish oil. A recent study on B16 melanoma on C57BL/6 mice carrying the fat-1 gene, suppressed the melanoma by changing the n-6/n-3 ratio in tumors from 27:1 in wild type mice to 4.6:1 in fat-1 mice. In this project, a fat-1 gene, which encodes a fatty acyl desaturase that acts on substrates of 16-20 carbons and converts n-6 to n-3 fatty acids, was transfected into the human breast cancer cells MDA-MB-231, parental MCF-7 and tamoxifen-resistant MCF-7/TAM-R cells, Sk-BR3 and murine EMT6 mammary tumor cells. Both fat-1 transgenic mice and fat-1 gene treated breast cancer cells were employed to test our hypothesis that fat-1 suppresses the growth of both estrogen receptor (ER) positive and ER negative breast cancer cells that respond poorly to endocrine therapies. We have also treated the breast cancer cell lines with docosahexaenoic acid (DHA, n-3 fatty acid), arachidonic acid (AA, n-6 fatty acid) with a vehicle control. We found that for the ER negative human breast cancer cells, MDA- MB-231 and SK-BR-3 cells, the cell proliferation rate of DHA treated cells decreased 50%, compared to the corresponding control cells treated with AA and vehicle control. The fatty acid analysis of the fat-1 gene expressing breast cancer cells MDA-MB-231 and MCF-7 showed 30% and 46% reduction of n-6/n-3 ratio, respectively, and ∼30% reduction of cell proliferation rate. The fat-1 transfected MDA-MB-231 cells have ∼4-fold increase of cell apoptosis by Tunel assay. Fat-1 gene expression also suppresses the growth of tamoxifen resistant human breast cancer cells MCF-7F/Tam-R. These results indicate that fat-1 or n-3 fatty acid suppresses breast cancer cells in an ER independent way. Normal human mammary epithelial cells treated with DHA, AA and BSA showed no significant difference of growth rates, suggesting that the n-3 suppression effect is breast cancer selective. In a preliminary study, the growth rate of the EMT6 mammary tumors were significantly reduced when the cell line was treated with fat-1 gene before inoculation into the FVB/NJ mice. The transgenic mice expressing fat-1 gene are also used to investigate the breast cancer suppression effect of fat-1 gene in vivo. The underlying mechanism of the breast cancer suppression effect by fat-1 gene is currently under investigation. This study may provide a potential adjuvant therapeutic method for hormonal resistant human breast cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 865. doi:10.1158/1538-7445.AM2011-865
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-865
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
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    detail.hit.zdb_id: 410466-3
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