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  • 1
    In: Journal of Urology, Ovid Technologies (Wolters Kluwer Health), Vol. 183, No. 5 ( 2010-05), p. 2062-2069
    Type of Medium: Online Resource
    ISSN: 0022-5347 , 1527-3792
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    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2010
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  • 2
    In: Carcinogenesis, Oxford University Press (OUP), Vol. 43, No. 6 ( 2022-06-27), p. 538-546
    Abstract: Helicobacter pylori infection has been suggested to be associated with lung cancer risk. However, information is lacking on whether the association differs by H. pylori antigen. We conducted a nested case-control study within the Southern Community Cohort Study, including 295 incident lung cancer cases and 295 controls. Helicobacter pylori multiplex serology assay was performed to detect antibodies to 15 H. pylori proteins. Conditional logistic regression was used to estimate odds ratios (ORs) and confidence intervals (95% CIs) after adjustment for covariates. Overall H. pylori+ was associated with a non-statistically significant increased risk of lung cancer (OR: 1.29; 95% CI: 0.85–1.95). Significant associations, however, were observed for H. pylori+ VacA+ (OR: 1.64; 95% CI: 1.02–2.62) and H. pylori+ Catalase+ (OR: 1.75; 95% CI: 1.11–2.77). The positive association of H. pylori+ Catalase+ with lung cancer risk was predominantly seen among African Americans (OR: 2.09; 95% CI: 1.11–3.95) but not European Americans (OR: 1.20; 95% CI: 0.56–2.54). Among participants who smoked ≥ 30 pack-years, overall H. pylori+ (OR: 1.85; 95% CI: 1.02–3.35), H. pylori+ CagA+ (OR: 2.77; 95% CI: 1.35–5.70), H. pylori+ VacA+ (OR: 2.53; 95% CI: 1.25–5.13) and H. pylori+ HP1564+ (OR: 2.01; 95% CI: 1.07–3.77) were associated with increased risk of lung cancer. Our study provides novel evidence that associations of H. pylori infection with lung cancer risk differ by H. pylori biomarker, may be more evident among African Americans and may be modified by smoking habits. Furthermore, studies are warranted to confirm our findings.
    Type of Medium: Online Resource
    ISSN: 0143-3334 , 1460-2180
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
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  • 3
    Online Resource
    Online Resource
    Editorial Office of Chinese Journal of Cancer ; 2011
    In:  Chinese Journal of Cancer Vol. 30, No. 2 ( 2011-2-5), p. 138-143
    In: Chinese Journal of Cancer, Editorial Office of Chinese Journal of Cancer, Vol. 30, No. 2 ( 2011-2-5), p. 138-143
    Type of Medium: Online Resource
    ISSN: 1000-467X , 1944-446X
    Language: Unknown
    Publisher: Editorial Office of Chinese Journal of Cancer
    Publication Date: 2011
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    detail.hit.zdb_id: 2922913-3
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  • 4
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2010
    In:  Breast Cancer Research and Treatment Vol. 119, No. 2 ( 2010-1), p. 431-436
    In: Breast Cancer Research and Treatment, Springer Science and Business Media LLC, Vol. 119, No. 2 ( 2010-1), p. 431-436
    Type of Medium: Online Resource
    ISSN: 0167-6806 , 1573-7217
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2010
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  • 5
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2023
    In:  Cancer Research Vol. 83, No. 7_Supplement ( 2023-04-04), p. 4201-4201
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 83, No. 7_Supplement ( 2023-04-04), p. 4201-4201
    Abstract: Introduction: Lung cancer is the leading cause of cancer death in the United States (U.S.). Lung cancer disproportionately affects African Americans (AAs) more than other racial/ethnic groups. Previous studies have linked liver diseases to lung cancer risk; however, few studies have evaluated the associations of circulating liver enzyme levels with lung cancer risk. In this study, we evaluated the associations of the serum alanine transaminase (ALT) and alkaline phosphatase (ALP) levels with the risk of subsequently developing lung cancer. Methods: We conducted a nested case-control study within the Southern Community Cohort Study, a well-conducted prospective cohort study in the southern U.S. mainly consisting of low-income AAs and European Americans (EAs). We included 552 incident lung cancer cases and 1,039 controls individually matched on age, sex, recruitment sites, and date of blood draw. Baseline serum levels of ALT and ALP were measured using the Beckman Coulter clinical chemistry analyzer. Conditional logistic regression and generalized estimating models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) after adjusting for age, education, household income, body mass index (BMI), smoking status, pack-years, alcohol consumption, physical activity levels, history of chronic obstructive pulmonary disease, hypertension, and diabetes. Results: Higher serum levels of ALT were associated with a lower overall risk of lung cancer. Compared with the lowest tertile, participants in the second and third tertiles had OR (95% CI) of 0.74 (0.48-1.14) and 0.47 (0.28-0.78) (Ptrend & lt; 0.01). The inverse association was observed in both AAs and EAs. However, the inverse associations between serum ALT levels and lung cancer risk were more evident among men [ORT3 vs T1 = 0.36 (0.18-0.70)], current smokers [ORT3 vs T1 =0.65 (0.47-0.90)] , participants with lower BMI [ORT3 vs T1=0.55 (0.38-0.79)], or lower physical activity [ORT3 vs T1 = 0.55 (0.37-0.83)] . Stratified analyses by time interval between blood collection and lung cancer diagnosis showed that the inverse associations were observed in both those diagnosed within [ORT3 vs T1 =0.48 (0.23-1.00)] and after [ORT3 vs T1 = 0.36 (0.19-0.69)] a median follow up time of 3 years. The serum ALT level was not associated with overall lung cancer; however, higher serum ALP levels were significantly associated with increased lung cancer risk among AA men [ORT3 vs T1 = 1.98 (1.18-3.34)]. Conclusion: Our results indicate that in a predominantly low-income AA and EA population, serum ALT levels may be related to a lower risk of lung cancer. Further studies are warranted to confirm our findings and elucidate the potential underlying mechanisms of the associations. Citation Format: Shuai Xu, Hui Cai, Jie Wu, Hyung-Suk Yoon, Regina Courtney, Xiao-Ou Shu, William J. Blot, Wei Zheng, Qiuyin Cai. Associations of pre-diagnostic serum liver enzymes levels with lung cancer risk: results from the Southern Community Cohort Study. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 4201.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
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  • 6
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 891-891
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 891-891
    Abstract: Signal-induced proliferation-associated gene 1 (Sipa1), encodes a GTPase-activating protein (GAP), was identified as a candidate host metastasis-regulatory factor in mice. Several epidemiological studies have shown that SIPA1 may play an important role in breast cancer risk and metastasis with inconsistent results. We evaluated functional single nucleotide polymorphisms (SNPs) in SIPA1 in relation to breast cancer risk and survival in Chinese women. Included in the study were 1,134 cases and 1,234 age frequency-matched community controls that participated in the Shanghai Breast Cancer Study, a large scale population-basd case-control study. Breast cancer patients were followed to determine intervals of overall survival and disease-free survival. Functional SNPs were genotyped using TaqMan assays. Additional SNPs in this gene region, both genotyped and imputed from a genome-wide association study, were also included in the analyses. The SIPA1 polymorphisms were not associated with breast cancer risk. We found SIPA1 polymorphisms were associated with breast cancer overall survival. Patients carrying the GA/AA genotypes in the synonymous exonic SNP rs746429 were associated with a marginally significant poor overall survival (HR =1.2, 95% CI, 0.9-1.6) as compared with the common GG genotype. Furthermore, this association was more evident among patients with an early stage cancer (HR =1.4, 95% CI, 1.0-1.9) than those with a late stage cancer (HR=1.2, 95% CI, 0.7-2.1). Patients carrying the AA genotype of rs3741378, a nonsynonymous exonic SNP, were associated with a better overall survival (HR =0.6, 95% CI, 0.4-1.0) as compared to those with the common GG genotype. We found that the SIPA1 polymorphisms were not associated with disease-free survival. Our findings suggested that common SIPA1 genetic polymorphisms may be associated with breast cancer progression. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 891.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 7
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2006
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 15, No. 2 ( 2006-02-01), p. 403-404
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 15, No. 2 ( 2006-02-01), p. 403-404
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2006
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 8
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Research Vol. 76, No. 14_Supplement ( 2016-07-15), p. 3455-3455
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 14_Supplement ( 2016-07-15), p. 3455-3455
    Abstract: Lung cancer is the leading cause of cancer death in the United States. The lungs are inhabited by diverse microbial communities. Bacterial infection in the lungs, such as a history of pneumonia and tuberculosis, has been associated with increased risk of lung cancer. Recent studies have found that the oral microbiome is the primary source of the bacterial microbiota in the lungs and that the bacterial species detected in the lungs overlap those found in the mouth. Therefore, readily-accessible oral samples may be used to investigate the role of bacteria in lung cancer etiology. In this study, we evaluated the association of the oral microbiome with subsequent risk of developing lung cancer. We conducted a nested case-control study using resources of the Southern Community Cohort Study, a well-characterized prospective cohort study of approximately 86,000 adult men and women, two-thirds of whom are African American. DNA was isolated from pre-diagnostic mouth rinse samples of 177 lung cancer cases and 177 controls matched on age, race, sex, smoking, and date of sample collection. The V4 domain of microbial 16S rRNA gene was sequenced. Sequencing libraries were prepared using the NEXTflex 16S V4 Amplicon-Seq Kit and sequenced with paired-end 150 bp using Illumina MiSeq. Sequencing data were processed using QIIME, and sequence reads were clustered into Operational Taxonomic Units (OTUs). On average, 82,254 sequencing reads were obtained for each sample. Duplicated quality control samples (n = 18; 2 samples each repeated for 9 times) showed very similar microbiome compositions, indicating high data quality. A total of 693 OTUs were observed and classified to 11 phyla. The observed composition was similar to the oral microbiome data from other studies, including the Human Microbiome Project. Multiple oral bacteria differed between lung cancer cases and controls. For example, Order CW040 was associated with increased lung cancer risk with OR of 3.64 (P = 0.0098). Family Tissierellaceae and Genus Parvimonas were associated with decreased risk of lung cancer with ORs of 0.42 (P = 0.0025) and 0.41 (P = 0.0014), respectively. Some of the associations differed by race. Among the lung cancer-associated oral bacteria, Family Fusobacteriaceae, Family Neisseriaceae, and Order Bacteroidales were among the most abundant bacteria found in the lungs. In summary, our study suggests that certain bacteria in the mouth are associated with substantial development of lung cancer and that the oral microbiome plays an important role in lung cancer etiology. Further studies with a larger sample size and with more comprehensive investigation are needed to confirm these findings. Citation Format: Qiuyin Cai, Jirong Long, Hua Xie, Xiaofei Wang, Jie Wu, Regina Courtney, Xiao Ou Shu, Wei Zheng, William J. Blot. Association of oral microbiome with lung cancer risk: Results from the Southern Community Cohort Study. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3455.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
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  • 9
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 16_Supplement ( 2020-08-15), p. 1052-1052
    Abstract: Lung cancer is the leading cause of cancer death in the United States and many other countries. Helicobacter pylori (H. pylori), a Group 1 carcinogen classified by IARC, is a common bacteria infecting humans. Emerging evidence supports a possible etiological role of H. pylori infection in lung cancer. H. pylori has evolved over time to become highly genetically diverse, with substantial variations in the presence or levels of virulence factors. To evaluate the associations of lung cancer risk with H. pylori seropositivity, overall and by antigen-specific biomarkers, we conducted a nested case-control study using resources from the Southern Community Cohort Study (SCCS) including ~86,000 participants, two-thirds of whom are African American. A total of 295 incident lung cancer cases and 295 matched controls were included in this study. Controls were matched to cases on age, sex, race, recruitment site and date of blood draw. H. pylori multiplex serology assay was performed to detect levels of IgA, IgM and IgG antibodies to 15 H. pylori proteins. Overall H. pylori seropositivity (H. pylori+) was defined as being positive to any 4 or more H. pylori antigens. Individual H. pylori antigens were considered as seropositive only when the sample was simultaneously considered overall H. pylori+, which ensured that antigen-specific seropositivity was not based on cross-reactive antibody responses from infection with other pathogens expressing homologous proteins. Multivariable logistic regression models were used to estimate odds ratios (ORs) and corresponding confidence intervals (95% CIs) for lung cancer risk associated with seropositivity of H. pylori after adjusting for age, smoking status, pack-years, alcohol consumption, education, household income, BMI and history of COPD. Overall H. pylori+ was associated with a non-statistically significant increased lung cancer risk (OR, 1.29; 95% CI, 0.85-1.95). Associations were stronger for H. pylori+ VacA+ (OR, 1.64; 95% CI, 1.02-2.62) and H. pylori+ Catalase+ (OR, 1.75; 95% CI, 1.11-2.77), the latter more so among African Americans (OR, 2.09; 95% CI, 1.11-3.95) than European Americans (OR, 1.20; 95% CI, 0.56-2.54). Among people who smoked ≥ 30 pack-years, overall H. pylori+ (OR, 1.85; 95% CI, 1.02-3.35), H. pylori+ CagA+ (OR, 2.77; 95% CI, 1.35-5.70), H. pylori+ VacA+ (OR, 2.53; 95% CI, 1.25-5.13) and H. pylori+ Omp+ (OR, 2.01; 95% CI, 1.07-3.77) were associated with increased lung cancer risk. Among current and former smokers, significant interactions were observed for H. pylori+ CagA+ (p for interaction = 0.01) and H. pylori+ VacA+ (p for interaction = 0.03) between those who smoked ≥ 30 pack-years and those who smoked & lt; 30 pack-years. In summary, our results indicate that H. pylori infection may be associated with an elevated risk of lung cancer, and the associated risk might differ by antigen-specific H. pylori biomarkers and smoking amount. Further studies are warranted to confirm our findings. Citation Format: Hyung-Suk Yoon, Wei Zheng, Hui Cai, Jie Wu, Wanqing Wen, Regina Courtney, Angelika Michel, Michael Pawlita, Tim Waterboer, Qiuyin Cai. Associations of Helicobacter pylori biomarkers with lung cancer risk among low-income and African American populations: Results from the Southern Community Cohort Study [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 1052.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 10
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 2781-2781
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 2781-2781
    Abstract: Alternative splicing generates different transcripts from the same precursor mRNA. ERBB2 proto-oncogene is involved in the growth, invasion, and prognosis of breast cancer. The ERBB2-sp is a splice variant of ERBB2 that lacks the intracellular and transmembrane domains, which may alter the function of the ERBB2 gene. We hypothesize that the ERBB2-sp and the wild type ERBB2 gene may play a different role in the development and prognosis of breast cancer, and thus compared ERBB2 and ERBB2-sp mRNA expression in tumor tissue and adjacent non-tumor tissue in both breast cancer patients and benign breast disease (BBD) patients. Included in the study were 515 patients diagnosed with breast cancer and 206 patients diagnosed with BBD. These women were recruited as part of the Shanghai Breast Cancer Study and they provided samples of tumor tissue and adjacent non-tumor tissue to the study. Tumor tissues from patients with breast cancer had substantially higher levels of ERBB2 expression than those from patients with BBD (81vs 37, P & lt; 0.0001). On the other hand, adjacent non-tumor tissues from patients with breast cancer had substantially lower levels of ERBB2 expression than those from patients with BBD (20 vs 34, p=0.0254). In breast cancer cases, ERBB2 expression in tumor tissue was significantly higher than that in their paired adjacent non-tumor tissue (p=0.0028). No significant difference of ERBB-sp expression levels was found in any of the following comparisons, tumor tissues or adjacent normal tissues between breast cancer patients and BBD controls as well as between the tumor tissues and adjacent normal tissues in both breast cancer and BBD patients. In the comparison of tumor tissues between breast cancer patients and BBD controls, the ratio of ERBB2 to ERBB2-sp expression levels (ERBB2 /ERBB2-sp index) in tumor tissue was associated with a significantly increased breast cancer risk in a linear manner, with adjusted odds ratios (95% CI) increased from 1.00 (reference) to 1.33 (0.84-2.13), 1.82 (1.13-2.94), and 2.63(1.55-4.43) (P for trend & lt;0.001) from the lowest to the highest quintiles of expression groups. However, there were no apparent associations of expressions of ERBB2 and ERBB2-sp, or ERBB2/ERBB2-sp index in cancer tissue with either overall survival or disease-free survival. Our findings suggest that the expression of ERBB2 and its splice variant ERBB2-sp may play a different role in the development, but not prognosis, of breast cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2781.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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    detail.hit.zdb_id: 410466-3
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