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  • American Association for Cancer Research (AACR)  (178)
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  • American Association for Cancer Research (AACR)  (178)
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  • 1
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 22 ( 2016-11-15), p. 6520-6532
    Abstract: The Jumonji domain–containing chromatin remodeling factor JMJD3 has important roles in development and cancer. Here, we report a pivotal role for JMJD3 in sustaining the phenotype of aggressive hepatocellular carcinomas. Expression levels of JMJD3 in clinical specimens of hepatocellular carcinoma correlated inversely with patient survival. In hepatocellular carcinoma cells, we found that enforcing its overexpression induced epithelial–mesenchymal transition (EMT), invasive migration, stem cell–like traits, and metastatic properties. Conversely, silencing JMJD3 in hepatocellular carcinoma cells overexpressing it inhibited these aggressive phenotypes. Mechanistically, JMJD3 modulated H3K27me3 in the SLUG gene promoter, a histone mark associated with active SLUG transcription. SLUG silencing blocked JMJD3-induced EMT, stemness, and metastasis. Furthermore, SLUG expression in hepatocellular carcinoma clinical specimens correlated positively with JMJD3 expression. Our results establish JMJD3 as a critical driver of hepatocellular carcinoma stem cell–like and metastatic behaviors, with implications for prognosis and treatment. Cancer Res; 76(22); 6520–32. ©2016 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
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  • 2
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 27, No. 15 ( 2021-08-01), p. 4186-4194
    Abstract: Previous studies suggest that a cumulative cisplatin dose of 200 mg/m2 might be adequate in the intensity-modulated radiation therapy (IMRT) era for locoregionally advanced nasopharyngeal carcinoma (LANPC). However, two cycles of once-every-3-weeks cisplatin at 100 mg/m2 has never been prospectively compared with standard once-a-week cisplatin regimen. Patients and Methods: This trial was conducted at three hospitals from 2011 to 2016. Patients who met the eligibility criteria were recruited (ChiCTR-TRC-12001979) and randomly assigned (1:1) via a computer-generated sequence to receive once-every-3-weeks cisplatin at 100 mg/m2 for two cycles or once-a-week cisplatin at 40 mg/m2 for six cycles concurrently with IMRT. Primary endpoint was failure-free survival and between-group absolute difference of 10% as the noninferiority margin. Results: A total of 510 patients were enrolled. Median follow-up time was 58.3 months with 85.4% of 3-year failure-free survival in the once-every-3-weeks group and 85.6% in the once-a-week group. An absolute difference of −0.2% (95% confidence interval, −6.3 to 5.9; Pnoninferiority = 0.0016). Acute toxicities of grade 3 or higher occurred in 55.8% in the once-every-3-weeks group and 66.3% in the once-a-week group (P = 0.015). The most common acute toxicities were hematologic abnormalities, including leukopenia (16% vs. 27%; P = 0.0022) and thrombocytopenia (1% vs. 5%; P = 0.015). The late grade 3–4 auditory loss rate was significantly lower in the once-every-3-weeks group than the once-a-week group (6% vs. 13%; P = 0.0039). Conclusions: Once-every-3-weeks cisplatin as concurrent chemoradiotherapy is noninferior to once-a-week cisplatin in the treatment efficacy in the LANPC. Although both regimens are well tolerated, severe acute toxicities and late-onset auditory loss are higher in the once-a-week group.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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  • 3
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 21, No. 6 ( 2012-06-01), p. 980-987
    Abstract: Background: Genome-wide association studies (GWAS) have identified more than 100 genetic loci for various cancers. However, only one is for endometrial cancer. Methods: We conducted a three-stage GWAS including 8,492 endometrial cancer cases and 16,596 controls. After analyzing 585,963 single-nucleotide polymorphisms (SNP) in 832 cases and 2,682 controls (stage I) from the Shanghai Endometrial Cancer Genetics Study, we selected the top 106 SNPs for in silico replication among 1,265 cases and 5,190 controls from the Australian/British Endometrial Cancer GWAS (stage II). Nine SNPs showed results consistent in direction with stage I with P & lt; 0.1. These nine SNPs were investigated among 459 cases and 558 controls (stage IIIa) and six SNPs showed a direction of association consistent with stages I and II. These six SNPs, plus two additional SNPs selected on the basis of linkage disequilibrium and P values in stage II, were investigated among 5,936 cases and 8,166 controls from an additional 11 studies (stage IIIb). Results: SNP rs1202524, near the CAPN9 gene on chromosome 1q42.2, showed a consistent association with endometrial cancer risk across all three stages, with ORs of 1.09 [95% confidence interval (CI), 1.03–1.16] for the A/G genotype and 1.17 (95% CI, 1.05–1.30) for the G/G genotype (P = 1.6 × 10−4 in combined analyses of all samples). The association was stronger when limited to the endometrioid subtype, with ORs (95% CI) of 1.11 (1.04–1.18) and 1.21 (1.08–1.35), respectively (P = 2.4 × 10−5). Conclusions: Chromosome 1q42.2 may host an endometrial cancer susceptibility locus. Impact: This study identified a potential genetic locus for endometrial cancer risk. Cancer Epidemiol Biomarkers Prev; 21(6); 980–7. ©2012 AACR.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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  • 4
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2006
    In:  Clinical Cancer Research Vol. 12, No. 10 ( 2006-05-15), p. 3193-3199
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 12, No. 10 ( 2006-05-15), p. 3193-3199
    Abstract: Purpose: Quercetin is a potent chemotherapeutic drug. Clinical trials exploring different schedules of administration of quercetin have been hampered by its extreme water insolubility. To overcome this limitation, this study is aimed to develop liposomal quercetin and investigate its distribution in vivo and antitumor efficacy in vivo and in vitro. Experimental Design: Quercetin was encapsulated in polyethylene glycol 4000 liposomes. Biodistribution of liposomal quercetin i.v. at 50 mg/kg in tumor-bearing mice was detected by high-performance liquid chromatography. Induction of apoptosis by liposomal quercetin in vitro was tested. The antitumor activity of liposomal quercetin was evaluated in the immunocompetent C57BL/6N mice bearing LL/2 Lewis lung cancer and in BALB/c mice bearing CT26 colon adenocarcinoma and H22 hepatoma. Tumor volume and survival time were observed. The mechanisms underlying the antitumor effect of quercetin in vivo was investigated by detecting the microvessel density, apoptosis, and heat shock protein 70 expression in tumor tissues. Results: Liposomal quercetin could be dissolved in i.v. injection and effectively accumulate in tumor tissues. The half-time of liposomal quercetin was 2 hours in plasma. The liposomal quercetin induced apoptosis in vitro and significantly inhibited tumor growth in vivo in a dose-dependent manner. The optimal dose of liposomal quercetin resulted in a 40-day survival rate of 40%. Quantitative real-time PCR showed that liposomal quercetin down-regulated the expression of heat shock protein 70 in tumor tissues. Immunohistochemistry analysis showed that liposomal quercetin inhibited tumor angiogenesis as assessed by CD31 and induced tumor cell apoptosis. Conclusions: Our data indicated that pegylated liposomal quercetin can significantly improve the solubility and bioavailability of quercetin and can be a potential application in the treatment of tumor.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2006
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  • 5
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2020
    In:  Clinical Cancer Research Vol. 26, No. 14 ( 2020-07-15), p. 3760-3770
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 26, No. 14 ( 2020-07-15), p. 3760-3770
    Abstract: Adults with T-cell lymphoblastic lymphoma (T-LBL) generally benefit from treatment with acute lymphoblastic leukemia (ALL)-like regimens, but approximately 40% will relapse after such treatment. We evaluated the value of CpG methylation in predicting relapse for adults with T-LBL treated with ALL-like regimens. Experimental Design: A total of 549 adults with T-LBL from 27 medical centers were included in the analysis. Using the Illumina Methylation 850K Beadchip, 44 relapse-related CpGs were identified from 49 T-LBL samples by two algorithms: least absolute shrinkage and selector operation (LASSO) and support vector machine–recursive feature elimination (SVM-RFE). We built a four-CpG classifier using LASSO Cox regression based on association between the methylation level of CpGs and relapse-free survival in the training cohort (n = 160). The four-CpG classifier was validated in the internal testing cohort (n = 68) and independent validation cohort (n = 321). Results: The four-CpG–based classifier discriminated patients with T-LBL at high risk of relapse in the training cohort from those at low risk (P & lt; 0.001). This classifier also showed good predictive value in the internal testing cohort (P & lt; 0.001) and the independent validation cohort (P & lt; 0.001). A nomogram incorporating five independent prognostic factors including the CpG-based classifier, lactate dehydrogenase levels, Eastern Cooperative Oncology Group performance status, central nervous system involvement, and NOTCH1/FBXW7 status showed a significantly higher predictive accuracy than each single variable. Stratification into different subgroups by the nomogram helped identify the subset of patients who most benefited from more intensive chemotherapy and/or sequential hematopoietic stem cell transplantation. Conclusions: Our four-CpG–based classifier could predict disease relapse in patients with T-LBL, and could be used to guide treatment decision.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 6
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 13_Supplement ( 2019-07-01), p. 1597-1597
    Abstract: Background: Recently, kinase domain duplications (KDD) in BRAF, EGFR, MET and FGFR1 were reported, along with responses to tyrosine kinase inhibitors (TKI). However, its frequency and clinical outcomes in advanced cancer patients are larglely uncertain. We assessed the frequency of KDD across 14, 491 advanced cancers to reveal the landscape in a wide variety of subtypes. Methods: A multicenter study in China was initiated from July 2013, and advanced cancer patients have been enrolled as of September 2018. We analyzed data from 14, 491 clinical advanced cancer cases, each of which had results from next-generation sequencing (NGS)-based 381 genes panel assay, analogous to the index patient. Results: Of this entire cohort [6837 lung cancer (47.18%), 1894 breast cancer (13.07%), 1325 colorectal cancer (9.14%), 710 urinary system tumor (4.90%), 536 gynecological tumor (3.70%), 592 hepatobiliary cancer (4.09%), 221 gastric cancer (1.53%), 312 soft tissue sarcoma (2.15%), 260 head and neck cancer (1.79%) and 1804 others (12.45%)], 71 patients were identified with KDD, including EGFR (16), BRAF (12), MET (11), FGFR3 (8), RET (3), PDGFRA (3), ROS1 (3), FGFR1 (2), ERBB2 (2), SOX17 (2), ALK (2), KIT (1), NTRK1 (1), BAP1 (1), TMPRSS2 (1), ERBB4 (1), VHL (1), NTRK3 (1). KDD were seen in 0.39% (27/6837) of lung cancer [EGFR(9), BRAF (2), MET (6), FGFR3 (2), RET (1), PDGFRA (1), ROS1 (2), ERBB2 (1), ALK (1), NTRK1 (1), and ERBB4 (1)] ; 0.21%(4/1894) of breast cancer [BRAF (1), FGFR3 (2), FGFR1 (1)]; 0.60%(8/1325) of colorectal cancer [EGFR (1), BRAF (3), FGFR3 (2), RET (1), ROS1 (1)] ; 0.28%(2/710) of urinary system tumor [TMPRSS2(1), VHL (1)]; 0.19%(1/536) of gynecological tumor [SOX17 (1)] ; 0.17%(1/592) of hepatobiliary cancer [EGFR (1)]; 0.45%(1/221) of gastric cancer [ERBB2 (1)] ; 0.96%(3/312) of soft tissue sarcoma [EGFR (1), FGFR3 (1), PDGFRA (1)]; 0.77%(2/260) of head and neck cancer [BRAF (2)] ; and 1.22%(22/1804) of others [EGFR (4), BRAF (4), MET (5), FGFR3 (1), RET (1), PDGFRA (1), FGFR1 (1), SOX17 (1), ALK (1), KIT (1), BAP1 (1), and NTRK3 (1)]; KDD possibly related to target resistance were seen in ERBB2 amplification gastric cancer and ALK-related NSCLC. Conclusion: Diverse KDD are found across diverse tumor types and may underlie acquired resistance, and can benefit from matched targeted treatment. In addition, for short- or long-term responses to targeted treatment, we can use the NGS assay to explore differential gene alter in the future. Citation Format: Chun-wei Xu, Wen-xian Wang, Xiao-jia Wang, You-cai Zhu, Qu-xia Zhang, Yong Fang, Xiu-yu Cai, Yu Chen, Li Lin, Hong Wang, Mei-yu Fang, Yin-bin Zhang, Shi-jie Lan, Xin Liu, Xing-xiang Pu, Zong-yang Yu, Bing Wan, Jian-ying Li, Xian-bin Liang, Li-ping Wang, Wu Zhuang, Ling Lin, Gang Chen, Tang-feng Lv, Yong Song. Real-world large-scale study kinase domain duplications across diverse tumor types in Chinese populations [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 1597.
    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: 2019
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  • 7
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 15 ( 2014-08-01), p. 4090-4098
    Abstract: We investigated the relationship between telomere length and lung cancer in a pooled analysis from three prospective cohort studies: the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial, conducted among men and women in the United States, and previously published data from the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Trial conducted among male smokers in Finland, and the Shanghai Women's Health Study (SWHS), which is comprised primarily of never-smokers. The pooled population included 847 cases and 847 controls matched by study, age, and sex. Leukocyte telomere length was measured by a monochrome multiplex qPCR assay. We used conditional logistic regression models to calculate ORs and their 95% confidence intervals (CI) for the association between telomere length and lung cancer risk, adjusted for age and pack-years of smoking. Longer telomere length was associated with increased lung cancer risk in the pooled analysis [OR (95% CI) by quartile: 1.00; 1.24 (0.90–1.71); 1.27 (0.91–1.78); and 1.86 (1.33–2.62); P trend = 0.000022] . Findings were consistent across the three cohorts and strongest for subjects with very long telomere length, i.e., lung cancer risks for telomere length [OR (95% CI)] in the upper half of the fourth quartile were 2.41 (1.28–4.52), 2.16 (1.11–4.23), and 3.02(1.39–6.58) for the PLCO trial, the ATBC trial, and the SWHS, respectively. In addition, the association persisted among cases diagnosed more than 6 years after blood collection and was particularly evident for female adenocarcinoma cases. Telomere length in white blood cell DNA may be a biomarker of future increased risk of lung cancer in diverse populations. Cancer Res; 74(15); 4090–8. ©2014 AACR.
    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: 2014
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  • 8
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 13_Supplement ( 2018-07-01), p. 4974-4974
    Abstract: The lung cancer rate among never-smokers is the highest among Asian women, however its etiology and any relevant non-smoking related biomarkers are still unclear. Pre-diagnostic lung cancer-related metabolic biomarkers may provide novel insights into lung cancer mechanisms, and may contribute to the discovery of etiologic factors for the high lung cancer prevalence among Asian women. We evaluated the role of the urinary metabolome in lung cancer development among female never-smokers in China by conducting a nested case-control study of 275 lung cancer cases and 289 healthy controls from the Shanghai Women's Health Study, a prospective cohort comprised of 73,363 Chinese female never-smokers. Metabolic profiling of urinary chemical features was conducted using ultrahigh-performance liquid chromatography - tandem mass spectrometry (UPLC-MS) (39,409 spectral features) and 600 MHz 1H nuclear magnetic resonance (NMR) spectroscopy (386 features). Unconditional logistic regression models were used to estimate the odds ratios (ORs) and 95% confidence intervals (CIs) for the association between each log-transformed metabolite level and lung cancer risk, adjusting for potential confounders such as age, body mass index, history of respiratory disease and passive smoking. Spearman correlation and linear regression were used to estimate associations between the most significant metabolites and pre-diagnosis dietary factors. Three detected UPLC-MS urinary metabolites were negatively associated with lung cancer risk with a false discovery rate of less than 10%: pos_2.61_127.0382m/z (OR = 0.57, 95% CI = 0.46-0.72, P = 1.98 x 10-6), neg_2.60_369.0408m/z (OR = 0.97, 95% CI = 0.96-0.98, P = 1.36 x 10-6), and pos_2.61_184.0325n (OR = 0.55, 95% CI = 0.43-0.71, P = 4.91 x 10-6). These were strongly correlated with each other (rho & gt; 0.65, p & lt; 0.0001). The significant metabolite (pos_2.61_127.0382m/z) was identified as 5-methyl-2-furoic acid and was moderately correlated with self-reported dietary intake of soy (rho = 0.21, p & lt; 0.001). In conclusion, we identified a metabolite in urine (5-methyl-2-furoic acid) that provides support for the protective association of soy-based foods on lung cancer risk that was previously observed in this population of never-smoking women. Further studies are warranted to replicate these findings. Citation Format: Wei Jie Seow, Xiao-Ou Shu, Jeremy Nicholson, Elaine Holmes, Wei Hu, Qiuyin Cai, Yu-Tang Gao, Yong-Bing Xiang, Steve Moore, Bryan A. Bassig, Jason Yy Wong, Jinming Zhang, Bu-Tian Ji, Claire Boulange, Manuja Kaluarachchi, Kyrillos F. Adesina-Georgiadis, Anisha Wijeyesekera, Wei Zheng, Paul Elliot, Nathaniel Rothman, Qing Lan. Prospective study of untargeted urinary metabolomics and risk of lung cancer among female never-smokers in Shanghai, China [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 4974.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 9
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 4160-4160
    Abstract: Background: There is growing evidence that longer telomere length is associated with higher risk of lung cancer. We investigated this association in the prospective Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial, which was conducted in the United States. We also combined these data with two previously published prospective cohorts: the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) trial conducted among ever smoking males in Finland and the Shanghai Women's Health Study (SWHS) which comprised primarily of never-smoking women, resulting in a pooled analysis on a total of 847 cases and 847 controls matched by age, sex and study. Methods: Blood samples were collected prior to diagnosis of lung cancer and telomere length was measured using the same monochrome multiplex quantitative PCR method in all three studies. We used conditional logistic regression models to calculate odds ratios (OR) and their 95% confidence intervals (CI) for the association between telomere length and lung cancer risk adjusted for age, to account for residual confounding, and pack-years of smoking as continuous variables. Analyses by telomere length quartile retaining the initial categorization used in each study, and using categorization based on telomere length in pooled controls, produced similar findings and results are presented for the former. Results: In the PLCO Trial, increasing telomere length was significantly associated with lung cancer risk (adjusted OR [95% CI] by quartile: 1.00; 1.11 [0.65-1.92] ; 1.20 [0.66-2.15]; and 1.83 [1.05-3.19] ; P-trend = 0.011), consistent with results from the ATBC and SWHS studies. In the pooled analyses, the adjusted OR (95% CI) by quartile was 1.00; 1.24 (0.90-1.72); 1.27 (0.91-1.77); and 1.87 (1.33-2.63); P-trend = 0.000022. This positive association was particularly evident for adenocarcinoma cases, especially those diagnosed more than 6 years after blood collection (n=115; adjusted OR [95% CI] by quartile: 1.00; 2.48 [0.85-7.23] ; 2.05 [0.81-5.15]; and 3.59 [1.38-9.34] ; P-trend = 0.0027). Conclusion: Telomere length in white blood cell DNA may be an important biomarker of future increased risk of lung cancer in diverse populations. Citation Format: Wei Jie Seow, Richard Cawthon, Mark Purdue, Wei Hu, Yu-Tang Gao, Wen-Yi Huang, Stephanie J. Weinstein, Bu-Tian Ji, Jarmo Virtamo, Dean Hosgood, Bryan Bassig, Xiaoou Shu, Qiuyin Cai, Yongbin Xiang, Shen Min, Wong-Ho Chow, Sonja Berndt, Christopher Kim, Unhee Lim, Demetrius Albanes, Neil E. Caporaso, Stephen Chanock, Wei Zheng, Nathaniel Rothman, Qing Lan. Telomere length in white blood cell DNA and lung cancer: a pooled analysis of three prospective cohorts. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4160. doi:10.1158/1538-7445.AM2014-4160
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
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    detail.hit.zdb_id: 1432-1
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  • 10
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 23, No. 12 ( 2014-12-01), p. 2977-2980
    Abstract: Background: We previously reported that higher levels of mitochondrial DNA copy number (mtDNA CN) were associated with lung cancer risk among male heavy smokers (i.e., ≥20 cigarettes per day) in the Alpha-Tocopherol Beta-Carotene (ATBC) study. Here, we present two additional prospective investigations nested in the Prostate, Lung, Colorectal, and Ovarian (PLCO) cancer screening trial and the Shanghai Women's Health Study (SWHS), and pooled with previously published data from ATBC. Materials: All DNA were extracted from peripheral whole blood samples using the phenol–chloroform method, and mtDNA CN was assayed by fluorescence-based qPCR. Multivariate unconditional logistic regression models were used to estimate ORs and 95% confidence intervals for the association of mtDNA CN and lung cancer risk. Results: Overall, mtDNA CN was not associated with lung cancer risk in the PLCO, SWHS, or pooled populations (all P trends & gt; 0.42, P heterogeneity = 0.0001), and mtDNA CN was inversely associated with lung cancer risk among male smokers in PLCO, the opposite direction observed in ATBC. In addition, the mtDNA CN association observed among male heavy smokers in ATBC was the opposite direction in PLCO. Conclusions: mtDNA CN was not consistently associated with lung cancer risk across three prospective study populations from Europe, Asia, and the United States. Impact: This pooled study suggests no consistent association between prediagnostic mtDNA CN levels and lung cancer risk across several populations. Cancer Epidemiol Biomarkers Prev; 23(12); 2977–80. ©2014 AACR.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
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    detail.hit.zdb_id: 1153420-5
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