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Differences in risk factors for molecular subtypes of clear cell renal cell carcinoma

MP. Purdue, J. Rhee, L. Moore, X. Gao, X. Sun, E. Kirk, V. Bencko, V. Janout, D. Mates, D. Zaridze, S. Petruzella, AA. Hakimi, WM. Linehan, SJ. Chanock, P. Brennan, H. Furberg, M. Troester, N. Rothman

. 2021 ; 149 (7) : 1448-1454. [pub] 20210610

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural

Perzistentní odkaz   https://www.medvik.cz/link/bmc21024917

Grantová podpora
P30 CA008748 NCI NIH HHS - United States

The ccA and ccB molecular subtypes of clear cell renal cell carcinoma (ccRCC) have well-characterized prognostic relevance. However, it is not known whether they possess distinct etiologies. We investigated the relationships between these subtypes and RCC risk factors within a case-control study conducted in Eastern Europe. We analyzed risk factor data for ccA (n = 144) and ccB (n = 106) cases and 1476 controls through case-only and case-control comparisons to assess risk factor differences across subtypes using logistic and polytomous regression models. We also performed a meta-analysis summarizing case-only results from our study and three patient cohorts. Patients with ccB tumors had poorer survival than those with ccA tumors and were more likely to be male (case-only odds ratio [OR] 2.68, 95% confidence interval [CI] 1.43-5.03). In case-control analyses, body mass index was significantly associated with ccA tumors (OR 2.45, 95% CI 1.18-5.10 for ≥35 vs <25 kg/m2 ) but not with ccB tumors (1.52, 0.56-4.12), while trichloroethylene was associated with ccB but not ccA (OR 3.09, 95% CI 1.11-8.65 and 1.25, 0.36-4.39 respectively for ≥1.58 ppm-years vs unexposed). A polygenic risk score of genetic variants identified from genome-wide association studies was associated with both ccA and, in particular, ccB (OR 1.82, 1.11-2.99 and 2.87, 95% CI 1.64-5.01 respectively for 90th vs 10th percentile). In a meta-analysis of case-only results including three patient cohorts, we still observed the ccB excess for male sex and the ccA excess for obesity. In conclusion, our findings suggest the existence of etiologic heterogeneity across ccRCC molecular subtypes for several risk factors.

Citace poskytuje Crossref.org

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$a The ccA and ccB molecular subtypes of clear cell renal cell carcinoma (ccRCC) have well-characterized prognostic relevance. However, it is not known whether they possess distinct etiologies. We investigated the relationships between these subtypes and RCC risk factors within a case-control study conducted in Eastern Europe. We analyzed risk factor data for ccA (n = 144) and ccB (n = 106) cases and 1476 controls through case-only and case-control comparisons to assess risk factor differences across subtypes using logistic and polytomous regression models. We also performed a meta-analysis summarizing case-only results from our study and three patient cohorts. Patients with ccB tumors had poorer survival than those with ccA tumors and were more likely to be male (case-only odds ratio [OR] 2.68, 95% confidence interval [CI] 1.43-5.03). In case-control analyses, body mass index was significantly associated with ccA tumors (OR 2.45, 95% CI 1.18-5.10 for ≥35 vs <25 kg/m2 ) but not with ccB tumors (1.52, 0.56-4.12), while trichloroethylene was associated with ccB but not ccA (OR 3.09, 95% CI 1.11-8.65 and 1.25, 0.36-4.39 respectively for ≥1.58 ppm-years vs unexposed). A polygenic risk score of genetic variants identified from genome-wide association studies was associated with both ccA and, in particular, ccB (OR 1.82, 1.11-2.99 and 2.87, 95% CI 1.64-5.01 respectively for 90th vs 10th percentile). In a meta-analysis of case-only results including three patient cohorts, we still observed the ccB excess for male sex and the ccA excess for obesity. In conclusion, our findings suggest the existence of etiologic heterogeneity across ccRCC molecular subtypes for several risk factors.
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$a Rhee, Jongeun $u Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA
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$a Moore, Lee $u Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA
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$a Gao, Xiaohua $u Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
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$a Sun, Xuezheng $u Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
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$a Kirk, Erin $u Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
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$a Bencko, Vladimir $u First Faculty of Medicine, Institute of Hygiene and Epidemiology, Charles University, Prague, Czech Republic
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$a Janout, Vladimir $u Faculty of Health Sciences, Palacky University, Olomouc, Czech Republic
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$a Mates, Dana $u Department of Environmental Health, Institute of Public Health, Bucharest, Romania
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$a Zaridze, David $u Institute of Carcinogenesis, Cancer Research Centre, Moscow, Russia
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$a Petruzella, Stacey $u Departments of Surgery and Epidemiology, Memorial Sloan Kettering Cancer Center, New York, New York, USA
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$a Hakimi, Abraham Ari $u Departments of Surgery and Epidemiology, Memorial Sloan Kettering Cancer Center, New York, New York, USA
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$a Linehan, William Marston $u Department of Health and Human Services, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA
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$a Chanock, Stephen J $u Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA
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$a Brennan, Paul $u Section of Genetics, International Agency for Research on Cancer, Lyon, France
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$a Furberg, Helena $u Departments of Surgery and Epidemiology, Memorial Sloan Kettering Cancer Center, New York, New York, USA
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$a Troester, Melissa $u Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
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$a Rothman, Nathaniel $u Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA
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