Second Primary Cancers After Kidney Cancers, and Kidney Cancers as Second Primary Cancers.

Cancer etiology Cancer incidence Relative risk Second primary cancer Sex difference

Journal

European urology open science
ISSN: 2666-1683
Titre abrégé: Eur Urol Open Sci
Pays: Netherlands
ID NLM: 101771568

Informations de publication

Date de publication:
Feb 2021
Historique:
accepted: 16 12 2020
entrez: 2 8 2021
pubmed: 3 8 2021
medline: 3 8 2021
Statut: epublish

Résumé

Second primary cancers (SPCs) are increasing due to improving survival in first primary cancers. Previous studies on SPCs in renal cell carcinoma (RCC) have focused on treatment and other risk factors, but data of RCC as an SPC are scarce. In this study, we want to elucidate the risk for any SPC after RCC, and in reverse order, for RCC as an SPC after any cancer. We additionally consider how family histories influence the risks. Patient data were obtained from the Swedish Cancer Registry from years 1990 through 2015, and family data were obtained from the Multigeneration Register. We employed standardized incidence ratios to estimate bidirectional relative risks of subsequent cancer associated with RCC. We identified 17 587 RCCs (60% in male patients). The highest increases for SPCs were observed for nervous system hemangioblastoma (HB; 26.8), adrenal (12.09) tumors, and renal pelvic cancer (6.32). In the reverse order, RCC as an SPC, nervous system HB (17.01), and adrenal tumors (15.34) were associated with the highest risks. Risks for many other sites (12 sites and subsites) were increased bidirectionally. For women, a total of seven sites and subsites were increased bidirectionally, and many were shared with men. The only significant sex difference in SPCs was the higher lung cancer risk in women (2.41) than in men (1.28). Patients with a family history of HBs or of prostate, colorectal and lung cancers showed high risks of these cancers as SPCs after RCC. Family history accounted for 30% of prostate cancers after RCC. The bidirectional study design was able to suggest risk factors for SPCs and offered a clinical take-home message urging to consider strategies for early detection and prevention of SPCs. Readily available information on lifestyle (eg, smoking) and family history (eg, prostate cancer) may reveal targets for risk reduction with prognostic benefits. Close to 10% of kidney cancer patients develop another cancer. The cause for these other cancers may not depend on kidney cancer.

Sections du résumé

BACKGROUND BACKGROUND
Second primary cancers (SPCs) are increasing due to improving survival in first primary cancers. Previous studies on SPCs in renal cell carcinoma (RCC) have focused on treatment and other risk factors, but data of RCC as an SPC are scarce.
OBJECTIVE OBJECTIVE
In this study, we want to elucidate the risk for any SPC after RCC, and in reverse order, for RCC as an SPC after any cancer. We additionally consider how family histories influence the risks.
DESIGN SETTING AND PARTICIPANTS METHODS
Patient data were obtained from the Swedish Cancer Registry from years 1990 through 2015, and family data were obtained from the Multigeneration Register.
OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS METHODS
We employed standardized incidence ratios to estimate bidirectional relative risks of subsequent cancer associated with RCC.
RESULTS AND LIMITATIONS CONCLUSIONS
We identified 17 587 RCCs (60% in male patients). The highest increases for SPCs were observed for nervous system hemangioblastoma (HB; 26.8), adrenal (12.09) tumors, and renal pelvic cancer (6.32). In the reverse order, RCC as an SPC, nervous system HB (17.01), and adrenal tumors (15.34) were associated with the highest risks. Risks for many other sites (12 sites and subsites) were increased bidirectionally. For women, a total of seven sites and subsites were increased bidirectionally, and many were shared with men. The only significant sex difference in SPCs was the higher lung cancer risk in women (2.41) than in men (1.28). Patients with a family history of HBs or of prostate, colorectal and lung cancers showed high risks of these cancers as SPCs after RCC. Family history accounted for 30% of prostate cancers after RCC.
CONCLUSIONS CONCLUSIONS
The bidirectional study design was able to suggest risk factors for SPCs and offered a clinical take-home message urging to consider strategies for early detection and prevention of SPCs. Readily available information on lifestyle (eg, smoking) and family history (eg, prostate cancer) may reveal targets for risk reduction with prognostic benefits.
PATIENT SUMMARY RESULTS
Close to 10% of kidney cancer patients develop another cancer. The cause for these other cancers may not depend on kidney cancer.

Identifiants

pubmed: 34337496
doi: 10.1016/j.euros.2020.12.007
pii: S2666-1683(20)36385-0
pmc: PMC8317822
doi:

Types de publication

Journal Article

Langues

eng

Pagination

52-59

Informations de copyright

© 2021 The Authors.

Références

Cancer Lett. 2015 Dec 1;369(1):152-66
pubmed: 26319898
Int J Cancer. 2018 Nov 15;143(10):2449-2457
pubmed: 30238973
Nat Rev Cancer. 2013 Mar;13(3):153-9
pubmed: 23550303
Kidney Int. 2002 May;61(5):1806-13
pubmed: 11967031
Nat Rev Clin Oncol. 2013 May;10(5):289-301
pubmed: 23529000
Scand J Urol Nephrol. 2008;42(1):12-7
pubmed: 17853011
BMC Cancer. 2020 Jan 21;20(1):51
pubmed: 31964352
J Clin Pathol. 2016 Sep;69(9):750-3
pubmed: 27235536
J Clin Oncol. 2012 Oct 20;30(30):3734-45
pubmed: 23008293
J Clin Oncol. 2016 Jun 20;34(18):2172-81
pubmed: 27114602
Cancer Res Treat. 2018 Jan;50(1):293-301
pubmed: 28421722
Clin Lymphoma Myeloma. 2009 Jun;9(3):239-42
pubmed: 19525194
Am J Clin Oncol. 2013 Apr;36(2):132-42
pubmed: 22441339
J Invest Dermatol. 2020 Jan;140(1):48-55.e1
pubmed: 31288011
Eur J Cancer. 2014 Aug;50(12):2108-18
pubmed: 24923229
Cancer Med. 2020 Nov;9(21):8258-8265
pubmed: 32960498
Cancer. 2019 Jan 15;125(2):232-238
pubmed: 30561791
Acta Oncol. 2018 Apr;57(4):440-455
pubmed: 29226751
Urol Oncol. 2020 Jun;38(6):590-598
pubmed: 32057596
Eur Urol. 2018 Jan;73(1):111-122
pubmed: 28867446
Int J Cancer. 2012 Nov 1;131(9):2085-93
pubmed: 22307919
J Natl Cancer Inst. 2006 Jan 4;98(1):15-25
pubmed: 16391368
Lancet Haematol. 2018 Aug;5(8):e368-e377
pubmed: 30075833
J Urol. 2011 Jun;185(6):2045-9
pubmed: 21496838
Eur Urol. 2011 Nov;60(5):987-93
pubmed: 21621909
Biomed Res Int. 2015;2015:456040
pubmed: 26539495

Auteurs

Guoqiao Zheng (G)

Division of Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Faculty of Medicine, University of Heidelberg, Heidelberg, Germany.
Center for Primary Health Care Research, Lund University, Malmö, Sweden.

Kristina Sundquist (K)

Center for Primary Health Care Research, Lund University, Malmö, Sweden.
Department of Family Medicine and Community Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Department of Population Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Center for Community-based Healthcare Research and Education (CoHRE), Department of Functional Pathology, School of Medicine, Shimane University, Shimane, Japan.

Jan Sundquist (J)

Center for Primary Health Care Research, Lund University, Malmö, Sweden.
Department of Family Medicine and Community Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Department of Population Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Center for Community-based Healthcare Research and Education (CoHRE), Department of Functional Pathology, School of Medicine, Shimane University, Shimane, Japan.

Tianhui Chen (T)

Department of Cancer Prevention, Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Hangzhou, China.
Institute of Cancer and Basic Medicine, Chinese Academy of Sciences, Hangzhou, China.

Asta Försti (A)

Division of Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Center for Primary Health Care Research, Lund University, Malmö, Sweden.
Hopp Children's Cancer Center (KiTZ), Heidelberg, Germany.
Division of Pediatric Neurooncology, German Cancer Research Center (DKFZ), German Cancer Consortium (DKTK), Heidelberg, Germany.

Otto Hemminki (O)

Cancer Gene Therapy Group, Translational Immunology Research Program, University of Helsinki, Helsinki, Finland.
Comprehensive Cancer Center, Helsinki University Hospital, Helsinki, Finland.

Kari Hemminki (K)

Division of Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Center for Primary Health Care Research, Lund University, Malmö, Sweden.
Biomedical Center, Faculty of Medicine and Biomedical Center in Pilsen, Charles University in Prague, Pilsen, Czech Republic.

Classifications MeSH