Abstract
Background: Although rare in the general population, highly penetrant germline mutations in CDKN2A are responsible for 5%-40% of melanoma cases reported in melanoma-prone families. We sought to determine whether MELPREDICT was generalizable to a global series of families with melanoma and whether performance improvements can be achieved. Methods: In total, 2116 familial melanoma cases were ascertained by the international GenoMEL Consortium. We recapitulated the MELPREDICT model within our data (GenoMELPREDICT) to assess performance improvements by adding phenotypic risk factors and history of pancreatic cancer. We report areas under the curve (AUC) with 95% confidence intervals (CIs) along with net reclassification indices (NRIs) as performance metrics. Results: MELPREDICT performed well (AUC 0.752, 95% CI 0.730-0.775), and GenoMELPREDICT performance was similar (AUC 0.748, 95% CI 0.726-0.771). Adding a reported history of pancreatic cancer yielded discriminatory improvement (P < .0001) in GenoMELPREDICT (AUC 0.772, 95% CI 0.750-0.793, NRI 0.40). Including phenotypic risk factors did not improve performance. Conclusion: The MELPREDICT model functioned well in a global data set of familial melanoma cases. Adding pancreatic cancer history improved model prediction. GenoMELPREDICT is a simple tool for predicting CDKN2A mutational status among melanoma patients from melanoma-prone families and can aid in directing these patients to receive genetic testing or cancer risk counseling.
Original language | English |
---|---|
Pages (from-to) | 386-394 |
Number of pages | 9 |
Journal | Journal of the American Academy of Dermatology |
Volume | 81 |
Issue number | 2 |
DOIs | |
Publication status | Published - Aug 2019 |
Externally published | Yes |
Keywords*
- CDKN2A
- familial melanoma
- GenoMEL
- GenoMELPREDICT
- mutation prediction
Field of Science*
- 3.2 Clinical medicine
Publication Type*
- 1.1. Scientific article indexed in Web of Science and/or Scopus database
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In: Journal of the American Academy of Dermatology, Vol. 81, No. 2, 08.2019, p. 386-394.
Research output: Contribution to journal › Article › peer-review
TY - JOUR
T1 - Estimating CDKN2A mutation carrier probability among global familial melanoma cases using GenoMELPREDICT
AU - GenoMEL Study Group
AU - Kanetsky, Peter A.
A2 - Taylor, Nicholas J.
A2 - Mitra, Nandita
A2 - Qian, Lu
A2 - Avril, Marie Françoise
A2 - Bishop, D. Timothy
A2 - Bressac-de Paillerets, Brigitte
A2 - Bruno, William
A2 - Calista, Donato
A2 - Cuellar, Francisco
A2 - Cust, Anne E.
A2 - Demenais, Florence
A2 - Elder, David E.
A2 - Gerdes, Anne Marie
A2 - Ghiorzo, P.
A2 - Goldstein, Alisa M.
A2 - Grazziotin, Thais C.
A2 - Gruis, Nelleke A.
A2 - Hansson, J.
A2 - Harland, Mark
A2 - Hayward, Nicholas K.
A2 - Hocevar, M.
A2 - Höiom, Veronica
A2 - Holland, Elizabeth A.
A2 - Ingvar, Christian
A2 - Landi, Maria Teresa
A2 - Landman, Gilles
A2 - Larre-Borges, Alejandra
A2 - Mann, Graham J.
A2 - Nagore, Eduardo
A2 - Olsson, Håkan
A2 - Palmer, Jane M.
A2 - Perić, Barbara
A2 - Pjanova, Dace
A2 - Pritchard, Antonia L.
A2 - Puig, Susana
A2 - Schmid, H.
A2 - van der Stoep, Nienke
A2 - Tucker, Margaret A.
A2 - Wadt, Karin A.W.
A2 - Yang, Xiaohong R.
A2 - Newton-Bishop, Julia A.
N1 - Funding Information: We acknowledge the contributions of the participants and their families and the many clinicians, geneticists, genetic counsellors, and allied health professionals involved in their management. This work was performed in participation with the following members at the following study locations: Leeds, United Kingdom (Linda Whitaker, Paul Affleck, Jennifer H. Barrett, Jane Harrison, Mark M. Iles, Juliette Randerson-Moor, John C. Taylor, Kairen Kukalizch, Susan Leake, Birute Karpavicius, Sue Haynes, Tricia Mack, May Chan, and Yvonne Taylor); Barcelona, Spain (Paula Aguilera, Llúcia Alós, Celia Badenas, Alicia Barreiro, Neus Calbet, Cristina Carrera, Carlos Conill, Mireia Domínguez, Daniel Gabriel, Pablo Iglesias, Josep Malvehy, M. Eugenia Moliner, Javiera Pérez, Ramon Pigem, Miriam Potrony, Joan Anton Puig Butille, Ramon Rull, Marcelo Sánchez, Gemma Tell-Martí, Sergi Vidal-Sicart, and Oriol Yelamos) Valencia (Zaida García-Casado, Celia Requena, José Bañuls, Virtudes Soriano, José Antonio López-Guerrero, Manuel Moragón, Vicente Oliver); NCI at Cesena, Italy (Paola Minghetti, Laura Fontaine, Katie Beebe, and Giorgio Landi); Genoa, Italy (Giovanna Bianchi-Scarrà, Lorenza Pastorino, Virginia Andreotti, Claudia Martinuzzi, Bruna Dalmasso, Giulia Ciccarese, Francesco Spagnolo, and Paola Queirolo); Riga, Latvia (Kristine Azarjana, Simona Donina, Olita Heisele, Baiba Štreinerte, Aija Ozola and Ludmila Engele); Sydney, Australia (Caroline Watts, Gayathri St. George, Robyn Dalziell, and Kate McBride who assisted with recruitment of study participants; Leo Raudonikis who assisted with data management; and Chantelle Agha-Hamilton and Svetlana Pianova who assisted with biospecimen management); Montevideo, Uruguay (Virginia Barquet, Javiera Pérez, Miguel Martínez, Jimena Núñez, and Malena Scarone); São Paulo, Brazil (Dirce Maria Carraro, Alexandre Leon Ribeiro de Ávila, Luciana Facure Moredo, Bianca Costa Soares de Sá, Maria Isabel Waddington Achatz, and João Duprat); Porto Alegre, Brazil (Renan Rangel Bonamigo and Maria Carolina Widholzer Rey); Leiden, the Netherlands (Coby Out-Luiting, Clasine van der Drift, Leny van Mourik, Wilma Bergman, Femke de Snoo, Jeanet ter Huurne, and Frans van Nieuwpoort); Queensland, Australia (Nicholas Martin, Grant Montgomery, David Whiteman, Stuart MacGregor, David Duffy and Michael Gattas, along with Judith Symmons and Harry Beeby who assisted with data management); Stockholm, Sweden (Diana Lindén, RN, for excellent work collecting and entering data into the study data base and Rainer Tuominen for screening of CDKN2A ); Tel Aviv, Israel (Yael Laitman); Lund, Sweden (Anita Zander, RN, for invaluable help with the data from the Lund Melanoma Study Group and Kari Nielsen, Anna Måsbäck, Katja Harbst, Goran Jonsson, and Åke Borg); and the University of Pennsylvania, Philadelphia, Pennsylvania, USA (Patricia Van Belle, Althea Ruffin, Jillian Knorr and Wenting Zhou). Samples for CDKN2A analysis were obtained from the Biobank of the Instituto Valenciano de Oncología. We also wish to thank the French Familial Melanoma Study Group: P. Andry-Benzaquen, B. Bachollet, F. Bérard, P. Berthet, F. Boitier, V. Bonadona, JL. Bonafé, JM. Bonnetblanc, F. Cambazard, O. Caron, F. Caux, J. Chevrant-Breton, A. Chompret (deceased), S. Dalle, L. Demange (deceased), O. Dereure, MX. Doré, MS. Doutre, C. Dugast (deceased), E. Maubec, L. Faivre, F. Grange, Ph. Humbert, P. Joly, D. Kerob, B. Labeille, C. Lasset, MT. Leccia, G. Lenoir, D. Leroux, J. Levang, D. Lipsker, S. Mansard, L. Martin, T. Martin-Denavit, C. Mateus, JL. Michel, P. Morel, L. Olivier-Faivre, JL. Perrot, N. Poulalhon, C. Robert, S. Ronger-Savle, B. Sassolas, P. Souteyrand, D. Stoppa-Lyonnet, L. Thomas, P. Vabres, L. Vincent-Fetita, and E. Wierzbicka. We also thank Hamida Mohamdi for managing the French MELARISK database. We acknowledge the use of the Genetic Counseling Shared Resource at the University of Utah, Salt Lake City, Utah, USA, supported by National Institutes of Health grant P30CA042014 awarded to the Hunstman Cancer Institute. We thank Christophe Blondel at Gustave Roussy for technical assistance in CDKN2A genotyping and acknowledge the work of the Gustave Roussy Biobank (BB-0033-00074) in providing DNA resources. Funding Information: Funding sources: Supported by the Cancer Research UK Programme Award (nos. C588/A4994 and C588/A10589); a Cancer Research UK project grant (C8216/A6129); the US National Institutes of Health (CA83115 to Drs Kanetsky, Bishop, and Elder; CA5558 to Dr Landi; Dr Taylor was supported by CA147832 to Dr Kanetsky); the Intramural Research Program of the National Institutions of Health, National Cancer Institute (NCI), Division of Cancer Epidemiology and Genetics; the National Health and Medical Research Council of Australia (NHMRC 107359, 402761, 633004, 566946, 211172); the Cancer Council New South Wales (project grants 77/00, 06/10); the Cancer Institute New South Wales (CINSW 05/TPG/1-01, 10/TPG/1-02); the Cancer Council Victoria and the Cancer Council Queensland (project grant 371); Coordenação de Aperfeiçoamento de Pessoal de Nível Superior; Fundação de Amparo à Pesquisa do Estado de São Paulo (no. 2007/04313-2); the National Health and Medical Research Council of Australia and the NCI (CA88363); the Cancer Research Foundations of Radiumhemmet and the Swedish Cancer Society; the Paulsson Trust, Lund University; the Swedish Cancer Society and European Research Council Advanced Grant (ERC-2011-294576); the research at the Melanoma Unit in Barcelona is partially funded by Spanish Fondo de Investigaciones Sanitarias (grants PI15/00716 and PI15/00956); Centros de Investigación Biomédica en Red de Enfermedades Raras of the Instituto de Salud Carlos III, Spain, is co-financed by European Development Regional Fund “A way to achieve Europe”; the Agency for Management of University and Research Grants 2014_SGR_603 of the Catalan government, Spain; the European Commission under the 6th Framework Programme (contract no. LSHC-CT-2006-018702, GenoMEL) and the 7th Framework Programme, Diagnoptics; a grant from Fundació La Marató de TV3 201331-30, Catalonia, Spain; a grant from Fundación Científica de la Asociación Española Contra el Cáncer, Spain (GCB15152978SOEN); Centres de Recerca de Catalunya Programme/Generalitat de Catalunya; the Italian Association for Cancer Research (to Dr Ghiorzo); the Italian Ministry of Health-Ricerca Finalizzata 2016 (to IRCCS San Martino-IST, Genoa); the Programme Hospitalier de Recherche Clinique (PHRC-AOM-07-195) awarded to Dr Avril and Dr Demenais; a grant from the Institut National du Cancer (to Dr Bressac de-Paillerets for coordination of Melanoma Oncogenetics in France); the Comisión Honoraria de Lucha Contra el Cáncer, Comisión Sectorial de Investigación Científica, Fundación Manuel Pérez, Montevideo, Uruguay; the Dutch Cancer Society (UL 2012-5489 to Dr Gruis); a scholarship awarded by Consejo Nacional de Ciencia y Tecnología, Mexico (152256/158706 to Dr Cuellar); and a Career Development Fellowship from the National Health and Medical Research Council (1147843) and Cancer Institute New South Wales (15/CDF/1-14) to Dr Cust. Part of the work was carried out at the Esther Koplowitz Center, Barcelona.We acknowledge the contributions of the participants and their families and the many clinicians, geneticists, genetic counsellors, and allied health professionals involved in their management. This work was performed in participation with the following members at the following study locations: Leeds, United Kingdom (Linda Whitaker, Paul Affleck, Jennifer H. Barrett, Jane Harrison, Mark M. Iles, Juliette Randerson-Moor, John C. Taylor, Kairen Kukalizch, Susan Leake, Birute Karpavicius, Sue Haynes, Tricia Mack, May Chan, and Yvonne Taylor); Barcelona, Spain (Paula Aguilera, Llúcia Alós, Celia Badenas, Alicia Barreiro, Neus Calbet, Cristina Carrera, Carlos Conill, Mireia Domínguez, Daniel Gabriel, Pablo Iglesias, Josep Malvehy, M. Eugenia Moliner, Javiera Pérez, Ramon Pigem, Miriam Potrony, Joan Anton Puig Butille, Ramon Rull, Marcelo Sánchez, Gemma Tell-Martí, Sergi Vidal-Sicart, and Oriol Yelamos) Valencia (Zaida García-Casado, Celia Requena, José Bañuls, Virtudes Soriano, José Antonio López-Guerrero, Manuel Moragón, Vicente Oliver); NCI at Cesena, Italy (Paola Minghetti, Laura Fontaine, Katie Beebe, and Giorgio Landi); Genoa, Italy (Giovanna Bianchi-Scarrà, Lorenza Pastorino, Virginia Andreotti, Claudia Martinuzzi, Bruna Dalmasso, Giulia Ciccarese, Francesco Spagnolo, and Paola Queirolo); Riga, Latvia (Kristine Azarjana, Simona Donina, Olita Heisele, Baiba Štreinerte, Aija Ozola and Ludmila Engele); Sydney, Australia (Caroline Watts, Gayathri St. George, Robyn Dalziell, and Kate McBride who assisted with recruitment of study participants; Leo Raudonikis who assisted with data management; and Chantelle Agha-Hamilton and Svetlana Pianova who assisted with biospecimen management); Montevideo, Uruguay (Virginia Barquet, Javiera Pérez, Miguel Martínez, Jimena Núñez, and Malena Scarone); São Paulo, Brazil (Dirce Maria Carraro, Alexandre Leon Ribeiro de Ávila, Luciana Facure Moredo, Bianca Costa Soares de Sá, Maria Isabel Waddington Achatz, and João Duprat); Porto Alegre, Brazil (Renan Rangel Bonamigo and Maria Carolina Widholzer Rey); Leiden, the Netherlands (Coby Out-Luiting, Clasine van der Drift, Leny van Mourik, Wilma Bergman, Femke de Snoo, Jeanet ter Huurne, and Frans van Nieuwpoort); Queensland, Australia (Nicholas Martin, Grant Montgomery, David Whiteman, Stuart MacGregor, David Duffy and Michael Gattas, along with Judith Symmons and Harry Beeby who assisted with data management); Stockholm, Sweden (Diana Lindén, RN, for excellent work collecting and entering data into the study data base and Rainer Tuominen for screening of CDKN2A); Tel Aviv, Israel (Yael Laitman); Lund, Sweden (Anita Zander, RN, for invaluable help with the data from the Lund Melanoma Study Group and Kari Nielsen, Anna Måsbäck, Katja Harbst, Goran Jonsson, and Åke Borg); and the University of Pennsylvania, Philadelphia, Pennsylvania, USA (Patricia Van Belle, Althea Ruffin, Jillian Knorr and Wenting Zhou). Samples for CDKN2A analysis were obtained from the Biobank of the Instituto Valenciano de Oncología. We also wish to thank the French Familial Melanoma Study Group: P. Andry-Benzaquen, B. Bachollet, F. Bérard, P. Berthet, F. Boitier, V. Bonadona, JL. Bonafé, JM. Bonnetblanc, F. Cambazard, O. Caron, F. Caux, J. Chevrant-Breton, A. Chompret (deceased), S. Dalle, L. Demange (deceased), O. Dereure, MX. Doré, MS. Doutre, C. Dugast (deceased), E. Maubec, L. Faivre, F. Grange, Ph. Humbert, P. Joly, D. Kerob, B. Labeille, C. Lasset, MT. Leccia, G. Lenoir, D. Leroux, J. Levang, D. Lipsker, S. Mansard, L. Martin, T. Martin-Denavit, C. Mateus, JL. Michel, P. Morel, L. Olivier-Faivre, JL. Perrot, N. Poulalhon, C. Robert, S. Ronger-Savle, B. Sassolas, P. Souteyrand, D. Stoppa-Lyonnet, L. Thomas, P. Vabres, L. Vincent-Fetita, and E. Wierzbicka. We also thank Hamida Mohamdi for managing the French MELARISK database. We acknowledge the use of the Genetic Counseling Shared Resource at the University of Utah, Salt Lake City, Utah, USA, supported by National Institutes of Health grant P30CA042014 awarded to the Hunstman Cancer Institute. We thank Christophe Blondel at Gustave Roussy for technical assistance in CDKN2A genotyping and acknowledge the work of the Gustave Roussy Biobank (BB-0033-00074) in providing DNA resources. Funding sources: Supported by the Cancer Research UK Programme Award (nos. C588/A4994 and C588/A10589); a Cancer Research UK project grant ( C8216/A6129); the US National Institutes of Health ( CA83115 to Drs Kanetsky, Bishop, and Elder; CA5558 to Dr Landi; Dr Taylor was supported by CA147832 to Dr Kanetsky); the Intramural Research Program of the National Institutions of Health, National Cancer Institute (NCI), Division of Cancer Epidemiology and Genetics; the National Health and Medical Research Council of Australia ( NHMRC 107359, 402761, 633004, 566946, 211172); the Cancer Council New South Wales (project grants 77/00, 06/10); the Cancer Institute New South Wales (CINSW 05/TPG/1-01, 10/TPG/1-02); the Cancer Council Victoria and the Cancer Council Queensland (project grant 371); Coordenação de Aperfeiçoamento de Pessoal de Nível Superior; Fundação de Amparo à Pesquisa do Estado de São Paulo (no. 2007/04313-2); the National Health and Medical Research Council of Australia and the NCI ( CA88363); the Cancer Research Foundations of Radiumhemmet and the Swedish Cancer Society; the Paulsson Trust, Lund University; the Swedish Cancer Society and European Research Council Advanced Grant ( ERC-2011-294576); the research at the Melanoma Unit in Barcelona is partially funded by Spanish Fondo de Investigaciones Sanitarias (grants PI15/00716 and PI15/00956); Centros de Investigación Biomédica en Red de Enfermedades Raras of the Instituto de Salud Carlos III, Spain, is co-financed by European Development Regional Fund “A way to achieve Europe”; the Agency for Management of University and Research Grants 2014_SGR_603 of the Catalan government, Spain; the European Commission under the 6th Framework Programme (contract no. LSHC-CT-2006-018702, GenoMEL) and the 7th Framework Programme, Diagnoptics; a grant from Fundació La Marató de TV3 201331-30, Catalonia, Spain; a grant from Fundación Científica de la Asociación Española Contra el Cáncer, Spain ( GCB15152978SOEN); Centres de Recerca de Catalunya Programme/Generalitat de Catalunya; the Italian Association for Cancer Research (to Dr Ghiorzo); the Italian Ministry of Health-Ricerca Finalizzata 2016 (to IRCCS San Martino- IST, Genoa); the Programme Hospitalier de Recherche Clinique ( PHRC-AOM-07-195) awarded to Dr Avril and Dr Demenais; a grant from the Institut National du Cancer (to Dr Bressac de-Paillerets for coordination of Melanoma Oncogenetics in France); the Comisión Honoraria de Lucha Contra el Cáncer, Comisión Sectorial de Investigación Científica, Fundación Manuel Pérez, Montevideo, Uruguay; the Dutch Cancer Society ( UL 2012-5489 to Dr Gruis); a scholarship awarded by Consejo Nacional de Ciencia y Tecnología, Mexico ( 152256/158706 to Dr Cuellar); and a Career Development Fellowship from the National Health and Medical Research Council (1147843) and Cancer Institute New South Wales ( 15/CDF/1-14) to Dr Cust. Part of the work was carried out at the Esther Koplowitz Center, Barcelona. Publisher Copyright: © 2019 American Academy of Dermatology, Inc.
PY - 2019/8
Y1 - 2019/8
N2 - Background: Although rare in the general population, highly penetrant germline mutations in CDKN2A are responsible for 5%-40% of melanoma cases reported in melanoma-prone families. We sought to determine whether MELPREDICT was generalizable to a global series of families with melanoma and whether performance improvements can be achieved. Methods: In total, 2116 familial melanoma cases were ascertained by the international GenoMEL Consortium. We recapitulated the MELPREDICT model within our data (GenoMELPREDICT) to assess performance improvements by adding phenotypic risk factors and history of pancreatic cancer. We report areas under the curve (AUC) with 95% confidence intervals (CIs) along with net reclassification indices (NRIs) as performance metrics. Results: MELPREDICT performed well (AUC 0.752, 95% CI 0.730-0.775), and GenoMELPREDICT performance was similar (AUC 0.748, 95% CI 0.726-0.771). Adding a reported history of pancreatic cancer yielded discriminatory improvement (P < .0001) in GenoMELPREDICT (AUC 0.772, 95% CI 0.750-0.793, NRI 0.40). Including phenotypic risk factors did not improve performance. Conclusion: The MELPREDICT model functioned well in a global data set of familial melanoma cases. Adding pancreatic cancer history improved model prediction. GenoMELPREDICT is a simple tool for predicting CDKN2A mutational status among melanoma patients from melanoma-prone families and can aid in directing these patients to receive genetic testing or cancer risk counseling.
AB - Background: Although rare in the general population, highly penetrant germline mutations in CDKN2A are responsible for 5%-40% of melanoma cases reported in melanoma-prone families. We sought to determine whether MELPREDICT was generalizable to a global series of families with melanoma and whether performance improvements can be achieved. Methods: In total, 2116 familial melanoma cases were ascertained by the international GenoMEL Consortium. We recapitulated the MELPREDICT model within our data (GenoMELPREDICT) to assess performance improvements by adding phenotypic risk factors and history of pancreatic cancer. We report areas under the curve (AUC) with 95% confidence intervals (CIs) along with net reclassification indices (NRIs) as performance metrics. Results: MELPREDICT performed well (AUC 0.752, 95% CI 0.730-0.775), and GenoMELPREDICT performance was similar (AUC 0.748, 95% CI 0.726-0.771). Adding a reported history of pancreatic cancer yielded discriminatory improvement (P < .0001) in GenoMELPREDICT (AUC 0.772, 95% CI 0.750-0.793, NRI 0.40). Including phenotypic risk factors did not improve performance. Conclusion: The MELPREDICT model functioned well in a global data set of familial melanoma cases. Adding pancreatic cancer history improved model prediction. GenoMELPREDICT is a simple tool for predicting CDKN2A mutational status among melanoma patients from melanoma-prone families and can aid in directing these patients to receive genetic testing or cancer risk counseling.
KW - CDKN2A
KW - familial melanoma
KW - GenoMEL
KW - GenoMELPREDICT
KW - mutation prediction
UR - http://www.scopus.com/inward/record.url?scp=85068769924&partnerID=8YFLogxK
U2 - 10.1016/j.jaad.2019.01.079
DO - 10.1016/j.jaad.2019.01.079
M3 - Article
C2 - 30731170
AN - SCOPUS:85068769924
SN - 0190-9622
VL - 81
SP - 386
EP - 394
JO - Journal of the American Academy of Dermatology
JF - Journal of the American Academy of Dermatology
IS - 2
ER -