NF1-mutated melanomas reveal distinct clinical characteristics depending on tumour origin and respond favourably to immune checkpoint inhibitors

Carl M. Thielmann; Eleftheria Chorti; Johanna Matull; Rajmohan Murali; Anne Zaremba; Georg Lodde; Philipp Jansen; Luisa Richter; Julia Kretz; Inga Möller; Antje Sucker; Rudolf Herbst; Patrick Terheyden; Jochen Utikal; Claudia Pföhler; Jens Ulrich; Alexander Kreuter; Peter Mohr; Ralf Gutzmer; Friedegund Meier; Edgar Dippel; Michael Weichenthal; Annette Paschen; Elisabeth Livingstone; Lisa Zimmer; Dirk Schadendorf; Eva Hadaschik; Selma Ugurel; Klaus G. Griewank

doi:10.1016/j.ejca.2021.09.035

NF1-mutated melanomas reveal distinct clinical characteristics depending on tumour origin and respond favourably to immune checkpoint inhibitors

Carl M. Thielmann, Eleftheria Chorti, Johanna Matull, Rajmohan Murali, Anne Zaremba, Georg Lodde, Philipp Jansen, Luisa Richter, Julia Kretz, Inga Möller, Antje Sucker, Rudolf Herbst, Patrick Terheyden, Jochen Utikal, Claudia Pföhler, Jens Ulrich, Alexander Kreuter, Peter Mohr, Ralf Gutzmer, Friedegund MeierEdgar Dippel, Michael Weichenthal, Annette Paschen, Elisabeth Livingstone, Lisa Zimmer, Dirk Schadendorf, Eva Hadaschik, Selma Ugurel, Klaus G. Griewank^*

^*Corresponding author for this work

Clinic of Dermatology, Allergology and Venerology

25 Citations (Scopus)

Abstract

Background: NF1-mutated tumours represent a small subset (10–15%) of melanomas, not sufficiently analysed in large clinical cohorts. This study investigated the largest multicentre collection of NF1-mutated melanomas to date. Methods: This study analysed a multicentre tumour tissue sample cohort from 266 patients with NF1-mutated melanoma. Targeted next-generation sequencing of the TERT promoter and 29 relevant melanoma genes was performed. Survival was compared with NF1 wild-type cohorts from the Tissue Registry in Melanoma project (n = 432). Results: Most NF1-mutated melanoma arose in the head-and-neck region of patients >60 years. NF1 alterations were frequently inactivating, primarily non-sense, less frequently truncating mutations. Non-inactivating NF1 mutations more frequently co-occurred with activating BRAF and RAS mutations. NF1-mutated tumours had higher numbers of gene mutations and UV signature C>T and CC>TT transitions than BRAF, RAS and triple wild-type melanomas. NF1-mutated acral and mucosal melanomas harboured a different mutation signature and were frequent in women (69% and 83%, respectively), differing from non-acral cutaneous NF1-mutated melanomas (men 73%, women 27%). Overall survival in stage IV disease was comparable for patients with NF1-mutated or wild-type melanoma. However, in patients receiving first-line immune checkpoint inhibitor treatment, better median overall survival (mOS) was observed for NF1-mutated than wild-type tumours (mOS = not reached vs mOS = 25.82, p = 0.0154, n = 80 and 432, respectively). Conclusions: Cutaneous, acral and mucosal NF1-mutated melanomas vary in clinical and genetic characteristics and demonstrate a favourable outcome on immune checkpoint inhibition therapy.

Original language	English
Journal	European Journal of Cancer
Volume	159
Pages (from-to)	113-124
Number of pages	12
ISSN	0959-8049
DOIs	https://doi.org/10.1016/j.ejca.2021.09.035
Publication status	Published - 12.2021

Funding

CMT was supported as a Junior Clinician Scientist within the University Medicine Essen Academy (UMEA) funded by the Faculty of Medicine , University of Duisburg-Essen . This research was funded in part through the NIH/NCI Cancer Centr e Support Grant P30 CA008748 . This work was partly funded by the Deutsche Forschungsgemeinschaft – SCHA 422/17-1 and HO 6389/2-1 (KFO 337) . This work was in part supported by Bristol Myers Squibb for the multicentre translational study ‘Tissue Registry in Melanoma’ (TRIM) within the framework of the skin cancer registry ADOREG of the German Dermatologic Cooperative Oncology Group (DeCOG). CMT was supported as a Junior Clinician Scientist within the University Medicine Essen Academy (UMEA) funded by the Faculty of Medicine, University of Duisburg-Essen. This research was funded in part through the NIH/NCI Cancer Centre Support Grant P30 CA008748. This work was partly funded by the Deutsche Forschungsgemeinschaft ? SCHA 422/17-1 and HO 6389/2-1 (KFO 337). This work was in part supported by Bristol Myers Squibb for the multicentre translational study ?Tissue Registry in Melanoma? (TRIM) within the framework of the skin cancer registry ADOREG of the German Dermatologic Cooperative Oncology Group (DeCOG).The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: C.M.T. reported no relevant conflicts of interest. E.C. reported no relevant conflicts of interest. J.M. declares travel support from Bristol Myers Squibb, Novartis and Sun Pharmaceutical Industries, outside the submitted work. R.M. reported no relevant conflicts of interest. A.Z. declares travel support from Novartis, Sanofi Genzyme and Bristol-Myers Squibb, outside the submitted work. G.L. declares travel support from Sun Pharma, outside the submitted work. P.J. reported no relevant conflicts of interest. L.R. reported no relevant conflicts of interest. J.K. reported no relevant conflicts of interest. I.M. reported no relevant conflicts of interest. A.S. reported no relevant conflicts of interest. R.H. declares speakers and advisory board honoraria from BMS, MSD, Novartis, Pierre Fabre, Roche and Sun Pharma, outside the submitted work. P.T. declares honoraria from Bristol-Myers Squibb, Novartis, Merck Sharp and Dohme, Pierre-Fabre, CureVac, Merck Serono, Sanofi, Roche, Kyowa Kirin, Biofrontera; travel support from Bristol-Myers Squibb and Pierre-Fabre, outside the submitted work. J.U. declares advisory board or has received honoraria and travel support from Amgen, Bristol Myers Squibb, GSK, LeoPharma, Merck Sharp and Dohme, Novartis, Pierre Fabre, Roche, Sanofi, outside the submitted work. C.P. served as consultant and/or has received honoraria from Bristol-Myers Squibb, Merck Sharp & Dohme, Novartis, Sanofi, Sun Pharma, Pierre Fabre, AbbVie, Kyona Kirin and Amgen and received travel support from Amgen, Merck Sharp and Dohme, Bristol-Myers Squibb, Pierre Fabre, Sun Pharma and Novartis, outside the submitted work. J.Ul declares travel support: Medac, Sun Pharma; consulting: Bristol-Myers Squibb, Sun Pharma; lectures: Bristol-Myers Squibb, MSD, Merck, Novartis, Roche, Sanofi, Sun Pharma; grants: Novartis, outside the submitted work. A.K. reported no relevant conflicts of interest. P.M. declares research support (to institution): Bristol-MyersSquibb, Novartis, MSD. Honoraria for lectures (personally): Roche Pharma, Bristol-MyersSquibb, Novartis, MSD, Almirall-Hermal, Amgen, Merck-Serono, Bayer, Pierre-Fabre, Sanofi. Honoraria for advisory boards: Bayersdorf, Roche Pharma, Bristol-MyersSquibb, Novartis, MSD, Almirall-Hermal, Amgen, Pierre-Fabre, Merck-Serono, SUN, Merck-Serono, Sanofi, outside the submitted work. R.G. invited speaker: Roche, BMS, MSD, Novartis, Amgen, Merck Serono, Almirall Hermal, SUN, Sanofi, Pierre-Fabre. Advisory board: BMS, Roche, Novartis, Almirall Hermal, MSD, Amgen, SUN, Sanofi, Pierre-Fabre, 4SC, Bayer, MerckSerono, Pfizer, Immunocore. Research grants: Novartis, Pfizer, Johnson and Johnson, Amgen, Merck-Serono, SUN Pharma, Sanofi. Travel/meeting support: Roche, BMS, SUN, Merck-Serono, Pierre-Fabre, outside the submitted work. F.M. declares travel support or/and speaker's fees or/and advisor's honoraria by Novartis, Roche, BMS, MSD and Pierre Fabre and research funding from Novartis and Roche, outside the submitted work. E.D. reported no relevant conflicts of interest. M.W. reported no relevant conflicts of interest. A.P. reported no relevant conflicts of interest. E.L. served as consultant and/or has received honoraria from Bristol-Myers Squibb, Merck Sharp and Dohme, Novartis, Medac, Sanofi, Sun Pharma and travel support from Amgen, Merck Sharp and Dohme, Bristol-Myers Squibb, Pierre Fabre, Sun Pharma and Novartis, outside the submitted work. LZ served as consultant and/or has received honoraria from Bristol-Myers Squibb, Merck Sharp and Dohme, Novartis, Pierre-Fabre, Sun Pharma and Sanofi; Research funding to institution: Novartis; travel support from Merck Sharp and Dohme, Bristol-Myers Squibb, Amgen, Pierre-Fabre, Sanofi, Sun Pharma and Novartis, outside the submitted work. D.S. reports personal fees and non-financial support from Roche/Genentech, grants, personal fees, non-financial support and others from BMS, personal fees from Merck Sharp and Dohme, personal fees and non-financial support from Merck Serono, grant, personal fees and non-financial support from Amgen, personal fees from Immunocore, personal fees from Incyte, personal fees from 4SC, personal fees from Pierre Fabre, personal fees and non-financial support from Sanofi/Regeneron, personal fees from Array BioPharma, personal fees from Pfizer, personal fees from Philogen, personal fees from Regeneron, personal fees from Nektar, personal fees from Sandoz, grants, personal fees and non-financial support from Novartis, personal fees and non-financial support from SunPharma, Replimune, Helsinn, OncoSec and InFlaRx outside the submitted work. E.H. reported no relevant conflicts of interest. S.U. declares research support from Bristol Myers Squibb and Merck Serono; speakers and advisory board honoraria from Bristol Myers Squibb, Merck Sharp and Dohme, Merck Serono, Novartis and Roche, and travel support from Bristol Myers Squibb, and Merck Sharp and Dohme, outside the submitted work. K.G. reported no relevant conflicts of interest. The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: C.M.T. reported no relevant conflicts of interest. E.C. reported no relevant conflicts of interest. J.M. declares travel support from Bristol Myers Squibb, Novartis and Sun Pharmaceutical Industries, outside the submitted work. R.M. reported no relevant conflicts of interest. A.Z. declares travel support from Novartis, Sanofi Genzyme and Bristol-Myers Squibb, outside the submitted work. G.L. declares travel support from Sun Pharma, outside the submitted work. P.J. reported no relevant conflicts of interest. L.R. reported no relevant conflicts of interest. J.K. reported no relevant conflicts of interest. I.M. reported no relevant conflicts of interest. A.S. reported no relevant conflicts of interest. R.H. declares speakers and advisory board honoraria from BMS , MSD , Novartis , Pierre Fabre , Roche and Sun Pharma , outside the submitted work. P.T. declares honoraria from Bristol-Myers Squibb , Novartis , Merck Sharp and Dohme , Pierre-Fabre , CureVac , Merck Serono , Sanofi , Roche , Kyowa Kirin , Biofrontera ; travel support from Bristol-Myers Squibb and Pierre-Fabre, outside the submitted work. J.U. declares advisory board or has received honoraria and travel support from Amgen, Bristol Myers Squibb, GSK, LeoPharma, Merck Sharp and Dohme, Novartis, Pierre Fabre, Roche, Sanofi, outside the submitted work. C.P. served as consultant and/or has received honoraria from Bristol-Myers Squibb , Merck Sharp & Dohme , Novartis , Sanofi , Sun Pharma , Pierre Fabre , AbbVie , Kyona Kirin and Amgen and received travel support from Amgen, Merck Sharp and Dohme, Bristol-Myers Squibb, Pierre Fabre, Sun Pharma and Novartis, outside the submitted work. J.Ul declares travel support: Medac, Sun Pharma; consulting: Bristol-Myers Squibb , Sun Pharma ; lectures: Bristol-Myers Squibb, MSD, Merck, Novartis, Roche, Sanofi, Sun Pharma; grants: Novartis, outside the submitted work. A.K. reported no relevant conflicts of interest. P.M. declares research support (to institution): Bristol-MyersSquibb , Novartis , MSD . Honoraria for lectures (personally): Roche Pharma , Bristol-MyersSquibb , Novartis , MSD , Almirall-Hermal , Amgen , Merck-Serono , Bayer , Pierre-Fabre , Sanofi . Honoraria for advisory boards: Bayersdorf , Roche Pharma , Bristol-MyersSquibb , Novartis , MSD , Almirall-Hermal , Amgen , Pierre-Fabre , Merck-Serono , SUN , Merck-Serono , Sanofi , outside the submitted work. R.G. invited speaker: Roche, BMS, MSD, Novartis, Amgen, Merck Serono, Almirall Hermal, SUN, Sanofi, Pierre-Fabre. Advisory board: BMS, Roche, Novartis, Almirall Hermal, MSD, Amgen, SUN, Sanofi, Pierre-Fabre, 4SC, Bayer, MerckSerono, Pfizer, Immunocore. Research grants: Novartis , Pfizer , Johnson and Johnson , Amgen , Merck-Serono , SUN Pharma , Sanofi . Travel/meeting support: Roche, BMS, SUN, Merck-Serono, Pierre-Fabre, outside the submitted work. F.M. declares travel support or/and speaker's fees or/and advisor's honoraria by Novartis , Roche , BMS , MSD and Pierre Fabre and research funding from Novartis and Roche , outside the submitted work. E.D. reported no relevant conflicts of interest. M.W. reported no relevant conflicts of interest. A.P. reported no relevant conflicts of interest. E.L. served as consultant and/or has received honoraria from Bristol-Myers Squibb , Merck Sharp and Dohme , Novartis , Medac , Sanofi , Sun Pharma and travel support from Amgen, Merck Sharp and Dohme, Bristol-Myers Squibb, Pierre Fabre, Sun Pharma and Novartis, outside the submitted work. LZ served as consultant and/or has received honoraria from Bristol-Myers Squibb , Merck Sharp and Dohme , Novartis , Pierre-Fabre , Sun Pharma and Sanofi ; Research funding to institution: Novartis ; travel support from Merck Sharp and Dohme, Bristol-Myers Squibb, Amgen, Pierre-Fabre, Sanofi, Sun Pharma and Novartis, outside the submitted work. D.S. reports personal fees and non-financial support from Roche/Genentech, grants, personal fees, non-financial support and others from BMS, personal fees from Merck Sharp and Dohme, personal fees and non-financial support from Merck Serono, grant, personal fees and non-financial support from Amgen, personal fees from Immunocore, personal fees from Incyte, personal fees from 4SC, personal fees from Pierre Fabre, personal fees and non-financial support from Sanofi/Regeneron, personal fees from Array BioPharma, personal fees from Pfizer, personal fees from Philogen, personal fees from Regeneron, personal fees from Nektar, personal fees from Sandoz, grants, personal fees and non-financial support from Novartis, personal fees and non-financial support from SunPharma, Replimune, Helsinn, OncoSec and InFlaRx outside the submitted work. E.H. reported no relevant conflicts of interest. S.U. declares research support from Bristol Myers Squibb and Merck Serono ; speakers and advisory board honoraria from Bristol Myers Squibb , Merck Sharp and Dohme , Merck Serono , Novartis and Roche , and travel support from Bristol Myers Squibb, and Merck Sharp and Dohme, outside the submitted work. K.G. reported no relevant conflicts of interest.

Research Areas and Centers

Academic Focus: Center for Infection and Inflammation Research (ZIEL)
Research Area: Luebeck Integrated Oncology Network (LION)
Centers: University Cancer Center Schleswig-Holstein (UCCSH)

DFG Research Classification Scheme

2.22-14 Hematology, Oncology
2.22-19 Dermatology
2.21-05 Immunology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.ejca.2021.09.035

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Thielmann, C. M., Chorti, E., Matull, J., Murali, R., Zaremba, A., Lodde, G., Jansen, P., Richter, L., Kretz, J., Möller, I., Sucker, A., Herbst, R., Terheyden, P., Utikal, J., Pföhler, C., Ulrich, J., Kreuter, A., Mohr, P., Gutzmer, R., ... Griewank, K. G. (2021). NF1-mutated melanomas reveal distinct clinical characteristics depending on tumour origin and respond favourably to immune checkpoint inhibitors. European Journal of Cancer, 159, 113-124. https://doi.org/10.1016/j.ejca.2021.09.035

@article{0aae8bbfdb92479fba69a7bd0b52c94b,

title = "NF1-mutated melanomas reveal distinct clinical characteristics depending on tumour origin and respond favourably to immune checkpoint inhibitors",

abstract = "Background: NF1-mutated tumours represent a small subset (10–15\%) of melanomas, not sufficiently analysed in large clinical cohorts. This study investigated the largest multicentre collection of NF1-mutated melanomas to date. Methods: This study analysed a multicentre tumour tissue sample cohort from 266 patients with NF1-mutated melanoma. Targeted next-generation sequencing of the TERT promoter and 29 relevant melanoma genes was performed. Survival was compared with NF1 wild-type cohorts from the Tissue Registry in Melanoma project (n = 432). Results: Most NF1-mutated melanoma arose in the head-and-neck region of patients >60 years. NF1 alterations were frequently inactivating, primarily non-sense, less frequently truncating mutations. Non-inactivating NF1 mutations more frequently co-occurred with activating BRAF and RAS mutations. NF1-mutated tumours had higher numbers of gene mutations and UV signature C>T and CC>TT transitions than BRAF, RAS and triple wild-type melanomas. NF1-mutated acral and mucosal melanomas harboured a different mutation signature and were frequent in women (69\% and 83\%, respectively), differing from non-acral cutaneous NF1-mutated melanomas (men 73\%, women 27\%). Overall survival in stage IV disease was comparable for patients with NF1-mutated or wild-type melanoma. However, in patients receiving first-line immune checkpoint inhibitor treatment, better median overall survival (mOS) was observed for NF1-mutated than wild-type tumours (mOS = not reached vs mOS = 25.82, p = 0.0154, n = 80 and 432, respectively). Conclusions: Cutaneous, acral and mucosal NF1-mutated melanomas vary in clinical and genetic characteristics and demonstrate a favourable outcome on immune checkpoint inhibition therapy.",

author = "Thielmann, \{Carl M.\} and Eleftheria Chorti and Johanna Matull and Rajmohan Murali and Anne Zaremba and Georg Lodde and Philipp Jansen and Luisa Richter and Julia Kretz and Inga M{\"o}ller and Antje Sucker and Rudolf Herbst and Patrick Terheyden and Jochen Utikal and Claudia Pf{\"o}hler and Jens Ulrich and Alexander Kreuter and Peter Mohr and Ralf Gutzmer and Friedegund Meier and Edgar Dippel and Michael Weichenthal and Annette Paschen and Elisabeth Livingstone and Lisa Zimmer and Dirk Schadendorf and Eva Hadaschik and Selma Ugurel and Griewank, \{Klaus G.\}",

note = "Publisher Copyright: {\textcopyright} 2021 Elsevier Ltd",

year = "2021",

month = dec,

doi = "10.1016/j.ejca.2021.09.035",

language = "English",

volume = "159",

pages = "113--124",

journal = "European Journal of Cancer",

issn = "0959-8049",

publisher = "Elsevier Ltd",

}

Thielmann, CM, Chorti, E, Matull, J, Murali, R, Zaremba, A, Lodde, G, Jansen, P, Richter, L, Kretz, J, Möller, I, Sucker, A, Herbst, R, Terheyden, P, Utikal, J, Pföhler, C, Ulrich, J, Kreuter, A, Mohr, P, Gutzmer, R, Meier, F, Dippel, E, Weichenthal, M, Paschen, A, Livingstone, E, Zimmer, L, Schadendorf, D, Hadaschik, E, Ugurel, S & Griewank, KG 2021, 'NF1-mutated melanomas reveal distinct clinical characteristics depending on tumour origin and respond favourably to immune checkpoint inhibitors', European Journal of Cancer, vol. 159, pp. 113-124. https://doi.org/10.1016/j.ejca.2021.09.035

TY - JOUR

T1 - NF1-mutated melanomas reveal distinct clinical characteristics depending on tumour origin and respond favourably to immune checkpoint inhibitors

AU - Thielmann, Carl M.

AU - Chorti, Eleftheria

AU - Matull, Johanna

AU - Murali, Rajmohan

AU - Zaremba, Anne

AU - Lodde, Georg

AU - Jansen, Philipp

AU - Richter, Luisa

AU - Kretz, Julia

AU - Möller, Inga

AU - Sucker, Antje

AU - Herbst, Rudolf

AU - Terheyden, Patrick

AU - Utikal, Jochen

AU - Pföhler, Claudia

AU - Ulrich, Jens

AU - Kreuter, Alexander

AU - Mohr, Peter

AU - Gutzmer, Ralf

AU - Meier, Friedegund

AU - Dippel, Edgar

AU - Weichenthal, Michael

AU - Paschen, Annette

AU - Livingstone, Elisabeth

AU - Zimmer, Lisa

AU - Schadendorf, Dirk

AU - Hadaschik, Eva

AU - Ugurel, Selma

AU - Griewank, Klaus G.

PY - 2021/12

Y1 - 2021/12

N2 - Background: NF1-mutated tumours represent a small subset (10–15%) of melanomas, not sufficiently analysed in large clinical cohorts. This study investigated the largest multicentre collection of NF1-mutated melanomas to date. Methods: This study analysed a multicentre tumour tissue sample cohort from 266 patients with NF1-mutated melanoma. Targeted next-generation sequencing of the TERT promoter and 29 relevant melanoma genes was performed. Survival was compared with NF1 wild-type cohorts from the Tissue Registry in Melanoma project (n = 432). Results: Most NF1-mutated melanoma arose in the head-and-neck region of patients >60 years. NF1 alterations were frequently inactivating, primarily non-sense, less frequently truncating mutations. Non-inactivating NF1 mutations more frequently co-occurred with activating BRAF and RAS mutations. NF1-mutated tumours had higher numbers of gene mutations and UV signature C>T and CC>TT transitions than BRAF, RAS and triple wild-type melanomas. NF1-mutated acral and mucosal melanomas harboured a different mutation signature and were frequent in women (69% and 83%, respectively), differing from non-acral cutaneous NF1-mutated melanomas (men 73%, women 27%). Overall survival in stage IV disease was comparable for patients with NF1-mutated or wild-type melanoma. However, in patients receiving first-line immune checkpoint inhibitor treatment, better median overall survival (mOS) was observed for NF1-mutated than wild-type tumours (mOS = not reached vs mOS = 25.82, p = 0.0154, n = 80 and 432, respectively). Conclusions: Cutaneous, acral and mucosal NF1-mutated melanomas vary in clinical and genetic characteristics and demonstrate a favourable outcome on immune checkpoint inhibition therapy.

AB - Background: NF1-mutated tumours represent a small subset (10–15%) of melanomas, not sufficiently analysed in large clinical cohorts. This study investigated the largest multicentre collection of NF1-mutated melanomas to date. Methods: This study analysed a multicentre tumour tissue sample cohort from 266 patients with NF1-mutated melanoma. Targeted next-generation sequencing of the TERT promoter and 29 relevant melanoma genes was performed. Survival was compared with NF1 wild-type cohorts from the Tissue Registry in Melanoma project (n = 432). Results: Most NF1-mutated melanoma arose in the head-and-neck region of patients >60 years. NF1 alterations were frequently inactivating, primarily non-sense, less frequently truncating mutations. Non-inactivating NF1 mutations more frequently co-occurred with activating BRAF and RAS mutations. NF1-mutated tumours had higher numbers of gene mutations and UV signature C>T and CC>TT transitions than BRAF, RAS and triple wild-type melanomas. NF1-mutated acral and mucosal melanomas harboured a different mutation signature and were frequent in women (69% and 83%, respectively), differing from non-acral cutaneous NF1-mutated melanomas (men 73%, women 27%). Overall survival in stage IV disease was comparable for patients with NF1-mutated or wild-type melanoma. However, in patients receiving first-line immune checkpoint inhibitor treatment, better median overall survival (mOS) was observed for NF1-mutated than wild-type tumours (mOS = not reached vs mOS = 25.82, p = 0.0154, n = 80 and 432, respectively). Conclusions: Cutaneous, acral and mucosal NF1-mutated melanomas vary in clinical and genetic characteristics and demonstrate a favourable outcome on immune checkpoint inhibition therapy.

UR - https://www.scopus.com/pages/publications/85118500481

U2 - 10.1016/j.ejca.2021.09.035

DO - 10.1016/j.ejca.2021.09.035

M3 - Journal articles

C2 - 34742158

AN - SCOPUS:85118500481

SN - 0959-8049

VL - 159

SP - 113

EP - 124

JO - European Journal of Cancer

JF - European Journal of Cancer

ER -

NF1-mutated melanomas reveal distinct clinical characteristics depending on tumour origin and respond favourably to immune checkpoint inhibitors

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