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1. Diagnostic Concordance in Tertiary (Dermatologists-to-Experts) Teledermoscopy: A Final Diagnosis-Based Study on 290 Cases

Author

Anne Marchetti, Stephane Dalle, Delphine Maucort Boulch, Mona Amini-Adl, Sébastien Debarbieux, Nicolas Poulalhon, Marie Perier-Muzet, Alice Phan, and Luc Thomas

Subjects
teledermoscopy, tertiary teledermatology, nail, pediatric, dermoscopy, Dermatology, RL1-803
Abstract

Background: Teledermoscopy (TDS) improves diagnostic accuracy and decreases the number of unnecessary consultations. Objectives: To determine the diagnostic concordance in tertiary (dermatologist-to-experts) TDS with histopathology/follow-up–based diagnosis. Methods: A descriptive retrospective cohort study including 290 requests. Results: Perfect diagnostic concordance was found in 202 (69.7%) cases and partial agreement in 29 (10%). Disagreement was found in 59 (20.3%) cases. Perfect concordance on the benign/malignant nature of the lesion was found in 227 (78.3%) cases and disagreement in 63 (21.7%). In onychology, diagnostic concordance was perfect in 43 (76.8%) cases, partial in 7 (12.5%), and there was disagreement in 6 (10.7%). Final concordance on the benign/malignant nature of the lesion was perfect in 48 (85.7%) and there was disagreement in 8 (14.3%) nail cases. For pediatric requests, diagnostic concordance was perfect in 29 (65.9%) cases, partial in 5 (11.4%), and there was disagreement in 10 (22.7%). Final concordance on the benign/malignant nature of the lesion was observed in 34 (77.3%) cases, disagreement in 10 (22.7%). Conclusions: This study confirms that tertiary TDS improves diagnostic accuracy of pigmented skin lesions. Moreover, it shows encouraging results in unusual conditions such as ungual and pediatric skin tumors. The main limitation was the retrospective nature and the “real-life” setting of our study that could have created a selection bias toward inclusion of the most difficult cases.

Published
2020
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2. Frequency and Genomic Aspects of Intrinsic Resistance to Vismodegib in Locally Advanced Basal Cell Carcinoma

Author

Andrey A. Yurchenko, Oltin T. Pop, Meriem Ighilahriz, Ismael Padioleau, Fatemeh Rajabi, Hayley J. Sharpe, Nicolas Poulalhon, Brigitte Dreno, Amir Khammari, Marc Delord, Antonio Alberti, Nadem Soufir, Maxime Battistella, Samia Mourah, Fanny Bouquet, Ariel Savina, Andrej Besse, Max Mendez-Lopez, Florent Grange, Sandrine Monestier, Laurent Mortier, Nicolas Meyer, Caroline Dutriaux, Caroline Robert, Philippe Saiag, Florian Herms, Jerome Lambert, Frederic J. de Sauvage, Nicolas Dumaz, Lukas Flatz, Nicole Basset-Seguin, Sergey I. Nikolaev, Pecqueret, Valérie, Biomarqueurs prédictifs et nouvelles stratégies moléculaires en thérapeutique anticancéreuse (U981), Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Prédicteurs moléculaires et nouvelles cibles en oncologie (PMNCO), Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Brustzentrum Kantonsspital St. Gallen, Immunologie humaine, physiopathologie & immunothérapie (HIPI (UMR_S_976 / U976)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), The Babraham Institute [Cambridge, UK], Centre Hospitalier Lyon Sud [CHU - HCL] (CHLS), Hospices Civils de Lyon (HCL), Centre de Recherche en Cancérologie et Immunologie Intégrée Nantes-Angers (CRCI2NA ), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Nantes Université - UFR de Médecine et des Techniques Médicales (Nantes Univ - UFR MEDECINE), Nantes Université - pôle Santé, Nantes Université (Nantes Univ)-Nantes Université (Nantes Univ)-Nantes Université - pôle Santé, Nantes Université (Nantes Univ)-Nantes Université (Nantes Univ), Centre d’Investigation Clinique de Nantes (CIC Nantes), Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre hospitalier universitaire de Nantes (CHU Nantes), Immunology and New Concepts in ImmunoTherapy (INCIT), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Nantes Université - UFR de Médecine et des Techniques Médicales (Nantes Univ - UFR MEDECINE), Centre hospitalier universitaire de Nantes (CHU Nantes), Université Paris Diderot, Sorbonne Paris Cité, Paris, France, Université Paris Diderot - Paris 7 (UPD7), Institut de Recherche Saint-Louis - Hématologie Immunologie Oncologie (Département de recherche de l’UFR de médecine, ex- Institut Universitaire Hématologie-IUH) (IRSL), Université Paris Cité (UPCité), Hopital Saint-Louis [AP-HP] (AP-HP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut ROCHE [Boulogne-Billancourt], Roche S.A.S, Centre Hospitalier Universitaire de Reims (CHU Reims), Hôpital de la Timone [CHU - APHM] (TIMONE), Equipe 3 - Facteurs de persistance des cellules leucémique - (INSERM U837), Institut pour la Recherche sur le Cancer de Lille (U837 INSERM - IRCL), Institut pour la recherche sur le cancer de Lille [Lille] (IRCL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut pour la recherche sur le cancer de Lille [Lille] (IRCL)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), CHU Bordeaux [Bordeaux], Institut Gustave Roussy (IGR), Oncologie dermatologique, Département de médecine oncologique [Gustave Roussy], Institut Gustave Roussy (IGR)-Institut Gustave Roussy (IGR), Hôpital Ambroise Paré [AP-HP], Service de Dermatologie [AP-HP Hôpital Saint-Louis], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Genentech, Inc., and Genentech, Inc. [San Francisco]

Subjects
Cancer Research, Skin Neoplasms, animal structures, integumentary system, Pyridines, [SDV]Life Sciences [q-bio], fungi, Antineoplastic Agents, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV] Life Sciences [q-bio], [SDV.CAN] Life Sciences [q-bio]/Cancer, Oncology, Carcinoma, Basal Cell, Humans, Anilides, Hedgehog Proteins, Cerebellar Neoplasms
Abstract

Purpose: Vismodegib is approved for the treatment of locally advanced basal cell carcinoma (laBCC), but some cases demonstrate intrinsic resistance (IR) to the drug. We sought to assess the frequency of IR to vismodegib in laBCC and its underlying genomic mechanisms. Experimental Design: Response to vismodegib was evaluated in a cohort of 148 laBCC patients. Comprehensive genomic and transcriptomic profiling was performed in a subset of five intrinsically resistant BCC (IR-BCC). Results: We identified that IR-BCC represents 6.1% of laBCC in the studied cohort. Prior treatment with chemotherapy was associated with IR. Genetic events that were previously associated with acquired resistance (AR) in BCC or medulloblastoma were observed in three out of five IR-BCC. However, IR-BCCs were distinct by highly rearranged polyploid genomes. Functional analyses identified hyperactivation of the HIPPO-YAP and WNT pathways at RNA and protein levels in IR-BCC. In vitro assay on the BCC cell line further confirmed that YAP1 overexpression increases the cell proliferation rate. Conclusions: IR to vismodegib is a rare event in laBCC. IR-BCCs frequently harbor resistance mutations in the Hh pathway, but also are characterized by hyperactivation of the HIPPO-YAP and WNT pathways.

Published
2022
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3. Supplementary Figure from Frequency and Genomic Aspects of Intrinsic Resistance to Vismodegib in Locally Advanced Basal Cell Carcinoma

Author

Sergey I. Nikolaev, Nicole Basset-Seguin, Lukas Flatz, Nicolas Dumaz, Frederic J. de Sauvage, Jerome Lambert, Florian Herms, Philippe Saiag, Caroline Robert, Caroline Dutriaux, Nicolas Meyer, Laurent Mortier, Sandrine Monestier, Florent Grange, Max Mendez-Lopez, Andrej Besse, Ariel Savina, Fanny Bouquet, Samia Mourah, Maxime Battistella, Nadem Soufir, Antonio Alberti, Marc Delord, Amir Khammari, Brigitte Dreno, Nicolas Poulalhon, Hayley J. Sharpe, Fatemeh Rajabi, Ismael Padioleau, Meriem Ighilahriz, Oltin T. Pop, and Andrey A. Yurchenko

Abstract

Supplementary Figure from Frequency and Genomic Aspects of Intrinsic Resistance to Vismodegib in Locally Advanced Basal Cell Carcinoma

Published
2023
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4. Data from Frequency and Genomic Aspects of Intrinsic Resistance to Vismodegib in Locally Advanced Basal Cell Carcinoma

Author

Sergey I. Nikolaev, Nicole Basset-Seguin, Lukas Flatz, Nicolas Dumaz, Frederic J. de Sauvage, Jerome Lambert, Florian Herms, Philippe Saiag, Caroline Robert, Caroline Dutriaux, Nicolas Meyer, Laurent Mortier, Sandrine Monestier, Florent Grange, Max Mendez-Lopez, Andrej Besse, Ariel Savina, Fanny Bouquet, Samia Mourah, Maxime Battistella, Nadem Soufir, Antonio Alberti, Marc Delord, Amir Khammari, Brigitte Dreno, Nicolas Poulalhon, Hayley J. Sharpe, Fatemeh Rajabi, Ismael Padioleau, Meriem Ighilahriz, Oltin T. Pop, and Andrey A. Yurchenko

Abstract

Purpose:Vismodegib is approved for the treatment of locally advanced basal cell carcinoma (laBCC), but some cases demonstrate intrinsic resistance (IR) to the drug. We sought to assess the frequency of IR to vismodegib in laBCC and its underlying genomic mechanisms.Experimental Design:Response to vismodegib was evaluated in a cohort of 148 laBCC patients. Comprehensive genomic and transcriptomic profiling was performed in a subset of five intrinsically resistant BCC (IR-BCC).Results:We identified that IR-BCC represents 6.1% of laBCC in the studied cohort. Prior treatment with chemotherapy was associated with IR. Genetic events that were previously associated with acquired resistance (AR) in BCC or medulloblastoma were observed in three out of five IR-BCC. However, IR-BCCs were distinct by highly rearranged polyploid genomes. Functional analyses identified hyperactivation of the HIPPO-YAP and WNT pathways at RNA and protein levels in IR-BCC. In vitro assay on the BCC cell line further confirmed that YAP1 overexpression increases the cell proliferation rate.Conclusions:IR to vismodegib is a rare event in laBCC. IR-BCCs frequently harbor resistance mutations in the Hh pathway, but also are characterized by hyperactivation of the HIPPO-YAP and WNT pathways.

Published
2023
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5. Dermatoscopic and clinical features of congenital or congenital-type nail matrix nevi: A multicenter prospective cohort study by the International Dermoscopy Society

Author

Félix Pham, Amélie Boespflug, Gérard Duru, Alice Phan, Nicolas Poulalhon, Laura Weiler, Masaru Tanaka, Aimilios Lallas, Dai Ogata, Anne Céline Davaine, Philippe Bahadoran, Xavier Balguerie, Grażyna Kamińska-Winciorek, Isabelle Tromme, Osvaldo Correia, Moon-Bum Kim, Ashfaq A. Marghoob, null Linda Martin, Pascale Guitera, Mariame Meziane, Juliette Miquel, Je-Ho Mun, Giuseppe Argenziano, Didier Bessis, Johnny Bourke, Zeljko Mijuskovic, Christine Chiaverini, Cloé Corven-Benoit, Catherine Droitcourt, François Skowron, Myriam Marque, Iris Zalaudek, Cliff Rosendahl, David Moreno-Ramirez, Pierre Vabres, Holger Haenssle, Josep Malvehy, Susana Puig, Caroline Robert, Thomas R. Schopf, Alon Scope, Stéphane Dalle, Luc Thomas, UCL - SSS/IRSS - Institut de recherche santé et société, UCL - (SLuc) Service de dermatologie, Pham, Félix, Boespflug, Amélie, Duru, Gérard, Phan, Alice, Poulalhon, Nicola, Weiler, Laura, Tanaka, Masaru, Lallas, Aimilio, Ogata, Dai, Davaine, Anne Céline, Bahadoran, Philippe, Balguerie, Xavier, Kamińska-Winciorek, Grażyna, Tromme, Isabelle, Correia, Osvaldo, Kim, Moon-Bum, Marghoob, Ashfaq A, Linda Martin, Null, Guitera, Pascale, Meziane, Mariame, Miquel, Juliette, Mun, Je-Ho, Argenziano, Giuseppe, Bessis, Didier, Bourke, Johnny, Mijuskovic, Zeljko, Chiaverini, Christine, Corven-Benoit, Cloé, Droitcourt, Catherine, Skowron, Françoi, Marque, Myriam, Zalaudek, Iri, Rosendahl, Cliff, Moreno-Ramirez, David, Vabres, Pierre, Haenssle, Holger, Malvehy, Josep, Puig, Susana, Robert, Caroline, Schopf, Thomas R, Scope, Alon, Dalle, Stéphane, Thomas, Luc, Pham, F., Boespflug, A., Duru, G., Phan, A., Poulalhon, N., Weiler, L., Tanaka, M., Lallas, A., Ogata, D., Davaine, A. C., Bahadoran, P., Balguerie, X., Kaminska-Winciorek, G., Tromme, I., Correia, O., Kim, M. -B., Marghoob, A. A., Linda, Martin, Guitera, P., Meziane, M., Miquel, J., Mun, J. -H., Argenziano, G., Bessis, D., Bourke, J., Mijuskovic, Z., Chiaverini, C., Corven-Benoit, C., Droitcourt, C., Skowron, F., Marque, M., Zalaudek, I., Rosendahl, C., Moreno-Ramirez, D., Vabres, P., Haenssle, H., Malvehy, J., Puig, S., Robert, C., Schopf, T. R., Scope, A., Dalle, S., and Thomas, L.

Subjects
Adult, Subungual melanoma, Skin Neoplasms, nevus of the nail unit, Dermoscopy, dermatoscopy, Dermatology, congenital nail matrix nevu, Longitudinal melanonychia, Melanonychia striata, Diagnosis, Differential, Nail Diseases, Congenital, children, Dermatoscopy, Humans, Prospective Studies, Child, Melanoma, Nevus, Children, melanonychia striata, Pediatric, congenital, congenital nail matrix nevus, longitudinal melanonychia, pediatric, subungual melanoma, Infant, Newborn, Congenital nail matrix nevus, Nevus of the nail unit, Child, Preschool
Abstract

Background: Congenital nail matrix nevi (NMN) are difficult to diagnose because they feature clinical characteristics suggestive of adult subungual melanoma. Nail matrix biopsy is difficult to perform, especially in children. Objective: To describe the initial clinical and dermatoscopic features of NMN appearing at birth (congenital) or after birth but before the age of 5 years (congenital-type). Methods: We conducted a prospective, international, and consecutive data collection in 102 hospitals or private medical offices across 30 countries from 2009 to 2019. Results: There were 69 congenital and 161 congenital-type NMNs. Congenital and congenital-type NMN predominantly displayed an irregular pattern of longitudinal microlines (n = 146, 64%), reminiscent of subungual melanoma in adults. The distal fibrillar (“brush-like”) pattern, present in 63 patients (27.8%), was more frequently encountered in congenital NMN than in congenital-type NMN (P = .012). Moreover, congenital NMN more frequently displayed a periungual pigmentation (P = .029) and Hutchinson's sign (P = .027) than did congenital-type NMN. Limitations: Lack of systematic biopsy-proven diagnosis and heterogeneity of clinical and dermatoscopic photographs. Conclusion: Congenital and congenital-type NMN showed worrisome clinical and dermatoscopic features similar to those observed in adulthood subungual melanoma. The distal fibrillar (“brush-like”) pattern is a suggestive feature of congenital and congenital-type NMN.

Published
2022

6. Atypical extensive lupus tumidus‐like eruption as an early presentation of VEXAS syndrome

Author

S. Debarbieux, Estelle Bourbon, Olivier Harou, Maël Heiblig, Nicolas Poulalhon, Emmanuel Ribereau-Gayon, Claire Theillac, Brigitte Balme, Pierre Sujobert, and Stéphane Dalle

Subjects
medicine.medical_specialty, Systemic lupus erythematosus, business.industry, MEDLINE, Dermatology, Exanthema, medicine.disease, Lupus Erythematosus, Discoid, Lupus Erythematosus, Cutaneous, medicine, Humans, Presentation (obstetrics), business
Published
2021
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7. Cemiplimab for locally advanced and metastatic cutaneous squamous-cell carcinomas: Real-life experience from the French CAREPI study group

Author

Pierre-Emmanuel Stoebner, Christophe Bedane, A. Jannic, Marc Dumas, Marie Moncourier, Sandrine Mansard, Anne-Bénédicte Duval-Modeste, David Solub, Sophie Darras, Suzanne Devaux, Julia Sanchez, Nicolas Meyer, Laurent Misery, Valentine Heidelberger, Raoul Triller, Ingrid Kupfer-Bessaguet, Nathalie Beneton, Florence Brunet-Possenti, Gaëlle Quéreux, E. Maubec, Sophie Dalac, François Skowron, Safia Abed, Caroline Gaudy-Marqueste, Laurent Mortier, Monica Dinulescu, F. Herms, Lucie Peuvrel, Marouane Boubaya, Candice Hober, Pierre Guillet, Mahtab Samimi, Yves Reguerre, Nicolas Poulalhon, Anne Pham-Ledard, Stéphanie Catala, Eve-Marie Neidhardt, Romain Lesbazeilles, Jean-Philippe Arnault, Brigitte Dréno, Olivier Collard, Philippe Celerier, Julie De Quatrebarbes, Youssef Tazi, Pierre Combe, Caroline Jacobzone, Élodie Archier, F. Aubin, Dominique Spaeth, Clémence Berthin, Nora Kramkimel, Florent Grange, Candice Lesage, Lisa Fredeau, A. Schoeffler, Marc Pracht, Bertille Bonniaud, Laure Cesaire, Maxime Etienne, Olivier Lauche, CHU Lille, Hôpital Avicenne [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), CHU Bordeaux [Bordeaux], Université de Bordeaux (UB), Hopital Saint-Louis [AP-HP] (AP-HP), Hôpital Saint-Louis de La Rochelle (CH La Rochelle), Université de Bourgogne (UB), Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon), Centre Hospitalier Le Mans (CH Le Mans), Hôpital Pontchaillou, Hôpital Henri Mondor, Institut Universitaire du Cancer de Toulouse - Oncopole (IUCT Oncopole - UMR 1037), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Hôpital Charles Nicolle [Rouen], CHU Rouen, Normandie Université (NU)-Normandie Université (NU), Hôpital Côte de Nacre [CHU Caen], CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN)-Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN), Centre Léon Bérard [Lyon], Hôpital Saint-Joseph [Marseille], Centre hospitalier universitaire de Nantes (CHU Nantes), Université de Nantes (UN), Centre d’Investigation Clinique de Nantes (CIC Nantes), Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre hospitalier universitaire de Nantes (CHU Nantes), Clinical and Translational Research in Skin Cancer (CRCINA-ÉQUIPE 2), Centre de Recherche en Cancérologie et Immunologie Nantes-Angers (CRCINA), Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM), Hôpital Cochin [AP-HP], Centre Hospitalier Universitaire de Reims (CHU Reims), Centre Hospitalier de Valence (CH DE VALENCE), Centre hospitalier de Valence, CH Annecy Genevois, CHU de Nîmes, Institut des Biomolécules Max Mousseron [Pôle Chimie Balard] (IBMM), Ecole Nationale Supérieure de Chimie de Montpellier (ENSCM)-Institut de Chimie du CNRS (INC)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Centre Hospitalier Lyon Sud [CHU - HCL] (CHLS), Hospices Civils de Lyon (HCL), CHU Amiens-Picardie, Hopital d'instruction des armées Sainte-Anne [Toulon] (HIA), CH Boulogne sur Mer, Hôpital Robert Ballanger [Aulnay-sous-Bois], Centre Hospitalier de la Côte Basque (CHCB), Centre Hospitalier Universitaire [Grenoble] (CHU), Université de Bretagne Occidentale, CHU Clermont-Ferrand, Centre Hospitalier Intercommunal de Cornouaille (CHIC), Centre Hospitalier Intercommunal de Cornouaille [Quimper] (CHI Cornouaille [Quimper]), AP-HP - Hôpital Bichat - Claude Bernard [Paris], Centre hospitalier universitaire de Poitiers (CHU Poitiers), Centre Hospitalier Georges Renon [Niort] (CH Georges Renon Niort), Clinique Saint Pierre, Perpignan, Centre Hospitalier Régional Universitaire de Tours (CHRU Tours), Infectiologie et Santé Publique (UMR ISP), Université de Tours (UT)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Clinique Sainte Anne [Strasbourg], Centre d'Oncologie de Gentilly, Institut de Cancérologie de la Loire Lucien Neuwirth, Centre Hospitalier Universitaire de Saint-Etienne [CHU Saint-Etienne] (CHU ST-E), Institut hospitalier Franco-Britannique [Levallois-Perret], CH René Dubos, Institut de Cancérologie de l'Ouest [Angers/Nantes] (UNICANCER/ICO), UNICANCER, Pôle Santé Léonard de Vinci, Partenaires INRAE, Centre Hospitalier Universitaire de La Réunion (CHU La Réunion), Centre hospitalier régional Metz-Thionville (CHR Metz-Thionville), CHU Limoges, Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes), Thérapies Laser Assistées par l'Image pour l'Oncologie - U 1189 (ONCO-THAI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), UFR Santé, Médecine et Biologie Humaine (UFR SMBH), Université Sorbonne Paris Nord, Toxicité environnementale, cibles thérapeutiques, signalisation cellulaire (T3S - UMR_S 1124), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), CHU Toulouse [Toulouse]-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre hospitalier universitaire de Toulouse - CHU Toulouse, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA), Centre Hospitalier Universitaire de Montpellier (CHU Montpellier ), Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie du CNRS (INC)-Université de Montpellier (UM)-Ecole Nationale Supérieure de Chimie de Montpellier (ENSCM), Le CHCB, Centre Hospitalier de la Côte Basque, Centre Hospitalier Universitaire de Saint-Etienne (CHU de Saint-Etienne), Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Toulouse [Toulouse], Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPC), Université de Tours-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, and Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP)

Subjects
Cancer Research, medicine.medical_specialty, cutaneous squamous cell carcinoma, Locally advanced, Best Overall Response, [SDV.CAN]Life Sciences [q-bio]/Cancer, Gastroenterology, Article, 030207 dermatology & venereal diseases, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Overall survival, Medicine, Adverse effect, Group performance, RC254-282, Immune status, business.industry, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, Mean age, medicine.disease, chronic dermatosis, Toxic epidermal necrolysis, 3. Good health, immunocompromised, real-life setting, Oncology, 030220 oncology & carcinogenesis, PD-1–blocking antibody, cemiplimab, business, [SDV.MHEP.DERM]Life Sciences [q-bio]/Human health and pathology/Dermatology
Abstract

Although cemiplimab has been approved for locally advanced (la) and metastatic (m) cutaneous squamous-cell carcinomas (CSCCs), its real-life value has not yet been demonstrated. An early-access program enrolled patients with la/mCSCCs to receive cemiplimab. Endpoints were best overall response rate (BOR), progression-free survival (PFS), overall survival (OS), duration of response (DOR) and safety. The 245 patients (mean age 77 years, 73% male, 49% prior systemic treatment, 24% immunocompromised, 27% Eastern Cooperative Oncology Group performance status (PS) ≥ 2) had laCSCCs (35%) or mCSCCs (65%). For the 240 recipients of ≥1 infusion(s), the BOR was 50.4% (complete, 21%, partial, 29%). With median follow-up at 12.6 months, median PFS was 7.9 months, and median OS and DOR were not reached. One-year OS was 73% versus 36%, respectively, for patients with PS &lt, 2 versus ≥ 2. Multivariate analysis retained PS ≥ 2 as being associated during the first 6 months with PFS and OS. Head-and-neck location was associated with longer PFS. Immune status had no impact. Severe treatment-related adverse events occurred in 9% of the patients, including one death from toxic epidermal necrolysis. Cemiplimab real-life safety and efficacy support its use for la/mCSCCs. Patients with PS ≥ 2 benefited less from cemiplimab, but it might represent an option for immunocompromised patients.

Published
2021
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8. Acute renal failure associated with the new BRAF inhibitor vemurafenib: A case series of 8 patients

Author

S. Amet, Gilbert Deray, Nicolas Poulalhon, Morgane Gosselin, Valérie Garrigue, Vincent Launay-Vacher, Thibault Fraisse, Sarah Zimner-Rapuch, and Nicolas Janus

Subjects
Oncology, Cancer Research, medicine.medical_specialty, business.industry, Melanoma, Dacarbazine, medicine.medical_treatment, Renal function, Cancer, medicine.disease, Surgery, Targeted therapy, Nephrotoxicity, Internal medicine, medicine, Vemurafenib, business, medicine.drug, Kidney disease
Abstract

BACKGROUND Vemurafenib is a BRAF inhibitor that has become the cornerstone of metastatic or inoperable melanoma therapy since its approval in 2011 in the United States and 2012 in Europe. This targeted therapy has shown impressive results in terms of increased progression-free and overall survival as compared to dacarbazine. The safety profile did not include any renal manifestations at that time. METHODS This report is the first case series of 8 patients who experienced significant to severe renal insufficiency under vemurafenib treatment. RESULTS This case series shows that vemurafenib may induce potentially severe acute renal failure, including renal sequelae and persistent kidney disease in some cases. CONCLUSIONS Further studies are needed to investigate the effects of vemurafenib on the kidneys. Meanwhile, renal function should be closely monitored in treated patients for early detection of any renal dysfunction occurrence. Cancer 2014;120:2158–2163. © 2014 American Cancer Society.

Published
2014
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9. Stevens–Johnson syndrome and toxic epidermal necrolysis induced by amifostine during head and neck radiotherapy

Author

Alexis Sidoroff, Maja Mockenhaupt, Nicolas Poulalhon, Batya Davidovici, Jean-Paul Fagot, Peggy Sekula, and Laurence Valeyrie-Allanore

Subjects
Adult, Male, medicine.medical_specialty, medicine.medical_treatment, Radiation-Protective Agents, Amifostine, Head and neck radiotherapy, medicine, Adverse Drug Reaction Reporting Systems, Humans, Radiology, Nuclear Medicine and imaging, Prospective Studies, Prospective cohort study, Aged, Chemotherapy, business.industry, Hematology, Middle Aged, Prodrug, medicine.disease, Dermatology, Cytoprotection, Toxic epidermal necrolysis, Europe, Radiation therapy, stomatognathic diseases, Oncology, Head and Neck Neoplasms, Stevens-Johnson Syndrome, Female, business, medicine.drug
Abstract

Amifostine is an organic thiophosphate prodrug used for cytoprotection against toxic effects of radiotherapy and chemotherapy. In a European prospective study of SJS/TEN, six patients were suspected to have SJS/TEN associated with amifostine. Our findings suggest that the risk of life-threatening cutaneous adverse reactions to amifostine could be significantly increased.

Published
2008
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10. Modulation of Collagen and MMP-1 Gene Expression in Fibroblasts by the Immunosuppressive Drug Rapamycin

Author

Dominique Farge, Laurence Michel, Nina Roos, Franck Verrecchia, Nicolas Poulalhon, Cindy Neuzillet, Charlotte Tacheau, and Alain Mauviel

Subjects
MAPK/ERK pathway, 0303 health sciences, Expression vector, Kinase, p38 mitogen-activated protein kinases, Cell Biology, Biology, Biochemistry, 3. Good health, 03 medical and health sciences, Transactivation, 0302 clinical medicine, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Gene expression, Cancer research, medicine, Phosphorylation, Fibroblast, Molecular Biology, 030304 developmental biology
Abstract

We have examined whether rapamycin, an immunosuppressive drug, may exert part of its antifibrotic activity by directly targeting fibroblast extracellular matrix deposition. Incubation of human lung fibroblast (WI-26) cultures with rapamycin led to dose- and time-dependent reduction in the expression of types I and III collagens, both at the protein and mRNA levels. Rapamycin had no effect on collagen promoter activity but accelerated mRNA decay, indicating post-transcriptional control of collagen gene expression. In contrast, rapamycin significantly enhanced the expression of interstitial collagenase (MMP-1) at the protein and mRNA levels and transcriptionally. We determined that rapamycin efficiently activates AP-1-driven transcription by rapidly inducing c-jun/AP-1 phosphorylation with activation of the c-Jun N-terminal kinase (JNK) cascade, resulting in enhanced binding of AP-1·DNA complex formation and AP-1-dependent gene transactivation. Conversely, the JNK inhibitor SP600125 inhibited rapamycin-induced MMP-1 gene transactivation and AP-1/DNA interactions. A c-jun antisense expression vector efficiently prevented rapamycin-induced MMP-1 gene transcription. Pharmacological inhibition of either ERK or p38 MAPK pathways was without effect on rapamycin-induced MMP-1 gene expression. It thus appears that rapamycin may exert direct antifibrotic activities independent from its immunosuppressive action.

Published
2006
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11. Acute renal failure associated with the new BRAF inhibitor vemurafenib: a case series of 8 patients

Author

Vincent, Launay-Vacher, Sarah, Zimner-Rapuch, Nicolas, Poulalhon, Thibault, Fraisse, Valérie, Garrigue, Morgane, Gosselin, Sabine, Amet, Nicolas, Janus, and Gilbert, Deray

Subjects
Adult, Aged, 80 and over, Male, Proto-Oncogene Proteins B-raf, Sulfonamides, Indoles, Skin Neoplasms, Antineoplastic Agents, Acute Kidney Injury, Middle Aged, Kidney, Kidney Function Tests, Severity of Illness Index, Drug Administration Schedule, Treatment Outcome, Vemurafenib, Humans, Female, Treatment Failure, Melanoma, Aged
Abstract

Vemurafenib is a BRAF inhibitor that has become the cornerstone of metastatic or inoperable melanoma therapy since its approval in 2011 in the United States and 2012 in Europe. This targeted therapy has shown impressive results in terms of increased progression-free and overall survival as compared to dacarbazine. The safety profile did not include any renal manifestations at that time.This report is the first case series of 8 patients who experienced significant to severe renal insufficiency under vemurafenib treatment.This case series shows that vemurafenib may induce potentially severe acute renal failure, including renal sequelae and persistent kidney disease in some cases.Further studies are needed to investigate the effects of vemurafenib on the kidneys. Meanwhile, renal function should be closely monitored in treated patients for early detection of any renal dysfunction occurrence. Cancer 2014;120:2158-2163. © 2014 American Cancer Society.

Published
2014

12. Special locations dermoscopy: facial, acral, and nail

Author

Luc, Thomas, Alice, Phan, Pauline, Pralong, Nicolas, Poulalhon, Sébastien, Debarbieux, and Stéphane, Dalle

Subjects
Diagnosis, Differential, Nail Diseases, Skin Neoplasms, Humans, Dermoscopy, Melanoma, Facial Dermatoses
Abstract

Although dermoscopy reflects the anatomy, skin anatomy is different on facial and acral skin as well as in the nail unit. Malignant patterns on acral sites include the parallel ridge pattern and irregular diffuse pigmentation, whose presence should lead to a biopsy. Malignant patterns on the face include features of follicular invasion (signet-ring images, annular granular images, and rhomboidal structures) and atypical vessels. Malignant patterns on the nail unit include the micro-Hutchinson sign and irregular longitudinal lines.

Published
2013

13. In vitro evidence for a direct antifibrotic role of the immunosuppressive drug mycophenolate mofetil

Author

Franck Verrecchia, Dominique Farge, Isabelle Madelaine, Nina Roos, Nicolas Poulalhon, Alain Mauviel, Bases Moleculaires de l'Homeostasie Cutanee : Inflammation, Reparation et Cancer, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de Médecine Interne [Saint-Louis], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Pharmacie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], and Verrecchia, Franck

Subjects
medicine.medical_treatment, MESH: Collagen Type I, 0302 clinical medicine, Fibrosis, Cell Movement, MESH: Cell Movement, Cells, Cultured, 0303 health sciences, MESH: Gene Expression Regulation, 3. Good health, medicine.anatomical_structure, Immunosuppressive drug, MESH: Fibrosis, Molecular Medicine, MESH: Immunosuppressive Agents, Matrix Metalloproteinase 1, Myofibroblast, Type I collagen, Immunosuppressive Agents, medicine.drug, MESH: Cells, Cultured, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, MESH: Actins, Mycophenolic acid, Collagen Type I, 03 medical and health sciences, medicine, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Fibroblast, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, 030304 developmental biology, MESH: Mycophenolic Acid, 030203 arthritis & rheumatology, Pharmacology, MESH: Humans, business.industry, [SDV.MHEP.DERM] Life Sciences [q-bio]/Human health and pathology/Dermatology, Fibroblasts, Mycophenolic Acid, medicine.disease, Actins, Transplantation, MESH: Matrix Metalloproteinase 1, Gene Expression Regulation, MESH: Fibroblasts, Immunology, Cancer research, business, Wound healing, [SDV.MHEP.DERM]Life Sciences [q-bio]/Human health and pathology/Dermatology
Abstract

International audience; The immunosuppressive drug mycophenolate mofetil (MMF) is used to prevent organ rejection after transplantation and has shown some efficacy to prevent the fibrotic complications that occur during autoimmune diseases such as systemic sclerosis or during graft-versus-host disease (GVHD). We tested the hypothesis that MMF may exert direct effects on fibroblast extracellular matrix remodeling. Incubation of human lung fibroblast cultures with MMF led to dose- and time-dependent reduction in the synthesis and expression of type I collagen. Inhibition of COL1A1 and COL1A2 mRNA steady-state levels occurred at the level of transcription via repression of their promoters. In contrast, MMF significantly enhanced the expression and the synthesis of interstitial collagenase (matrix metalloproteinase-1). MMF was also found to diminish the capacity of fibroblast to contract mechanically unloaded collagen lattices and to reduce the synthesis of alpha-smooth muscle actin, a marker of the contractile myofibroblast phenotype. In addition, MMF diminished the fibroblasts motility. In conclusion, we provide novel mechanism by which MMF alters fibroblast functions important for wound healing and implicated in the development of tissue fibrosis, e.g., collagen production, extracellular matrix contraction, and cell migration. Such properties may contribute to the beneficial therapeutic effects of MMF against fibrotic lesions developing in systemic sclerosis or during GVHD.

Published
2007
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14. Modulation of collagen and MMP-1 gene expression in fibroblasts by the immunosuppressive drug rapamycin. A direct role as an antifibrotic agent?

Author

Nicolas, Poulalhon, Dominique, Farge, Nina, Roos, Charlotte, Tacheau, Cindy, Neuzillet, Laurence, Michel, Alain, Mauviel, Franck, Verrecchia, Verrecchia, Franck, Bases Moleculaires de l'Homeostasie Cutanee : Inflammation, Reparation et Cancer, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de Médecine Interne [Saint-Louis], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)

Subjects
MESH: Gene Expression, Transcription, Genetic, RNA Stability, Gene Expression, MESH: Collagen Type I, Collagen Type I, Cell Line, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, Humans, MESH: Lung, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, RNA, Messenger, Lung, MESH: RNA, Messenger, Sirolimus, MESH: Humans, JNK Mitogen-Activated Protein Kinases, MESH: RNA Stability, MESH: JNK Mitogen-Activated Protein Kinases, Fibroblasts, [SDV.MHEP.DERM] Life Sciences [q-bio]/Human health and pathology/Dermatology, MESH: Gene Expression Regulation, MESH: Cell Line, Transcription Factor AP-1, MESH: Matrix Metalloproteinase 1, MESH: Transcription Factor, Gene Expression Regulation, MESH: Fibroblasts, MESH: Sirolimus, MESH: Immunosuppressive Agents, Matrix Metalloproteinase 1, Immunosuppressive Agents, [SDV.MHEP.DERM]Life Sciences [q-bio]/Human health and pathology/Dermatology
Abstract

International audience; We have examined whether rapamycin, an immunosuppressive drug, may exert part of its antifibrotic activity by directly targeting fibroblast extracellular matrix deposition. Incubation of human lung fibroblast (WI-26) cultures with rapamycin led to dose- and time-dependent reduction in the expression of types I and III collagens, both at the protein and mRNA levels. Rapamycin had no effect on collagen promoter activity but accelerated mRNA decay, indicating post-transcriptional control of collagen gene expression. In contrast, rapamycin significantly enhanced the expression of interstitial collagenase (MMP-1) at the protein and mRNA levels and transcriptionally. We determined that rapamycin efficiently activates AP-1-driven transcription by rapidly inducing c-jun/AP-1 phosphorylation with activation of the c-Jun N-terminal kinase (JNK) cascade, resulting in enhanced binding of AP-1.DNA complex formation and AP-1-dependent gene transactivation. Conversely, the JNK inhibitor SP600125 inhibited rapamycin-induced MMP-1 gene transactivation and AP-1/DNA interactions. A c-jun antisense expression vector efficiently prevented rapamycin-induced MMP-1 gene transcription. Pharmacological inhibition of either ERK or p38 MAPK pathways was without effect on rapamycin-induced MMP-1 gene expression. It thus appears that rapamycin may exert direct antifibrotic activities independent from its immunosuppressive action.

Published
2006
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