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51. Baseline Genomic Features in BRAFV600-Mutated Metastatic Melanoma Patients Treated with BRAF Inhibitor + MEK Inhibitor in Routine Care

Author

Louveau, Baptiste, primary, Jouenne, Fanelie, additional, Reger de Moura, Coralie, additional, Sadoux, Aurelie, additional, Baroudjian, Barouyr, additional, Delyon, Julie, additional, Herms, Florian, additional, De Masson, Adele, additional, Da Meda, Laetitia, additional, Battistella, Maxime, additional, Dumaz, Nicolas, additional, Lebbe, Celeste, additional, and Mourah, Samia, additional

Published
2019
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53. A targeted genomic alteration analysis predicts survival of melanoma patients under BRAF inhibitors

Author

Louveau, Baptiste, primary, Delyon, Julie, additional, De Moura, Coralie Reger, additional, Battistella, Maxime, additional, Jouenne, Fanelie, additional, Golmard, Lisa, additional, Sadoux, Aurelie, additional, Podgorniak, Marie-Pierre, additional, Chami, Ichrak, additional, Marco, Oren, additional, Caramel, Julie, additional, Dalle, Stephane, additional, Feugeas, Jean-Paul, additional, Dumaz, Nicolas, additional, Lebbe, Celeste, additional, and Mourah, Samia, additional

Published
2019
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54. Distinct expression patterns of the E3 ligase SIAH-1 and its partner Kid/KIF22 in normal tissues and in the breast tumoral processes

Author

Mourah Samia, Candeias Marco M, Powell Darren J, Podgorniak Marie-Pierre, Veiga Lucía, Fernandez Plinio, Bruzzoni-Giovanelli Heriberto, Calvo Fabien, and Marín Mónica

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract SIAH proteins are the human members of an highly conserved family of E3 ubiquitin ligases. Several data suggest that SIAH proteins may have a role in tumor suppression and apoptosis. Previously, we reported that SIAH-1 induces the degradation of Kid (KIF22), a chromokinesin protein implicated in the normal progression of mitosis and meiosis, by the ubiquitin proteasome pathway. In human breast cancer cells stably transfected with SIAH-1, Kid/KIF22 protein level was markedly reduced whereas, the Kid/KIF22 mRNA level was increased. This interaction has been further elucidated through analyzing SIAH and Kid/KIF22 expression in both paired normal and tumor tissues and cell lines. It was observed that SIAH-1 protein is widely expressed in different normal tissues, and in cells lines but showing some differences in western blotting profiles. Immunofluorescence microscopy shows that the intracellular distribution of SIAH-1 and Kid/KIF22 appears to be modified in human tumor tissues compared to normal controls. When mRNA expression of SIAH-1 and Kid/KIF22 was analyzed by real-time PCR in normal and cancer breast tissues from the same patient, a large variation in the number of mRNA copies was detected between the different samples. In most cases, SIAH-1 mRNA is decreased in tumor tissues compared to their normal counterparts. Interestingly, in all breast tumor tissues analyzed, variations in the Kid/KIF22 mRNA levels mirrored those seen with SIAH-1 mRNAs. This concerted variation of SIAH-1 and Kid/KIF22 messengers suggests the existence of an additional level of control than the previously described protein-protein interaction and protein stability regulation. Our observations also underline the need to re-evaluate the results of gene expression obtained by qRT-PCR and relate it to the protein expression and cellular localization when matched normal and tumoral tissues are analyzed.

Published
2010
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56. Early changes in coagulation but not inflammatory biomarkers under intermittent ART: the randomized ANRS 106 WINDOW trial

Author

Gallien, Sébastien, Charreau, Isabelle, Fonsart, Julien, Mourah, Samia, Kalidi, Issa, Delobel, Pierre, Marchou, Bruno, Aboulker, Jean?Pierre, and Molina, Jean?Michel

Subjects
Antiviral agents -- Patient outcomes, Immunity -- Identification and classification -- Health aspects, AIDS (Disease) -- Research, AIDS research, HIV infection -- Development and progression -- Drug therapy, Health
Abstract

Introduction: In the SMART trial, baseline plasma hsCRP, IL6 and D‐dimer levels were strongly correlated to all‐cause mortality. A case‐control study has shown an increase of IL‐6 and D‐dimer levels after one month of antiretroviral therapy (ART) interruption, which was correlated to viral load. Restarting ART was associated to a decrease in D‐dimer but not IL‐6 or hsCRP levels. We assessed biomarkers levels up to 96 weeks in ART‐experienced adults with plasma HIV RNA levels Methods: Stored plasma for 160 participants (80 IT and 80 CT), matched by age, sex and CDC classification, were analyzed blinded for IL‐6, sCD‐14, hsCRP and D‐dimer levels at baseline, week 8 (IT group only), week 16 and week 96. Lower levels of detection for IL‐6, sCD14, hsCRP and D‐Dimer were 1.5 pg/mL, 250 ng/mL, 0.03 µg/mL and 0.21 µg/mL, respectively. The primary objective was to compare changes in IL‐6, hsCRP, sCD14 and D‐dimer plasma levels from baseline to week 8, 16 and 96 in the IT and CT arms. Biomarkers levels were log10 transformed prior to analysis. Results: At baseline, patients were mostly men (86%), with a median age of 40 years, a CD4+ T‐cell count of 768/mm[sup.3], have received a median of 4.7 years of ART and 85% had HIV RNA Compared to baseline, D‐dimer levels significantly increased 8 weeks after ART interruption in the IT arm (+23% fold change, 95% CI +9% to +39%) but reverted to baseline levels at week 16 and remained unchanged at week 96. There was no significant change from baseline in the other biomarker levels in the IT arm. Similarly, no significant change from baseline in biomarker levels was seen in the CT arm up to 96 weeks. Conclusion: Coagulation and inflammatory biomarkers levels remained stable over 96 weeks in well‐suppressed HIV‐infected patient on ART. Following ART interruption there was a significant increase in D‐dimer but not in inflammatory biomarkers levels. This increase was reversed upon reintroduction of ART. These data suggest that ART interruption increases coagulation rather than inflammatory biomarkers., Table 1: Changes in biomarkers levels in participants from the intermittent (IT) vs continuous (CT) treatment arms through 96 weeks (*p=0.002, Wilcoxon test) IL‐6(pg/mL) sCD14(ng/mL) hsCRP(#x00B5;g/mL) D‐dimer(µg/mL) IT CT IT [...]

Published
2014
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60. VEGF121, is predictor for survival in activated B-cell-like diffuse large B-cell lymphoma and is related to an immune response gene signature conserved in cancers

Author

Broséus, Julien, primary, Mourah, Samia, additional, Ramstein, Gérard, additional, Bernard, Sophie, additional, Mounier, Nicolas, additional, Cuccuini, Wendy, additional, Gaulard, Philippe, additional, Gisselbrecht, Christian, additional, Brière, Josette, additional, Houlgatte, Rémi, additional, and Thieblemont, Catherine, additional

Published
2017
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61. Intermittent VersusContinuous Dosing of MAPK Inhibitors in the Treatment of BRAF-Mutated Melanoma

Author

Reger de Moura, Coralie, Vercellino, Laetitia, Jouenne, Fanélie, Baroudjian, Barouyr, Sadoux, Aurélie, Louveau, Baptiste, Delyon, Julie, Serror, Kevin, Goldwirt, Lauriane, Merlet, Pascal, Bouquet, Fanny, Battistella, Maxime, Lebbé, Céleste, and Mourah, Samia

Abstract

The development of BRAF and MEK inhibitors (BRAFi/MEKi) has led to major advances in melanoma treatment. However, the emergence of resistance mechanisms limits the benefit duration and a complete response occurs in less than 20% of patients receiving BRAFi ± MEKi. In this study, we evaluated the impact of an intermittent versus continuous dosing schedule of BRAF/MEK inhibition in a melanoma model mildly sensitive to a BRAF inhibitor. The combination of a BRAFi with three different MEKi was studied with a continuous or intermittent dosing schedule in vivo,in a xenografted melanoma model and ex vivousing histoculture drug response assays (HDRAs) of patient-derived xenografts (PDX). To further understand the underlying molecular mechanisms of therapeutic efficacy, a biomarker pharmacodynamic readout was evaluated.

Published
2020
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62. A Novel Case of Gorlin Syndrome Mosaicism Involving an SMO Gene Mutation: Clinical, Histological and Molecular Analysis of Basaloid Tumours.

Author

IGHILAHRIZ, Meriem, NIKOLAEV, Sergey, YURCHENKO, Andrey A., BATTISTELLA, Maxime, MOURAH, Samia, JOUENNE, Fanelie, BOURRAT, Emmanuelle, and BASSET-SEGUIN, Nicole

Subjects
BASAL cell nevus syndrome, GENETIC mutation, MOSAICISM, BASAL cell carcinoma, SKELETAL abnormalities, SOMATIC mutation
Abstract

Gorlin syndrome comprises multiple basal cell carcinomas (BCCs), basal cell naevi (BCNs), odontogenic keratocysts, skeletal abnormalities and other features (1). Identification of the PTCH1 gene as the candidate gene for Gorlin syndrome demonstrated that activation of the Hedgehog (Hh) pathway is the key driver in the physiology and pathology of BCC formation (2). Gorlin syndrome has been linked to germline mutations of various members of the Hh pathway, including mainly PTCH1 and also PTCH2 and SUFU; however, to date, SMO germline mutations have not been described. Recently, a case of Gorlin syndrome type 1 mosaicism presented a somatic mutation of SMO L412F (3). This mutation has been described as oncogenic, conferring constitutive activation of the Hh pathway (4). This paper describes a second case of Gorlin syndrome mosaicism with the same SMO L412F mutation observed in affected skin. A detailed molecular assessment of multiple BCNs and BCCs was performed to analyse the oncogenic steps of BCC formation in this patient. [ABSTRACT FROM AUTHOR]

Published
2021
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63. ZEB 1‐mediated melanoma cell plasticity enhances resistance to MAPK inhibitors

Author

Richard, Geoffrey, primary, Dalle, Stéphane, additional, Monet, Marie‐Ambre, additional, Ligier, Maud, additional, Boespflug, Amélie, additional, Pommier, Roxane M, additional, de la Fouchardière, Arnaud, additional, Perier‐Muzet, Marie, additional, Depaepe, Lauriane, additional, Barnault, Romain, additional, Tondeur, Garance, additional, Ansieau, Stéphane, additional, Thomas, Emilie, additional, Bertolotto, Corine, additional, Ballotti, Robert, additional, Mourah, Samia, additional, Battistella, Maxime, additional, Lebbé, Céleste, additional, Thomas, Luc, additional, Puisieux, Alain, additional, and Caramel, Julie, additional

Published
2016
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64. Correction: Validation of a preclinical model for assessment of drug efficacy in melanoma

Author

Delyon, Julie, primary, Varna, Mariana, additional, Feugeas, Jean-Paul, additional, Sadoux, Aurélie, additional, Yahiaoui, Saliha, additional, Podgorniak, Marie-Pierre, additional, Leclert, Geoffroy, additional, Dorval, Sarra Mazouz, additional, Dumaz, Nicolas, additional, Janin, Anne, additional, Mourah, Samia, additional, and Lebbé, Céleste, additional

Published
2016
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65. RecurrentNRASmutations in pulmonary Langerhans cell histiocytosis

Author

Mourah, Samia, primary, How-Kit, Alexandre, additional, Meignin, Véronique, additional, Gossot, Dominique, additional, Lorillon, Gwenaël, additional, Bugnet, Emmanuelle, additional, Mauger, Florence, additional, Lebbe, Celeste, additional, Chevret, Sylvie, additional, Tost, Jörg, additional, and Tazi, Abdellatif, additional

Published
2016
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66. Mechanisms Underpinning Increased Plasma Creatinine Levels in Patients Receiving Vemurafenib for Advanced Melanoma

Author

Hurabielle, Charlotte, primary, Pillebout, Evangéline, additional, Stehlé, Thomas, additional, Pagès, Cécile, additional, Roux, Jennifer, additional, Schneider, Pierre, additional, Chevret, Sylvie, additional, Chaffaut, Cendrine, additional, Boutten, Anne, additional, Mourah, Samia, additional, Basset-Seguin, Nicole, additional, Vidal-Petiot, Emmanuelle, additional, Lebbé, Céleste, additional, and Flamant, Martin, additional

Published
2016
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67. Validation of a preclinical model for assessment of drug efficacy in melanoma

Author

Delyon, Julie, primary, Varna, Mariana, additional, Feugeas, Jean-Paul, additional, Sadoux, Aurélie, additional, Yahiaoui, Saliha, additional, Podgorniak, Marie-Pierre, additional, Leclert, Geoffroy, additional, Dorval, Sarra Mazouz, additional, Dumaz, Nicolas, additional, Janin, Anne, additional, Mourah, Samia, additional, and Lebbé, Céleste, additional

Published
2016
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68. EMMPRIN/CD147 is a novel coreceptor of VEGFR-2 mediating its activation by VEGF

Author

Barcelona Supercomputing Center, Khayati, Farah, Pérez-Cano, Laura, Maouche, Kamel, Sadoux, Aurélie, Boutalbi, Zineb, Podgorniak, Marie-Pierre, Maskos, Uwe, Setterblad, Niclas, Janin, Anne, Calvo, Fabien, Lebbé, Céleste, Menashi, Suzanne, Fernández-Recio, Juan, Mourah, Samia, Barcelona Supercomputing Center, Khayati, Farah, Pérez-Cano, Laura, Maouche, Kamel, Sadoux, Aurélie, Boutalbi, Zineb, Podgorniak, Marie-Pierre, Maskos, Uwe, Setterblad, Niclas, Janin, Anne, Calvo, Fabien, Lebbé, Céleste, Menashi, Suzanne, Fernández-Recio, Juan, and Mourah, Samia

Abstract

EMMPRIN/CD147 is mainly known for its protease inducing function but a role in promoting tumor angiogenesis has also been demonstrated. This study provides evidence that EMMPRIN is a new coreceptor for the VEGFR-2 tyrosine kinase receptor in both endothelial and tumor cells, as it directly interacts with it and regulates its activation by its VEGF ligand, signalling and functional consequences both in vitro and in vivo. Computational docking analyses and mutagenesis studies identified a molecular binding site in the extracellular domain of EMMPRIN located close to the cell membrane and containing the amino acids 195/199. EMMPRIN is overexpressed in cancer and hence is able to further potentiate VEGFR-2 activation, suggesting that a combinatory therapy of an antiangiogenic drug together with an inhibitor of EMMPRIN/VEGFR-2 interaction may have a greater impact on inhibiting angiogenesis and malignancy., This work was supported by Institut National de la Santé et de la Recherche Médicale (INSERM), La Ligue Nationale contre le Cancer (LNCC), La Société Française de Dermatologie and Université Paris Diderot. F.K was supported by a PhD fellowship from Cancéropôle-Ile de France and from Fondation ARC pour la Recherche sur le Cancer. L.P.C was supported by a FPU fellowship from Spanish Ministry of Science. This work was supported by grant BIO2010–22324 from Plan NacionalI+D+iMICINN. We thank the core facility of the Institut Universitaire d’Hématologie for confocal microscopy analyses. The core facility is supported by grants from the Association Saint-Louis, Conseil Regional d’Ile-de-France, and the Ministère de la Recherche., Peer Reviewed, Postprint (published version)

Published
2015

70. PARKINInactivation Links Parkinson’s Disease to Melanoma

Author

Hu, Hui-Han, primary, Kannengiesser, Caroline, additional, Lesage, Suzanne, additional, André, Jocelyne, additional, Mourah, Samia, additional, Michel, Laurence, additional, Descamps, Vincent, additional, Basset-Seguin, Nicole, additional, Bagot, Martine, additional, Bensussan, Armand, additional, Lebbé, Céleste, additional, Deschamps, Lydia, additional, Saiag, Philippe, additional, Leccia, Marie-Thérèse, additional, Bressac-de-Paillerets, Brigitte, additional, Tsalamlal, Amel, additional, Kumar, Rajiv, additional, Klebe, Stephan, additional, Grandchamp, Bernard, additional, Andrieu-Abadie, Nathalie, additional, Thomas, Luc, additional, Brice, Alexis, additional, Dumaz, Nicolas, additional, and Soufir, Nadem, additional

Published
2015
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71. EMMPRIN/CD147 is a novel coreceptor of VEGFR-2 mediating its activation by VEGF

Author

Khayati, Farah, primary, Pérez-Cano, Laura, additional, Maouche, Kamel, additional, Sadoux, Aurélie, additional, Boutalbi, Zineb, additional, Podgorniak, Marie-Pierre, additional, Maskos, Uwe, additional, Setterblad, Niclas, additional, Janin, Anne, additional, Calvo, Fabien, additional, Lebbé, Céleste, additional, Menashi, Suzanne, additional, Fernandez-Recio, Juan, additional, and Mourah, Samia, additional

Published
2015
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72. Detection of BRAF V600 Mutations in Melanoma: Evaluation of Concordance between the Cobas® 4800 BRAF V600 Mutation Test and the Methods Used in French National Cancer Institute (INCa) Platforms in a Real-Life Setting

Author

Mourah, Samia, primary, Denis, Marc G., additional, Narducci, Fabienne Escande, additional, Solassol, Jérôme, additional, Merlin, Jean-Louis, additional, Sabourin, Jean-Christophe, additional, Scoazec, Jean-Yves, additional, Ouafik, L’Houcine, additional, Emile, Jean-François, additional, Heller, Remy, additional, Souvignet, Claude, additional, Bergougnoux, Loïc, additional, and Merlio, Jean-Philippe, additional

Published
2015
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73. VEGF and VEGFR-1 are coexpressed by epithelial and stromal cells of renal cell carcinoma.: VEGF and its receptors in renal cell carcinoma

Author

Rivet, Jacqueline, Mourah, Samia, Murata, Hideyuki, Mounier, Nicolas, Pisonero, Helena, Mongiat-Artus, Pierre, Teillac, Pierre, Calvo, Fabien, Janin, Anne, Dosquet, Christine, Ratajczak, Philippe, Gvh et Gvl : Physiopathologie Chez l'Homme et Chez l'Animal, Incidence et Role Therapeutique, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de pharmacologie expérimentale et clinique : cibles moléculaires en cancérologie ((U 716)), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Service d'Urologie [CHU 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), Hemostase, Endothelium, Angiogenese (UMR_S_553), Institut Universitaire d'Hématologie (IUH), Université Paris Diderot - Paris 7 (UPD7), and University Paris 7, Inserm, GIP/HMR, PHRC

Subjects
[SDV.CAN] Life Sciences [q-bio]/Cancer, MESH: laser microdissection, renal cell carcinoma, VEGF, VEGFR-1, VEGFR-2, [SDV.CAN]Life Sciences [q-bio]/Cancer
Abstract

International audience; BACKGROUND.: Tumor angiogenesis is a dynamic process that plays a major role in cancer progression. Vascular endothelial growth factor (VEGF) and its receptors play a pivotal role in angiogenesis. The expression of VEGF and its receptors VEGFR-1 and VEGFR-2 in renal cell carcinoma (RCC) was investigated in the perspective of anti-VEGF treatments. METHODS.: Total VEGF protein levels were quantified by enzyme-linked immunosorbent assay (ELISA) in tumor tissue samples from surgical specimens of 65 patients with clear cell RCC. At the cellular level the VEGF isoforms VEGFR-1 and VEGFR-2 mRNA were quantified by real-time quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) in laser-microdissected tumoral epithelial as stromal cells and in corresponding normal tissue compartments. Colocalization of VEGF and VEGFR-1 proteins was studied by triple immunofluorescent labeling. RESULTS.: Protein VEGF in cytosolic extracts was significantly higher in tumoral than in nontumoral tissue (P < .0001). Event-free survival was significantly longer for patients with cytosolic VEGF lower than the cutoff (75th percentile of VEGF protein levels, P = .02). In laser-microdissected epithelial cells, VEGF(121) and VEGFR-1 mRNA expressions were higher in RCC than in corresponding nontumoral kidney (P = .007 and P = .002, respectively); they were also higher in stromal cells of RCC compared with nontumoral kidney (P = .02 and P = .003, respectively). There was no differential VEGFR-2 expression in epithelial or in stromal cells of tumoral or nontumoral kidney. By immunofluorescent labeling VEGF and VEGFR-1 colocalized on RCC tumor epithelial and stromal cells. CONCLUSIONS.: Combined laser microdissection and quantitative RT-PCR, as triple immunofluorescent labeling, underlined the preferential expression of the most soluble VEGF isoform, VEGF(121), and its receptor VEGFR-1, but not VEGFR-2, in epithelial and stromal cells of RCC. Cancer 2008. (c) 2007 American Cancer Society.

Published
2008
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74. Clinical Spectrum, Quality of Life, BRAF Mutation Status and Treatment of Skin Involvement in Adult Langerhans Cell Histiocytosis.

Author

CRICKX, Etienne, BOUAZIZ, Jean-David, LORILLON, Gwenaël, DE MENTHON, Mathilde, CORDOLIANI, Florence, BUGNET, Emmanuelle, BAGOT, Martine, RYBOJAD, Michel, MOURAH, Samia, and TAZI, Abdellatif

Subjects
QUALITY of life, BRAF genes, GENETIC mutation, SKIN disease treatment, LANGERHANS-cell histiocytosis, THERAPEUTICS
Abstract

Langerhans cell histiocytosis is a rare histiocytic disorder for which skin involvement and management are poorly described in adults. The aim of this retrospective monocentric study in a national reference centre is to describe the clinical characteristics, quality of life, BRAF mutation status and outcomes of skin involvement in adult patients with Langerhans cell histiocytosis. Twenty-five patients (14 females, mean age 47 years) were included, with a median follow-up of 33 months (range 4-420 months). Patients experienced poor dermatological quality of life despite low body surface involvement. BRAFV600 mutations were detected in 8 of the 18 patients analysed (45%). Eight patients had an associated malignancy. Several treatment options were used and consisted of surgery, topical steroids and carmustine, thalidomide, methotrexate, vinblastine and steroids and cladribine. This study highlights the need to evaluate quality of life and to screen for associated malignancy in adult patients with Langerhans cell histiocytosis. [ABSTRACT FROM AUTHOR]

Published
2017
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75. A novel tumor suppressor function of Kindlin-3 in solid cancer

Author

Djaafri, Ibtissem, primary, Khayati, Farah, additional, Menashi, Suzanne, additional, Tost, Jorg, additional, Podgorniak, Marie-Pierre, additional, Sadoux, Aurelie, additional, Daunay, Antoine, additional, Teixeira, Luis, additional, Soulier, Jean, additional, Idbaih, Ahmed, additional, Setterblad, Niclas, additional, Fauvel, Françoise, additional, Calvo, Fabien, additional, Janin, Anne, additional, Lebbé, Celeste, additional, and Mourah, Samia, additional

Published
2014
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77. PARKIN Inactivation Links Parkinson's Disease to Melanoma.

Author

Hui-Han Hu, Kannengiesser, Caroline, Lesage, Suzanne, André, Jocelyne, Mourah, Samia, Michel, Laurence, Descamps, Vincent, Basset-Seguin, Nicole, Bagot, Martine, Bensussan, Armand, Lebbé, Céleste, Deschamps, Lydia, Saiag, Philippe, Leccia, Marie-Thérèse, Bressac-de-Paillerets, Brigitte, Tsalamlal, Amel, Kumar, Rajiv, Klebe, Stephan, Grandchamp, Bernard, and Andrieu-Abadie, Nathalie

Subjects
PROTEIN metabolism, DNA analysis, ENZYME metabolism, CELL lines, CELL physiology, ENZYMES, EPITHELIAL cells, GENES, GENETICS, MELANOMA, GENETIC mutation, PARKINSON'S disease, PROTEINS, SKIN tumors, WESTERN immunoblotting, RELATIVE medical risk, CASE-control method, SEQUENCE analysis, ODDS ratio, GENOTYPES
Abstract

Background: Melanoma incidence is higher in patients affected by Parkinson's disease (PD) and vice versa, but the genetic link shared by both diseases is unknown. As PARK2 is both a tumor suppressor gene and frequently mutated in young onset PD, we evaluated the role of PARK2 in melanoma predisposition and progression.Methods: An in-depth PARK2 gene dosage analysis and sequencing was performed on 512 French case patients and 562 healthy control patients, as well as sporadic tumors and melanoma cell lines. The frequency of genetic alterations was compared between case patients and control patients using two-sided Fisher's exact tests and odds ratio (OR) calculations. We used western blotting to determine PARKIN expression in melanocytes and melanoma cell lines and transfection followed by clonogenic assays to evaluate the effect of PARKIN expression on cellular proliferation. All statistical tests were two-sided.Results: Germline PARK2 mutations (including copy number variations, splicing, and putative deleterious missense mutations) were present in 25 case patients but only four control patients (OR = 3.95, 95% confidence interval = 1.34 to 15.75). Copy number variations (CNVs) and loss of heterozygosity were present in 60% and 74%, respectively, of primary tumors. PARKIN protein was expressed in melanocytes but not in most melanoma cell lines, and its expression decreased following melanocyte transformation by oncogenic NRAS. Re-expression of PARKIN in melanoma cell lines resulted in a drastic reduction of cell proliferation and inhibition of PARKIN in melanocytes stimulated their proliferation.Conclusion: Our results show an important role for PARK2 as a tumor suppressor both in melanoma predisposition and progression, which could explain the epidemiological association of these diseases. [ABSTRACT FROM AUTHOR]

Published
2016
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80. Invading Basement Membrane Matrix Is Sufficient for MDA-MB-231 Breast Cancer Cells to Develop a Stable In Vivo Metastatic Phenotype

Author

Abdelkarim, Mohamed, primary, Vintonenko, Nadejda, additional, Starzec, Anna, additional, Robles, Aniela, additional, Aubert, Julie, additional, Martin, Marie-Laure, additional, Mourah, Samia, additional, Podgorniak, Marie-Pierre, additional, Rodrigues-Ferreira, Sylvie, additional, Nahmias, Clara, additional, Couraud, Pierre-Olivier, additional, Doliger, Christelle, additional, Sainte-Catherine, Odile, additional, Peyri, Nicole, additional, Chen, Lei, additional, Mariau, Jérémie, additional, Etienne, Monique, additional, Perret, Gerard-Yves, additional, Crepin, Michel, additional, Poyet, Jean-Luc, additional, Khatib, Abdel-Majid, additional, and Di Benedetto, Mélanie, additional

Published
2011
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83. Soluble Isoforms of Vascular Endothelial Growth Factor Are Predictors of Response to Sunitinib in Metastatic Renal Cell Carcinomas

Author

Paule, Bernard, primary, Bastien, Laurence, additional, Deslandes, Emmanuelle, additional, Cussenot, Olivier, additional, Podgorniak, Marie-Pierre, additional, Allory, Yves, additional, Naïmi, Benyoussef, additional, Porcher, Raphael, additional, de La Taille, Alexandre, additional, Menashi, Suzanne, additional, Calvo, Fabien, additional, and Mourah, Samia, additional

Published
2010
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85. Abstract 2341: The Subtilisin-like proprotein convertases blockade inhibits the invasiveness of human primary melanoma with altered P53, CDKN2A and N-Ras genes

Author

Lalou, Claude, primary, Scamuffa, Nathalie, additional, Podgorniak, Marie-Pierre, additional, Plassa, Francois, additional, Mourah, Samia, additional, Soufir, Nadem, additional, Dumaz, Nicolas, additional, Calvo, Fabien, additional, Basset-Seguin, Nicole, additional, and KHATIB, Abdel-Majid, additional

Published
2010
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87. Extracellular Matrix Metalloproteinase Inducer Up-regulates the Urokinase-Type Plasminogen Activator System Promoting Tumor Cell Invasion

Author

Quemener, Cathy, primary, Gabison, Eric E., additional, Naïmi, Benyoussef, additional, Lescaille, Géraldine, additional, Bougatef, Faten, additional, Podgorniak, Marie Pierre, additional, Labarchède, Géraldine, additional, Lebbé, Celeste, additional, Calvo, Fabien, additional, Menashi, Suzanne, additional, and Mourah, Samia, additional

Published
2007
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88. Epstein-Barr Virus (EBV) Genome and Expression in Breast Cancer Tissue: Effect of EBV Infection of Breast Cancer Cells on Resistance to Paclitaxel (Taxol)

Author

Arbach, Hratch, primary, Viglasky, Viktor, additional, Lefeu, Florence, additional, Guinebretière, Jean-Marc, additional, Ramirez, Vanessa, additional, Bride, Nadège, additional, Boualaga, Nadia, additional, Bauchet, Thomas, additional, Peyrat, Jean-Philippe, additional, Mathieu, Marie-Christine, additional, Mourah, Samia, additional, Podgorniak, Marie-Pierre, additional, Seignerin, Jean-Marie, additional, Takada, Kenzo, additional, and Joab, Irène, additional

Published
2006
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90. Distinct expression patterns of the E3 ligaseSIAH-1 and its partner Kid/KIF22 in normaltissues and in the breast tumoral processes.

Author

Bruzzoni-Giovanelli, Heriberto, Fernandez, Plinio, Veiga, Lucía, Podgorniak, Marie-Pierre, Powell, Darren J., Candeias, Marco M., Mourah, Samia, Calvo, Fabien, and Marín, Mónica

Subjects
BREAST cancer, UBIQUITIN, LIGASES, APOPTOSIS, GENE expression, MITOSIS, MEIOSIS, CELL lines, IMMUNOFLUORESCENCE
Abstract

SIAH proteins are the human members of an highly conserved family of E3 ubiquitin ligases. Several data suggest that SIAH proteins may have a role in tumor suppression and apoptosis. Previously, we reported that SIAH-1 induces the degradation of Kid (KIF22), a chromokinesin protein implicated in the normal progression of mitosis and meiosis, by the ubiquitin proteasome pathway. In human breast cancer cells stably transfected with SIAH-1, Kid/KIF22 protein level was markedly reduced whereas, the Kid/KIF22 mRNA level was increased. This interaction has been further elucidated through analyzing SIAH and Kid/KIF22 expression in both paired normal and tumor tissues and cell lines. It was observed that SIAH-1 protein is widely expressed in different normal tissues, and in cells lines but showing some differences in western blotting profiles. Immunofluorescence microscopy shows that the intracellular distribution of SIAH-1 and Kid/KIF22 appears to be modified in human tumor tissues compared to normal controls. When mRNA expression of SIAH-1 and Kid/KIF22 was analyzed by real-time PCR in normal and cancer breast tissues from the same patient, a large variation in the number of mRNA copies was detected between the different samples. In most cases, SIAH-1 mRNA is decreased in tumor tissues compared to their normal counterparts. Interestingly, in all breast tumor tissues analyzed, variations in the Kid/KIF22 mRNA levels mirrored those seen with SIAH-1 mRNAs. This concerted variation of SIAH-1 and Kid/KIF22 messengers suggests the existence of an additional level of control than the previously described protein-protein interaction and protein stability regulation. Our observations also underline the need to re-evaluate the results of gene expression obtained by qRT-PCR and relate it to the protein expression and cellular localization when matched normal and tumoral tissues are analyzed. [ABSTRACT FROM AUTHOR]

Published
2010
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91. Methylation of specific CpG sites in the P2 promoter of parathyroid hormone-related proteindetermines the invasive potential of breast cancer cell lines

Author

Tost, Jörg, Hamzaoui, Hinda, Busato, Florence, Neyret, Aymeric, Mourah, Samia, Dupont, Jean-Michel, and Bouizar, Zhor

Abstract

Parathyroid hormone-related protein(PTHrP) is upregulated in primary breast cancers and a major candidate for osteoclastic bone resorption present at sites of breast cancer to bone metastases. Using a human model of mammary epithelial cell lines differing in tumorigenicity and PTHrPexpression, we investigated the role of epigenetic modifications for PTHrPexpression. Quantitative analysis of the DNA methylation patterns at a total of 104 CpGs in the promoter region of PTHrP by pyrosequencing showed the absence of methylation in all analyzed cell lines in the large CpG island upstream of exon 1C. In the second intron of promoter 2 (P2) a region was identified containing 4 CpG nucleotides for which differential methylation correlated with the PTHrP expression level. The functional importance of this control mechanism was confirmed by the ability of the demethylating agent 5'-azacytidine to induce PTHrPmRNA and iPTHrP protein expression in previously non-expressing cell lines and increase their production by metastatic NS2T2A1 cells. In particular, transcription from P2 was activated non-tumoral S1T3 cells upon treatment with 5'-azacytidine. Our findings support the hypothesis that the methylation status of specific CpG dinucleotides is the dominant mechanism involved in silencing of PTHrPexpression rather than the overall methylation of the CpG island. Methylation of the PTHrPP2 is a potential marker of breast cancer progression and might be used to evaluate the metastatic potential of breast tumors.

Published
2011
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93. Macrophage-derived CXCL9 and CXCL11, T-cell skin homing and disease control in mogamulizumab-treated CTCL patients

Author

Masson, Adèle de, Darbord, Delphine, Dobos, Gabor, Boisson, Marie, Roelens, Marie, Ram-Wolff, Caroline, Cassius, Charles, Le Buanec, Hélène, de la Grange, Pierre, Jouenne, Fanélie, Louveau, Baptiste, Sadoux, Aurélie, Bouaziz, Jean-David, Marie-Cardine, Anne, Bagot, Martine, Moins-Teisserenc, Hélène, Mourah, Samia, and Battistella, Maxime

Abstract

Cutaneous T-celllymphomas (CTCL) are rare malignanciesinvolvingprimarily the skin. Responses to treatment are usually short-lived in advanced CTCL. The determinants of long-term CTCL control are unclear. Mogamulizumab, an anti-human CCR4 antibodythatacts by antibody-dependentcellcytotoxicityagainst CCR4+ CTCL tumorcells and peripheral memory blood regulatory T cells, has been associatedwith long-lasting remissions and immune adverse events. Here, wereported skin rashes in 32% of 44 CTCL patients treatedwithmogamulizumab, associatedwithsignificantlyhigheroverallsurvival (hazard ratio, 0.16 (0.04-0.73, p=0.01)). Rash occurred in Sézary patients and wasassociatedwith longer time to progression. These rashes werecharacterized by a CD163+ granulomatous and/or CD8+ lichenoid skin infiltrate. High-throughputsequencinganalysis of TCRβ genes in skin, and blood flow cytometry, confirmed the depletion of CTCL tumorcells, and the recruitment of new reactive T-cell clones in skin at the time of skin rash. CXCL9 and CXCL11, two macrophage-derivedchemokinesthatrecruit CXCR3+ T-cells to skin, wereoverexpressed in skin rashes. A higherfrequency of TIGIT+ and PD1+ exhaustedreactive blood T-cellwasobserved at baseline in patients with rash, and thisfrequencydecreaseduponmogamulizumabtreatment. These data are consistent withmogamulizumab-induced long-term immune CTCL control by activation of the macrophagic and T-cellresponses in patients with rash.

Published
2021
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94. Poster Sessions.

Subjects
HIV-positive persons, HIV-positive women
Abstract

The article presents abstracts on HIV drug therapy including socio-economic factors among people diagnosed with HIV in Great Britain, care of HIV-infected patients in Belgium and HIV-infected women.

Published
2014

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