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5 results on '"Favrot, Marie-Christine"'

1. An apoptosis methylation prognostic signature for early lung cancer in the IFCT-0002 trial

Author

De Fraipont, Florence, Levallet, Guénaëlle, Creveuil, Christian, Bergot, Emmanuel, Beau-Faller, Michèle, Mounawar, Mounia, Richard, Nicolas, Antoine, Martine, Rouquette, Isabelle, Favrot, Marie-Christine, Debieuvre, Didier, Braun, Denis, Westeel, Virginie, Quoix, Elisabeth, Brambilla, Elisabeth, Hainaut, Pierre, Moro-Sibilot, Denis, Morin, Franck, Milleron, Bernard, Zalcman, Gérard, Renseigné, Non, INSERM U823, équipe 5 (cibles diagnostiques ou thérapeutiques et vectorisation de drogues dans le cancer du poumon), Institut d'oncologie/développement Albert Bonniot de Grenoble (INSERM U823), Université Joseph Fourier - Grenoble 1 (UJF)-CHU Grenoble-EFS-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Joseph Fourier - Grenoble 1 (UJF)-CHU Grenoble-EFS-Institut National de la Santé et de la Recherche Médicale (INSERM)-Biochimie des Cancers et Biothérapies, CHU Grenoble-Hôpital Michallon-Hôpital Michallon, Service de pneumologie [CHU Caen], Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU)-CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN)-Tumorothèque de Caen Basse-Normandie (TCBN), Laboratoire de Biochimie et de Biologie Moléculaire, CHU Strasbourg-Hôpital de Hautepierre [Strasbourg], Unit of Environment Cancer Epidemiology, IARC, Service de Génétique [CHU Caen], CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN)-Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN)-Université de Caen Normandie (UNICAEN), Normandie Université (NU), Interactions cellulaires tumorales et leur environnement et réponse aux agents anti-cancéreux, Université Pierre et Marie Curie - Paris 6 (UPMC), Intergroupe Francophone de Cancérologie Thoracique [Paris] (IFCT), Intergroupe Francophone de Cancérologie thoracique, Service d'anatomie pathologique [CHU Tenon], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Centre d'innovation en biologie (CIB), Université Joseph Fourier - Grenoble 1 (UJF)-CHU Grenoble, Service de Pneumologie, CHI de la Haute-Saône, Carcinogénèse épithéliale : facteurs prédictifs et pronostiques - UFC (EA 3181) (CEF2P / CARCINO), Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon), Service de pneumologie, CHU Strasbourg-Hopital Civil, INSERM U823, équipe 2 (Bases Moléculaires de la Progression des Cancers du Poumon), Université Joseph Fourier - Grenoble 1 (UJF)-CHU Grenoble-EFS-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Joseph Fourier - Grenoble 1 (UJF)-CHU Grenoble-EFS-Institut National de la Santé et de la Recherche Médicale (INSERM)-Département d'anatomie et cythologie pathologique, CHU Grenoble-Hôpital Michallon-Hôpital Michallon-Intergroupe Francophone de Cancérologie Thoracique [Paris] (IFCT), Intergroupe Francophone de Cancérologie thoracique-Intergroupe Francophone de Cancérologie thoracique, International Agency for Cancer Research (IACR), Université Joseph Fourier - Grenoble 1 (UJF)-CHU Grenoble-EFS-Institut National de la Santé et de la Recherche Médicale (INSERM), Pôle Médecine Aigüe Communautaire Pneumologie, CHU Grenoble, Amplitude Systèmes, CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut d'oncologie/développement Albert Bonniot de Grenoble ( INSERM U823 ), Université Joseph Fourier - Grenoble 1 ( UJF ) -CHU Grenoble-EFS-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université Joseph Fourier - Grenoble 1 ( UJF ) -CHU Grenoble-EFS-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Biochimie des Cancers et Biothérapies, Service de pneumologie [Caen], Université de Caen Normandie ( UNICAEN ), Normandie Université ( NU ) -Normandie Université ( NU ) -CHU Caen, Service de génétique, CHU Caen-Hôpital Clémenceau, Université Pierre et Marie Curie - Paris 6 ( UPMC ), Intergroupe Francophone de Cancérologie Thoracique [Paris] ( IFCT ), Assistance publique - Hôpitaux de Paris (AP-HP)-CHU Tenon [APHP], Centre d'innovation en biologie ( CIB ), Université Joseph Fourier - Grenoble 1 ( UJF ) -CHU Grenoble, Carcinogénèse épithéliale : facteurs prédictifs et pronostiques - UFC ( CEF2P / CARCINO ), Centre Hospitalier Régional Universitaire [Besançon] ( CHRU Besançon ) -Université Bourgogne Franche-Comté ( UBFC ) -Université de Franche-Comté ( UFC ), Université Joseph Fourier - Grenoble 1 ( UJF ) -CHU Grenoble-EFS-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université Joseph Fourier - Grenoble 1 ( UJF ) -CHU Grenoble-EFS-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Département d'anatomie et cythologie pathologique, CHU Grenoble-Hôpital Michallon-Hôpital Michallon-Intergroupe Francophone de Cancérologie Thoracique [Paris] ( IFCT ), International Agency for Cancer Research ( IACR ), International Agency for Cancer Research, Université Joseph Fourier - Grenoble 1 ( UJF ) -CHU Grenoble-EFS-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Carcinogénèse épithéliale : facteurs prédictifs et pronostiques - UFC (UR 3181) (CEF2P / CARCINO), Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Université de Franche-Comté (UFC), and Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)

Subjects
Oncology, Male, Cancer Research, Pathology, Lung Neoplasms, medicine.medical_treatment, Apoptosis, Deoxycytidine, Carboplatin, [ SDV.CAN ] Life Sciences [q-bio]/Cancer, chemistry.chemical_compound, 0302 clinical medicine, Carcinoma, Non-Small-Cell Lung, Epidermal growth factor receptor, RNA, Small Interfering, Promoter Regions, Genetic, Neoadjuvant therapy, Cytoskeleton, 0303 health sciences, biology, Methylation, Middle Aged, Prognosis, Neoadjuvant Therapy, 3. Good health, ErbB Receptors, Paclitaxel, 030220 oncology & carcinogenesis, DNA methylation, Female, RNA Interference, medicine.medical_specialty, Adenocarcinoma of Lung, Antineoplastic Agents, [SDV.CAN]Life Sciences [q-bio]/Cancer, Adenocarcinoma, Disease-Free Survival, 03 medical and health sciences, Internal medicine, medicine, Carcinoma, Biomarkers, Tumor, Humans, 030304 developmental biology, Chemotherapy, business.industry, Tumor Suppressor Proteins, Cancer, DNA Methylation, medicine.disease, Genes, p53, Gemcitabine, Death-Associated Protein Kinases, Genes, ras, chemistry, Calcium-Calmodulin-Dependent Protein Kinases, biology.protein, Cisplatin, Tumor Suppressor Protein p53, business, Apoptosis Regulatory Proteins
Abstract

Purpose: To evaluate prognostic and predictive molecular biomarkers in early-stage non–small cell lung carcinoma (NSCLC) receiving neoadjuvant chemotherapy. Experimental Design: The IFCT-0002 trial compared two neoadjuvant regimens in 528 stages I to II NSCLC patients. DNA extraction of snap-frozen surgical samples taken from 208 patients receiving gemcitabine-cisplatin or paclitaxel-carboplatin regimens allowed for the identification of 3p allelic imbalance, Ras association domain family 1A (RASSF1A) and death-associated protein kinase 1 (DAPK1) promoter methylation, and epidermal growth factor receptor, K-ras, and TP53 mutations. Multivariate analysis identified prognostic and predictive effects of molecular alterations. A Bootstrapping approach was used to assess stability of the prognostic models generating optimism corrected indexes. Results: RASSF1A methylation correlated significantly with shorter disease-free survival (DFS; adjusted HR = 1.88, 95% CI: 1.25–2.82, P = 0.0048) and shorter median overall survival (OS; adjusted HR = 2.01, 95% CI: 1.26–3.20, P = 0.020). A computed bootstrap resampling strategy led to a prognostic model, including RASSF1A, DAPK1, and tumor stage, dividing patients into three prognostic groups, with median OS ranging from 34 months for high-risk patients (HR for death = 3.85, 95% CI: 1.79–6.40) to more than 84 months for moderate (HR = 1.85, 95% CI: 0.97–3.52) and low-risk patients (reference group; P = 0.00044). In addition, RASSF1A methylation predicted longer DFS in patients treated with paclitaxel-carboplatin compared with gemcitabine-cisplatin (adjusted HR = 0.47, 95% CI: 0.23–0.97, Pinteraction = 0.042). Conclusions: Following neoadjuvant chemotherapy, RASSF1A methylation negatively impacted prognosis of early-stage NSCLC. Along with DAPK1 methylation and tumor stage, RASSF1A methylation allowed definition of three subgroups with strikingly different prognosis. Conversely, significantly longer DFS following paclitaxel-based neoadjuvant chemotherapy for patients whose tumors showed RASSF1A methylation suggested its predictive interest in stages I and II NSCLC. Clin Cancer Res; 18(10); 2976–86. ©2012 AACR.

Published
2012
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2. [Diagnosis of lung cancer. DNA microarrays in thoracic oncology]

Author

Moro-Sibilot, Denis, Diab, Samia, Lantuejoul, Sylvie, Favrot, Marie Christine, Groupe de Recherche Sur Le Cancer du Poumon : Bases Moléculaires de la Progression Tumorale, Dépistage et Thérapie Génique, Institut Albert Bonniot-Institut National de la Santé et de la Recherche Médicale (INSERM), and Salas, Danielle

Subjects
MESH: Pulmonary Disease (Specialty), MESH: Humans, Lung Neoplasms, [SDV.CAN] Life Sciences [q-bio]/Cancer, MESH: Oligonucleotide Array Sequence Analysis, Pulmonary Medicine, Humans, [SDV.CAN]Life Sciences [q-bio]/Cancer, Medical Oncology, MESH: Lung Neoplasms, MESH: Medical Oncology, Oligonucleotide Array Sequence Analysis
Abstract

National audience; DNA microarrays allow simultaneous measurement of the expression of several thousand genes in a biological specimen. This technique represents a major advance in the analysis of tumour biopsies. It may be used to refine the anatomical- pathological diagnosis at a molecular level and thus lead to better diagnostic and prognostic classification and improved therapeutic decisions.

Published
2007

3. [Aberrant methylation of tumor suppressor genes in head and neck squamous cell carcinoma: is it clinically relevant?]

Author

Righini, Christian, De Fraipont, Florence, Reyt, Emile, Favrot, Marie-Christine, Salas, Danielle, INSERM U823, équipe 5 (cibles diagnostiques ou thérapeutiques et vectorisation de drogues dans le cancer du poumon), Institut d'oncologie/développement Albert Bonniot de Grenoble (INSERM U823), Université Joseph Fourier - Grenoble 1 (UJF)-CHU Grenoble-EFS-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Joseph Fourier - Grenoble 1 (UJF)-CHU Grenoble-EFS-Institut National de la Santé et de la Recherche Médicale (INSERM), Service d'ORL et de chirurgie cervicale, and CHU Grenoble

Subjects
Chromosome Aberrations, MESH: Humans, MESH: Laryngeal Neoplasms, [SDV.CAN]Life Sciences [q-bio]/Cancer, MESH: Genes, Tumor Suppressor, DNA Methylation, Epigenesis, Genetic, MESH: Mouth Neoplasms, Oropharyngeal Neoplasms, MESH: DNA Methylation, [SDV.CAN] Life Sciences [q-bio]/Cancer, MESH: Oropharyngeal Neoplasms, MESH: Chromosome Aberrations, Humans, MESH: Gene Silencing, Genes, Tumor Suppressor, Mouth Neoplasms, MESH: Epigenesis, Genetic, Gene Silencing, Laryngeal Neoplasms
Abstract

International audience; During malignant transformation, the malignant cell accumulates epigenetic abnormalities that do not alter the DNA sequence but are transmissible during divisions and modify genes expression. The methylation of CpG islands in the tumor suppressor genes (TS genes) promoters inhibits their transcription ; it is a mecanism of gene inactivation as frequent as allelic deletions. The methylation profile (or panel of methylated genes in a tumor), similarly to allelic deletions, varies with the tumor histology. Within head and neck squamous cell carcinoma (oral cavity, larynx and oropharynx), 19 genes have been analysed, among them 5 are frequently methylated, i.e. : p16, ECAD, DAPK, MGMT et TIMP3. The method of methylation analysis, based on a bisulfite treatment followed by a PCR amplification, is sensitive and specific enough to allow the detection of abnormalities in biological fluid that drain the tumor or in circulating tumoral DNA. In the head and neck squamous cell carcinoma, correlation between the methylation profile in tumor and paired saliva is excellent ; thus methylation analysis in saliva is a very promising approach for early cancer detection in high risk patients or for the post treatment follow up and rapid diagnosis of relapse. The methylation signature might also reflect the tumor prognosis and complete the histology to define the diagnosis. Finally, DNA methylation is reversible with demethylating agents, a new avenue for cancer therapy in association with conventional chemotherapy.

Published
2006

4. Cooperation of amphiregulin and insulin-like growth factor-1 inhibits Bax- and Bad-mediated apoptosis via a protein kinase C-dependent pathway in non-small cell lung cancer cells

Author

Hurbin, Amandine, Coll, Jean-Luc, Dubrez-Daloz, Laurence, Mari, Bernard, Auberger, Patrick, Brambilla, Christian, Favrot, Marie-Christine, Groupe de Recherche Sur Le Cancer du Poumon : Bases Moléculaires de la Progression Tumorale, Dépistage et Thérapie Génique, Institut Albert Bonniot-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Mort cellulaire et cancer, Université de Bourgogne ( UB ) -IFR100 - Structure fédérative de recherche Santé-STIC-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Physiopathologie de la survie et de la mort cellulaire et infection virale, Institut National de la Santé et de la Recherche Médicale ( INSERM ) -IFR50-Université Nice Sophia Antipolis ( UNS ), Université Côte d'Azur ( UCA ) -Université Côte d'Azur ( UCA ), Institut Albert Bonniot-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Bourgogne (UB)-IFR100 - Structure fédérative de recherche Santé-STIC-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Nice Sophia Antipolis (... - 2019) (UNS), and COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-IFR50-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UCA)

Subjects
MESH: Signal Transduction, MESH : Staurosporine, MESH: Insulin-Like Growth Factor I, MESH : Insulin-Like Growth Factor I, MESH : Models, Biological, MESH : Proto-Oncogene Proteins c-bcl-2, [ SDV.CAN ] Life Sciences [q-bio]/Cancer, MESH : Culture Media, Serum-Free, MESH : Flavonoids, MESH : 1-Phosphatidylinositol 3-Kinase, MESH : Isoenzymes, MESH: Naphthalenes, MESH: Culture Media, Serum-Free, MESH: Enzyme Inhibitors, MESH: Isoenzymes, MESH : bcl-Associated Death Protein, MESH : Carrier Proteins, MESH: Cell Line, Tumor, MESH: Glycoproteins, MESH : Androstadienes, MESH : MAP Kinase Signaling System, MESH: Carrier Proteins, [SDV.CAN]Life Sciences [q-bio]/Cancer, MESH : Naphthalenes, MESH: bcl-Associated Death Protein, MESH: bcl-2-Associated X Protein, MESH : Lung Neoplasms, MESH : Protein Kinase C, MESH: Intercellular Signaling Peptides and Proteins, MESH : Intercellular Signaling Peptides and Proteins, MESH : Signal Transduction, MESH : Enzyme Inhibitors, MESH: Humans, MESH : Carcinoma, Non-Small-Cell Lung, MESH: MAP Kinase Signaling System, MESH : bcl-2-Associated X Protein, MESH : Cell Line, Tumor, MESH: Apoptosis, MESH : Humans, MESH: Models, Biological, MESH: 1-Phosphatidylinositol 3-Kinase, MESH: Protein Kinase C, MESH : Glycoproteins, MESH: Lung Neoplasms, MESH: Proto-Oncogene Proteins c-bcl-2, MESH: Androstadienes, MESH: Staurosporine, MESH: Flavonoids, MESH: Carcinoma, Non-Small-Cell Lung, MESH : Apoptosis
Abstract

International audience; Amphiregulin (AR) and insulin-like growth factor-1 (IGF1) are growth factors known to promote non-small cell lung cancer (NSCLC) survival. We have previously published that 1) AR and IGF1, secreted by H358 NSCLC cells, cooperate to protect those cells and H322 NSCLC cells from serum-starved apoptosis; 2) H358 cells resist Bax-induced apoptosis through an inhibition of Bax conformational change. We show here that the antiapoptotic activity of the AR/IGF1 combination is specifically abolished by the PKC inhibitors calphostin C and staurosporine, but not by the MAPK and phosphatidylinositol 3-kinase inhibitors PD98059 and wortmannin, suggesting the involvement of a PKC-dependent and MAPK- and phosphatidylinositol 3-kinase-independent survival pathway. The PKCdelta inhibitor rottlerin restores apoptosis induced by serum deprivation. In addition, phosphorylation of PKCdelta and PKCzeta/lambda, but not of PKCalpha/beta(II), increases in serum-starved H358 cells and in H322 cells treated with an AR/IGF1 combination and is blocked by calphostin C. The combination of AR and IGF1 increases p90(rsk) and Bad phosphorylation as well as inhibiting the conformational change of Bax by a PKC-dependent mechanism. Finally, PKCdelta, PKCzeta, or p90(rsk) small interfering RNAs block the antiapoptotic activity of AR/IGF1 combination but have no effect on partial apoptosis inhibition observed with each factor used alone. Constitutively active PKC expression inhibits serum deprivation-induced apoptosis, whereas a catalytically inactive form of p90(rsk) restores it. Thus, AR and IGF1 cooperate to prevent apoptosis by activating a specific PKC-p90(rsk)-dependent pathway, which leads to Bad and Bax inactivation. This signaling pathway is different to that used by single factor.

Published
2005
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5. Cooperation of amphiregulin and insulin-like growth factor-1 inhibits Bax- and Bad-mediated apoptosis via a protein kinase C-dependent pathway in non-small cell lung cancer cells

Author

Hurbin, Amandine, Coll, Jean-Luc, Dubrez-Daloz, Laurence, Mari, Bernard, Auberger, Patrick, Brambilla, Christian, Favrot, Marie-Christine, Hurbin, Amandine, Groupe de Recherche Sur Le Cancer du Poumon : Bases Moléculaires de la Progression Tumorale, Dépistage et Thérapie Génique, Institut Albert Bonniot-Institut National de la Santé et de la Recherche Médicale (INSERM), Mort cellulaire et cancer, Université de Bourgogne (UB)-IFR100 - Structure fédérative de recherche Santé-STIC-Institut National de la Santé et de la Recherche Médicale (INSERM), Physiopathologie de la survie et de la mort cellulaire et infection virale, Université Nice Sophia Antipolis (1965 - 2019) (UNS), and COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-IFR50-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UCA)

Subjects
MESH: Signal Transduction, MESH: Cell Line, Tumor, MESH: Insulin-Like Growth Factor I, MESH: Glycoproteins, MESH: Carrier Proteins, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.CAN] Life Sciences [q-bio]/Cancer, MESH: bcl-Associated Death Protein, MESH: bcl-2-Associated X Protein, MESH: Intercellular Signaling Peptides and Proteins, MESH: Humans, MESH: MAP Kinase Signaling System, MESH: Apoptosis, MESH: Models, Biological, MESH: Naphthalenes, MESH: 1-Phosphatidylinositol 3-Kinase, MESH: Culture Media, Serum-Free, MESH: Protein Kinase C, MESH: Lung Neoplasms, MESH: Proto-Oncogene Proteins c-bcl-2, MESH: Enzyme Inhibitors, MESH: Androstadienes, MESH: Isoenzymes, MESH: Staurosporine, MESH: Flavonoids, MESH: Carcinoma, Non-Small-Cell Lung
Abstract

International audience; Amphiregulin (AR) and insulin-like growth factor-1 (IGF1) are growth factors known to promote non-small cell lung cancer (NSCLC) survival. We have previously published that 1) AR and IGF1, secreted by H358 NSCLC cells, cooperate to protect those cells and H322 NSCLC cells from serum-starved apoptosis; 2) H358 cells resist Bax-induced apoptosis through an inhibition of Bax conformational change. We show here that the antiapoptotic activity of the AR/IGF1 combination is specifically abolished by the PKC inhibitors calphostin C and staurosporine, but not by the MAPK and phosphatidylinositol 3-kinase inhibitors PD98059 and wortmannin, suggesting the involvement of a PKC-dependent and MAPK- and phosphatidylinositol 3-kinase-independent survival pathway. The PKCdelta inhibitor rottlerin restores apoptosis induced by serum deprivation. In addition, phosphorylation of PKCdelta and PKCzeta/lambda, but not of PKCalpha/beta(II), increases in serum-starved H358 cells and in H322 cells treated with an AR/IGF1 combination and is blocked by calphostin C. The combination of AR and IGF1 increases p90(rsk) and Bad phosphorylation as well as inhibiting the conformational change of Bax by a PKC-dependent mechanism. Finally, PKCdelta, PKCzeta, or p90(rsk) small interfering RNAs block the antiapoptotic activity of AR/IGF1 combination but have no effect on partial apoptosis inhibition observed with each factor used alone. Constitutively active PKC expression inhibits serum deprivation-induced apoptosis, whereas a catalytically inactive form of p90(rsk) restores it. Thus, AR and IGF1 cooperate to prevent apoptosis by activating a specific PKC-p90(rsk)-dependent pathway, which leads to Bad and Bax inactivation. This signaling pathway is different to that used by single factor.

Published
2005
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