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41 results on '"Levallet, Jérôme"'

3. Multimodal evaluation of hypoxia in brain metastases of lung cancer and interest of hypoxia image-guided radiotherapy

Author

Corroyer-Dulmont, Aurélien, Valable, Samuel, Fantin, Jade, Chatre, Laurent, Toutain, Jérôme, Teulier, Sylvain, Bazille, Céline, Letissier, Elise, Levallet, Jérôme, Divoux, Didier, Ibazizène, Méziane, Guillouet, Stéphane, Perrio, Cécile, Barré, Louisa, Serres, Sébastien, Sibson, Nicola R., Chapon, Françoise, Levallet, Guénaëlle, and Bernaudin, Myriam

Published
2021
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4. Supplementary Table 1 from High TUBB3 Expression, an Independent Prognostic Marker in Patients with Early Non–Small Cell Lung Cancer Treated by Preoperative Chemotherapy, Is Regulated by K-Ras Signaling Pathway

Author

Levallet, Guénaëlle, primary, Bergot, Emmanuel, primary, Antoine, Martine, primary, Creveuil, Christian, primary, Santos, Adriana O., primary, Beau-Faller, Michelle, primary, de Fraipont, Florence, primary, Brambilla, Elisabeth, primary, Levallet, Jérôme, primary, Morin, Franck, primary, Westeel, Virginie, primary, Wislez, Marie, primary, Quoix, Elisabeth, primary, Debieuvre, Didier, primary, Dubois, Fatéméh, primary, Rouquette, Isabelle, primary, Pujol, Jean-Louis, primary, Moro-Sibilot, Denis, primary, Camonis, Jacques, primary, and Zalcman, Gérard, primary

Published
2023
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5. Supplementary Figure 2 from High TUBB3 Expression, an Independent Prognostic Marker in Patients with Early Non–Small Cell Lung Cancer Treated by Preoperative Chemotherapy, Is Regulated by K-Ras Signaling Pathway

Author

Levallet, Guénaëlle, primary, Bergot, Emmanuel, primary, Antoine, Martine, primary, Creveuil, Christian, primary, Santos, Adriana O., primary, Beau-Faller, Michelle, primary, de Fraipont, Florence, primary, Brambilla, Elisabeth, primary, Levallet, Jérôme, primary, Morin, Franck, primary, Westeel, Virginie, primary, Wislez, Marie, primary, Quoix, Elisabeth, primary, Debieuvre, Didier, primary, Dubois, Fatéméh, primary, Rouquette, Isabelle, primary, Pujol, Jean-Louis, primary, Moro-Sibilot, Denis, primary, Camonis, Jacques, primary, and Zalcman, Gérard, primary

Published
2023
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6. Supplementary Figure 5 from High TUBB3 Expression, an Independent Prognostic Marker in Patients with Early Non–Small Cell Lung Cancer Treated by Preoperative Chemotherapy, Is Regulated by K-Ras Signaling Pathway

Author

Levallet, Guénaëlle, primary, Bergot, Emmanuel, primary, Antoine, Martine, primary, Creveuil, Christian, primary, Santos, Adriana O., primary, Beau-Faller, Michelle, primary, de Fraipont, Florence, primary, Brambilla, Elisabeth, primary, Levallet, Jérôme, primary, Morin, Franck, primary, Westeel, Virginie, primary, Wislez, Marie, primary, Quoix, Elisabeth, primary, Debieuvre, Didier, primary, Dubois, Fatéméh, primary, Rouquette, Isabelle, primary, Pujol, Jean-Louis, primary, Moro-Sibilot, Denis, primary, Camonis, Jacques, primary, and Zalcman, Gérard, primary

Published
2023
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7. Supplementary Figure 3 from High TUBB3 Expression, an Independent Prognostic Marker in Patients with Early Non–Small Cell Lung Cancer Treated by Preoperative Chemotherapy, Is Regulated by K-Ras Signaling Pathway

Author

Levallet, Guénaëlle, primary, Bergot, Emmanuel, primary, Antoine, Martine, primary, Creveuil, Christian, primary, Santos, Adriana O., primary, Beau-Faller, Michelle, primary, de Fraipont, Florence, primary, Brambilla, Elisabeth, primary, Levallet, Jérôme, primary, Morin, Franck, primary, Westeel, Virginie, primary, Wislez, Marie, primary, Quoix, Elisabeth, primary, Debieuvre, Didier, primary, Dubois, Fatéméh, primary, Rouquette, Isabelle, primary, Pujol, Jean-Louis, primary, Moro-Sibilot, Denis, primary, Camonis, Jacques, primary, and Zalcman, Gérard, primary

Published
2023
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8. Supplementary Figure Legends 1-5 from High TUBB3 Expression, an Independent Prognostic Marker in Patients with Early Non–Small Cell Lung Cancer Treated by Preoperative Chemotherapy, Is Regulated by K-Ras Signaling Pathway

Author

Levallet, Guénaëlle, primary, Bergot, Emmanuel, primary, Antoine, Martine, primary, Creveuil, Christian, primary, Santos, Adriana O., primary, Beau-Faller, Michelle, primary, de Fraipont, Florence, primary, Brambilla, Elisabeth, primary, Levallet, Jérôme, primary, Morin, Franck, primary, Westeel, Virginie, primary, Wislez, Marie, primary, Quoix, Elisabeth, primary, Debieuvre, Didier, primary, Dubois, Fatéméh, primary, Rouquette, Isabelle, primary, Pujol, Jean-Louis, primary, Moro-Sibilot, Denis, primary, Camonis, Jacques, primary, and Zalcman, Gérard, primary

Published
2023
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9. Supplementary Figure 4 from High TUBB3 Expression, an Independent Prognostic Marker in Patients with Early Non–Small Cell Lung Cancer Treated by Preoperative Chemotherapy, Is Regulated by K-Ras Signaling Pathway

Author

Levallet, Guénaëlle, primary, Bergot, Emmanuel, primary, Antoine, Martine, primary, Creveuil, Christian, primary, Santos, Adriana O., primary, Beau-Faller, Michelle, primary, de Fraipont, Florence, primary, Brambilla, Elisabeth, primary, Levallet, Jérôme, primary, Morin, Franck, primary, Westeel, Virginie, primary, Wislez, Marie, primary, Quoix, Elisabeth, primary, Debieuvre, Didier, primary, Dubois, Fatéméh, primary, Rouquette, Isabelle, primary, Pujol, Jean-Louis, primary, Moro-Sibilot, Denis, primary, Camonis, Jacques, primary, and Zalcman, Gérard, primary

Published
2023
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10. Supplementary Figure 1 from High TUBB3 Expression, an Independent Prognostic Marker in Patients with Early Non–Small Cell Lung Cancer Treated by Preoperative Chemotherapy, Is Regulated by K-Ras Signaling Pathway

Author

Levallet, Guénaëlle, primary, Bergot, Emmanuel, primary, Antoine, Martine, primary, Creveuil, Christian, primary, Santos, Adriana O., primary, Beau-Faller, Michelle, primary, de Fraipont, Florence, primary, Brambilla, Elisabeth, primary, Levallet, Jérôme, primary, Morin, Franck, primary, Westeel, Virginie, primary, Wislez, Marie, primary, Quoix, Elisabeth, primary, Debieuvre, Didier, primary, Dubois, Fatéméh, primary, Rouquette, Isabelle, primary, Pujol, Jean-Louis, primary, Moro-Sibilot, Denis, primary, Camonis, Jacques, primary, and Zalcman, Gérard, primary

Published
2023
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12. A defect of amphiregulin release predicted longer survival independently of YAP expression in patients with pleural mesothelioma in the IFCT ‐0701 MAPS phase 3 trial

Author

Maille, Elodie, Levallet, Jérôme, Dubois, Fatéméh, Antoine, Martine, Danel, Claire, Creveuil, Christian, Mazieres, Julien, Margery, Jacques, Greillier, Laurent, Gounant, Valérie, Moro‐sibilot, Denis, Molinier, Olivier, Léna, Hervé, Monnet, Isabelle, Bergot, Emmanuel, Langlais, Alexandra, Morin, Franck, Sherpereel, Arnaud, Zalcman, Gérard, Levallet, Guénaëlle, Imagerie et Stratégies Thérapeutiques des pathologies Cérébrales et Tumorales (ISTCT), Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS), GIP Cyceron (Cyceron), Normandie Université (NU)-Normandie Université (NU)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN)-Tumorothèque de Caen Basse-Normandie (TCBN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Département de Pathologie [CHU Caen], Normandie Université (NU)-Normandie Université (NU)-CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN)-Tumorothèque de Caen Basse-Normandie (TCBN), CHU Tenon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Service Pneumologie et allergologie pédiatrique [CHU Toulouse], Pôle Enfants [CHU Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Institut Gustave Roussy (IGR), Département de médecine oncologique [Gustave Roussy], Service d'oncologie multidisciplinaire innovations thérapeutiques [Hôpital Nord - APHM], Assistance Publique - Hôpitaux de Marseille (APHM)- Hôpital Nord [CHU - APHM], Aix Marseille Université (AMU), Centre d'investigation Clinique [CHU Bichat] - Épidémiologie clinique (CIC 1425), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Pôle Thorax et Vaisseaux [CHU Grenoble], Centre Hospitalier Universitaire [Grenoble] (CHU), Centre Hospitalier Le Mans (CH Le Mans), Service de pneumologie [Rennes] = Pneumology [Rennes], CHU Pontchaillou [Rennes], Intergroupe Francophone de Cancérologie Thoracique [Paris] (IFCT), Intergroupe Francophone de Cancérologie thoracique, Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 (CIIL), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS), CHU Lille, Unité de génétique et biologie des cancers (U830), Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Brunaud, Carole, Service d'Anatomie et cytologie pathologiques [CHU Tenon], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)

Subjects
[SDV] Life Sciences [q-bio], Mesothelioma, Lung Neoplasms, Cell Line, Tumor, Pleural Neoplasms, [SDV]Life Sciences [q-bio], Mesothelioma, Malignant, Humans, malignant pleural mesothelioma, amphiregulin, YAP
Abstract

CERVOXY; International audience; The Hippo pathway effector YAP is dysregulated in malignant pleural mesothelioma (MPM). YAP’s target genes include the secreted growth factor amphiregulin (AREG), which is overexpressed in a wide range of epithelial cancers and plays an elusive role in MPM. We assayed the expression of YAP and AREG in MPM pathology samples and that of AREG additionally in plasma samples of patients from the randomized phase 3 IFCT-0701 Mesothelioma Avastin Cisplatin Pemetrexed Study (MAPS) using immunohistochemistry and ELISA assays, respectively. MPM patients frequently presented high levels of tumor AREG (64.3%), a high cytosolic AREG expression being predictive of a better prognosis with longer median overall and progression-free survival. Surprisingly, tumor AREG cytosolic expression was not correlated with secreted plasma AREG. By investigating the AREG metabolism and function in MPM cell lines H2452, H2052, MSTO-211H, and H28, in comparison with the T47D ER+ breast cancer cell line used as a positive control, we confirm that AREG is important for cell invasion, growth without anchorage, proliferation, and apoptosis in mesothelioma cells. Yet, most of these MPM cell lines failed to correctly execute AREG post-translational processing by metalloprotease ADAM17/tumor necrosis factor-alpha-converting enzyme (TACE) and extra-cell secretion. The favorable prognostic value of high cytosolic AREG expression in MPM patients could therefore be sustained by default AREG post-translational processing and release. Thus, the determination of mesothelioma cell AREG content could be further investigated as a prognostic marker for MPM patients and used as a stratification factor in future clinical trials.

Published
2022

13. Caractérisation de l’hypoxie dans les métastases cérébrales issues de cancer du poumon : de l’approche clinique à la pré-clinique

Author

Jade, Fantin, Aurélien, Corroyer-Dulmont, Samuel, Valable, Toutain, Jérôme, Sylvain, Teulier, Céline, Bazille, Levallet, Jérôme, Françoise, Chapon, Levallet, Guénaëlle, Bernaudin, Myriam, Imagerie et Stratégies Thérapeutiques des pathologies Cérébrales et Tumorales (ISTCT), Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS), Département de Pathologie [CHU Caen], Normandie Université (NU)-Normandie Université (NU)-CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN)-Tumorothèque de Caen Basse-Normandie (TCBN), 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), and Brunaud, Carole

Subjects
[SDV] Life Sciences [q-bio], [SDV]Life Sciences [q-bio]
Abstract

CERVOXY; International audience

Published
2021

16. Investigating Tunneling Nanotubes in Cancer Cells: Guidelines for Structural and Functional Studies through Cell Imaging

Author

Dubois, Fatéméh, Bénard, Magalie, Jean-Jacques, Bastien, Schapman, Damien, Roberge, Hélène, Lebon, Alexis, Goux, Didier, Monterroso, Baptiste, Elie, Nicolas, Komuro, Hitoshi, Bazille, Céline, Levallet, Jérôme, Bergot, Emmanuel, Levallet, Guénaëlle, and Galas, Ludovic

Subjects
Article Subject
Abstract

By allowing insured communication between cancer cells themselves and with the neighboring stromal cells, tunneling nanotubes (TNTs) are involved in the multistep process of cancer development from tumorigenesis to the treatment resistance. However, despite their critical role in the biology of cancer, the study of the TNTs has been announced challenging due to not only the absence of a specific biomarker but also the fragile and transitory nature of their structure and the fact that they are hovering freely above the substratum. Here, we proposed to review guidelines to follow for studying the structure and functionality of TNTs in tumoral neuroendocrine cells (PC12) and nontumorigenic human bronchial epithelial cells (HBEC-3, H28). In particular, we reported how crucial is it (i) to consider the culture conditions (culture surface, cell density), (ii) to visualize the formation of TNTs in living cells (mechanisms of formation, 3D representation), and (iii) to identify the cytoskeleton components and the associated elements (categories, origin, tip, and formation/transport) in the TNTs. We also focused on the input of high-resolution cell imaging approaches including Stimulated Emission Depletion (STED) nanoscopy, Transmitted and Scanning Electron Microscopies (TEM and SEM). In addition, we underlined the important role of the organelles in the mechanisms of TNT formation and transfer between the cancer cells. Finally, new biological models for the identification of the TNTs between cancer cells and stromal cells (liquid air interface, ex vivo, in vivo) and the clinical considerations will also be discussed.

Published
2020
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17. Cytosolic amphiregulin accumulation in malignant pleural mesothelioma cells predicts better survival of patient from the IFCT-GFPC-0701 MAPS Phase 3 trial

Author

Lainé, Baptiste, Maille, Elodie, Levallet, Jérôme, Dubois, Fatéméh, Antoine, Martine, Danel, Claire, Creveuil, Christian, Bergot, Emmanuel, Sherpereel, Arnaud, Langlais, Alexandra, Morin, Franck, Zalcman, Gérard, Levallet, Guénaëlle, Imagerie et Stratégies Thérapeutiques des pathologies Cérébrales et Tumorales (ISTCT), Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS), Service de pneumologie [CHU Caen], Normandie Université (NU)-Normandie Université (NU)-CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN)-Tumorothèque de Caen Basse-Normandie (TCBN), The departments of Pulmonary and Thoracic Oncology and Thoracic Surgery, Calmette Hospital, Lille, France, and Couteau, Florence

Subjects
[SDV] Life Sciences [q-bio], [SDV]Life Sciences [q-bio]
Abstract

CERVOXY COLL; National audience

Published
2019

18. L’expression cytosolique tumorale d’amphireguline prédit la meilleure survie des patients atteints de mésothéliome pleural malin : analyses chez 288 patients de la cohorte Bio-MAPS

Author

Lainé, Baptiste, Maille, Elodie, Dubois, Fatéméh, Levallet, Jérôme, Antoine, Martine, Danel, Claire, Creveuil, Christian, Bergot, Emmanuel, Sherpereel, Arnaud, Langlais, Alexandra, Morin, Franck, Zalcman, Gérard, Levallet, Guénaëlle, Imagerie et Stratégies Thérapeutiques des pathologies Cérébrales et Tumorales (ISTCT), Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS), CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN), and Couteau, Florence

Subjects
[SDV] Life Sciences [q-bio], [SDV]Life Sciences [q-bio]
Abstract

CERVOXY; National audience

Published
2019

19. Additional file 2: of NDR2 kinase contributes to cell invasion and cytokinesis defects induced by the inactivation of RASSF1A tumor-suppressor gene in lung cancer cells

Author

Keller, Maureen, Fatéméh Dubois, Teulier, Sylvain, Martin, Alexandre, Levallet, Jérôme, Maille, Elodie, Solenn Brosseau, Elie, Nicolas, Hergovich, Alexander, Bergot, Emmanuel, Camonis, Jacques, Zalcman, Gérard, and Levallet, Guénaëlle

Subjects
endocrine system
Abstract

Figure S1. NDR1 or NDR2 depletion abolishes mobility and metastasis properties in HBEC with RASSF1A depletion without lead to cells death. Figure S2: NDR2 depletion abolishes mobility and metastasis properties in HBEC with RASSF1A depletion without lead to cells death. Figure S3. NDR1 or NDR2 restores mobility and 3D migration in HBEC with respectively NDR1 or NDR2 depletion. Figure S4. NDR1/2 expression in shcontrol, shNDR1 or shNDR2 HBEC. Figure S5. NDR1orNDR2depletionpartlyabolishedEMTinRASSF1A-depletedH1299cells. Figure S6. NDR2depletionabolishesYAPactivationinRASSF1A-depletedA549orH1650cells. Figure S7. TheheparansulfateproteoglycanSyndecan-1(SDC-1)mediatestheinteractionandphosphorylationofGEF-H1byNDR2inHBEC-3cells. Figure S8. Sanger analysis of GEF-H1 S265A or S885A mutants. Figure S9. RASSF1A is not required for cleavage plan or equatorial structure of HBEC. Figure S10. RASSF1Adepletion induces defects on metaphase and anaphase and is required for mid body formationin HBEC cells. Figure S11. RASSF1A depletion leads to accumulation of enzymes involved in midbody cut (A) and alterations in the content of proteins crucial for intracellular traffic and mitosis (B) in HBEC cells. Figure S12. GEF-H1 silencing mimics cytokinesis failure induced by RASSF1A loss in HBEC-3 cells while NDR2 depletion in RASSF1A-depleted H1299 cells restores proper cytokinesis. Figure S13. RASSF1A/RhoB/GEF-H1/NDR2 mRNA impacts on survival from of 681 patients with NSCLC,TCGAcohort. (PDF 2685 kb)

Published
2019
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23. L’expression cytosolique tumorale d’amphiréguline prédit la meilleure survie des patients atteints de mésothéliome pleural malin : analyses chez 288 patients de la cohorte Bio-MAPS

Author

Levallet, Jérôme, primary, Maille, Elodie, additional, Dubois, Fatéméh, additional, Antoine, Martine, additional, Danel, Claire, additional, Creveuil, Christian, additional, Bergot, Emmanuel, additional, Sherpereel, Arnaud, additional, Langlais, Alexandra, additional, Morin, Franck, additional, Zalcman, Gérard, additional, and Levallet, Guénaëlle, additional

Published
2019
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27. High TUBB3 expression, an independent prognostic marker in patients with early non-small cell lung cancer treated by preoperative chemotherapy, is regulated by K-Ras signaling pathway

Author

Levallet , Guénaëlle, Bergot , Emmanuel, Antoine , Martine, Creveuil , Christian, Santos , Adriana O, Beau-Faller , Michelle, De Fraipont , Florence, Brambilla , Elisabeth, Levallet , Jérôme, Morin , Franck, Westeel , Virginie, Wislez , Marie, Quoix , Elisabeth, Debieuvre , Didier, Dubois , Fatéméh, Rouquette , Isabelle, Pujol , Jean-Louis, Moro-Sibilot , Denis, Camonis , Jacques, Zalcman , Gérard, Renseigné , Non, Service de pneumologie [Caen], Université de Caen Normandie ( UNICAEN ), Normandie Université ( NU ) -Normandie Université ( NU ) -CHU Caen, 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)-CHU Tenon [APHP], 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, 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, Amplitude Systèmes, Carcinogénèse épithéliale : facteurs prédictifs et pronostiques - UFC ( CEF2P / CARCINO ), Université Bourgogne Franche-Comté ( UBFC ) -Université de Franche-Comté ( UFC ) -Centre Hospitalier Régional Universitaire [Besançon] ( CHRU Besançon ), Service de pneumologie et réanimation [CHU Tenon], Service de pneumologie, CHU Strasbourg-Hopital Civil, Service de Pneumologie, CHI de la Haute-Saône, Institut de biologie et chimie des protéines [Lyon] ( IBCP ), Université Claude Bernard Lyon 1 ( UCBL ), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique ( CNRS ), 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, Institut Curie, Unité de génétique et biologie des cancers ( U830 ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut Curie-Institut National de la Santé et de la Recherche Médicale ( INSERM ), 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), Université Pierre et Marie Curie - Paris 6 (UPMC), Intergroupe Francophone de Cancérologie Thoracique [Paris] (IFCT), 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), 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, 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), 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 - Oncologie Thoracique - Maladies Pulmonaires Rares [CHU Tenon], CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut de biologie et chimie des protéines [Lyon] (IBCP), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), Université Joseph Fourier - Grenoble 1 (UJF)-CHU Grenoble-EFS-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Curie [Paris], Unité de génétique et biologie des cancers (U830), Université Paris Descartes - Paris 5 (UPD5)-Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), National Hospital Program for Clinical Research (PHRC), Association de Recherche contre le Cancer (ARC), Curie Institute grant for clinical research (CERC), National Program of Scientific Excellency from French National Cancer Institute (INCA), Comite du Calvados de la Ligue contre le Cancer grant, French Society of Pulmonary Medicine (Societe de Pneumologie de Langue Francaise, SPLF), ARC [3131, 4845], Fondation de France [2008 005019], Fondation de France/Programme tumeurs solides, 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), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-CHU Tenon [APHP], Université Bourgogne Franche-Comté [COMUE] (UBFC)-Centre Hospitalier Régional Universitaire [Besançon] (CHRU Besançon)-Université de Franche-Comté (UFC), Université Paris Descartes - Paris 5 (UPD5)-Institut Curie-Institut National de la Santé et de la Recherche Médicale (INSERM), Carcinogénèse épithéliale : facteurs prédictifs et pronostiques - UFC (EA 3181) ( CEF2P / CARCINO ), and Centre Hospitalier Régional Universitaire [Besançon] ( CHRU Besançon ) -Université Bourgogne Franche-Comté [COMUE] ( UBFC ) -Université de Franche-Comté ( UFC )

Subjects
Male, Cancer Research, Lung Neoplasms, medicine.medical_treatment, PROTEIN, [ SDV.CAN ] Life Sciences [q-bio]/Cancer, 0302 clinical medicine, ADJUVANT CHEMOTHERAPY, Tubulin, Carcinoma, Non-Small-Cell Lung, Antineoplastic Combined Chemotherapy Protocols, Medicine, GENE-EXPRESSION, 0303 health sciences, ISOTYPE, Middle Aged, Prognosis, Neoadjuvant Therapy, 3. Good health, Gene Expression Regulation, Neoplastic, Treatment Outcome, Oncology, 030220 oncology & carcinogenesis, Female, medicine.drug, Signal Transduction, Adult, GAMMA-TUBULIN, [SDV.CAN]Life Sciences [q-bio]/Cancer, Proto-Oncogene Proteins p21(ras), 03 medical and health sciences, CISPLATIN, BRONCHIAL EPITHELIAL-CELLS, Biomarkers, Tumor, Humans, Lung cancer, Protein kinase B, Survival analysis, 030304 developmental biology, III BETA-TUBULIN, Aged, Cisplatin, Chemotherapy, TUBB3, Taxane, business.industry, medicine.disease, Survival Analysis, Gemcitabine, RANDOMIZED-TRIAL, Immunology, Mutation, Cancer research, PACLITAXEL RESISTANCE, business
Abstract

We assessed the prognostic and predictive value of β-tubulin III (TUBB3) expression, as determined by immunohistochemistry, in 412 non–small cell lung cancer (NSCLC) specimens from early-stage patients who received neoadjuvant chemotherapy (paclitaxel- or gemcitabine-based) in a phase III trial (IFCT-0002). We also correlated TUBB3 expression with K-Ras and EGF receptor (EGFR) mutations in a subset of 208 cryopreserved specimens. High TUBB3 protein expression was associated with nonsquamous cell carcinomas (P < 0.001) and K-Ras mutation (P < 0.001). The 127 (30.8%) TUBB3-negative patients derived more than 1 year of overall survival advantage, with more than 84 months median overall survival versus 71.7 months for TUBB3-positive patients [HR, 1.58; 95% confidence interval (CI), 1.11–2.25)]. This prognostic value was confirmed in multivariate analysis (adjusted HR for death, 1.51; 95% CI, 1.04–2.21; P = 0.031) with a bootstrapping validation procedure. TUBB3 expression was associated with nonresponse to chemotherapy (adjusted HR, 1.31; 95% CI, 1.01–1.70; P = 0.044) but had no predictive value (taxane vs. gemcitabine). Taking account of these clinical findings, we further investigated TUBB3 expression in isogenic human bronchial cell lines only differing by K-Ras gene status and assessed the effect of K-Ras short interfering RNA (siRNA) mediated depletion, cell hypoxia, or pharmacologic inhibitors of K-Ras downstream effectors, on TUBB3 protein cell content. siRNA K-Ras knockdown, inhibition of RAF/MEK (MAP–ERK kinase) and phosphoinositide 3-kinase (PI3K)/AKT signaling, and hypoxia were shown to downregulate TUBB3 expression in bronchial cells. This study is the first one to identify K-Ras mutations as determinant of TUBB3 expression, a chemoresistance marker. Our in vitro data deserve studies combining standard chemotherapy with anti-MEK or anti-PI3K drugs in patients with TUBB3-overexpressing tumors. Mol Cancer Ther; 11(5); 1203–13. ©2012 AACR.

Published
2012

28. Expression of the cAMP-Phosphodiesterase PDE4D isoforms and age-related changes in follicle-stimulating hormone-stimulated PDE4 activities in immature rat sertoli cells

Author

Levallet, Guénaëlle, Levallet, Jérôme, Bouraïma-Lelong, Hélène, Bonnamy, Pierre-Jacques, Unité sous contrat aromatase et oestrogènes dans les gonades des mammifères, Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Recherche Agronomique (INRA), and ProdInra, Migration

Subjects
FOLLICLE-STIMULATING HORMONE, TESTIS, PHOSPHODIESTERASES, FSH, AMP-C, RAT, [SDV.BDLR]Life Sciences [q-bio]/Reproductive Biology, CYCLIC ADENOSINE MONOPHOSPHATE, [SDV.BDLR] Life Sciences [q-bio]/Reproductive Biology, ComputingMilieux_MISCELLANEOUS, SERTOLI CELLS
Abstract

International audience

Published
2007

37. Expression and Immunolocalization of Functional Cytochrome P450 Aromatase in Mature Rat Testicular Cells1

Author

Levallet, Jérôme, Bilinska, Barbara, Mittre, Hervé, Genissel, Christelle, Fresnel, Jacqueline, and Carreau, Serge

Abstract

Aromatase activity has been measured in Leydig cells and Sertoli cells from both immature and mature rats. Cytochrome P450 aromatase (P450arom) has been immunolocalized in germ cells of the rodent, bear, and rooster. Our purpose was to investigate expression of and to immunolocalize P450aromin adult rat testicular cells. After Western blotting with a specific anti-cytochrome P450aromantibody, we demonstrated the presence of a 55-kDa protein in mature rat seminiferous tubules and crude germ cell preparations. Immunoreactive aromatase was detected both in cultured rat Leydig cells and in testis sections (interstitial tissue and elongated spermatids showed positive immunoreactivity for P450arom). We next used reverse transcription-polymerase chain reaction to localize and quantify the P450arommRNA in the various testicular cells. In rat Leydig cells, the amount of P450arommRNA was 15 times higher than in Sertoli cells (34.1 ± 3.2 to 2.3 ± 0.2 × 10-3amol/106cells, respectively). In pachytene spermatocytes, round spermatids, and testicular spermatozoa the P450arommRNA levels were 38.7 ± 8.1, 20.4± 3.8, and < 1.3 × 10−3fmol/106cells, respectively. The aromatase activity was 2.5–4 times higher in testicular spermatozoa (8.48 ± 1.98 fmol/106cells per hour) than in other germ cells. These results indicate that in mature rats, not only Leydig cells and Sertoli cells but also germ cells have the capacity to express functional P450arom. According to the germ cell maturation state, there was an inverse relationship between P450arommRNA content and the biological activity of the protein. The expression of the functional P450aromin mature rat germ cells confirms the existence of an additional source of estrogens within the genital tract of the male.

Published
1998
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38. A defect of amphiregulin release predicted longer survival independently of YAP expression in patients with pleural mesothelioma in the IFCT-0701 MAPS phase 3 trial.

Author

Maille E, Levallet J, Dubois F, Antoine M, Danel C, Creveuil C, Mazieres J, Margery J, Greillier L, Gounant V, Moro-Sibilot D, Molinier O, Léna H, Monnet I, Bergot E, Langlais A, Morin F, Scherpereel A, Zalcman G, and Levallet G

Subjects
Amphiregulin genetics, Cell Line, Tumor, Humans, Lung Neoplasms genetics, Mesothelioma metabolism, Mesothelioma, Malignant, Pleural Neoplasms drug therapy, Pleural Neoplasms pathology
Abstract

The Hippo pathway effector YAP is dysregulated in malignant pleural mesothelioma (MPM). YAP's target genes include the secreted growth factor amphiregulin (AREG), which is overexpressed in a wide range of epithelial cancers and plays an elusive role in MPM. We assayed the expression of YAP and AREG in MPM pathology samples and that of AREG additionally in plasma samples of patients from the randomized phase 3 IFCT-0701 Mesothelioma Avastin Cisplatin Pemetrexed Study (MAPS) using immunohistochemistry and ELISA assays, respectively. MPM patients frequently presented high levels of tumor AREG (64.3%), a high cytosolic AREG expression being predictive of a better prognosis with longer median overall and progression-free survival. Surprisingly, tumor AREG cytosolic expression was not correlated with secreted plasma AREG. By investigating the AREG metabolism and function in MPM cell lines H2452, H2052, MSTO-211H and H28, in comparison with the T47D ER+ breast cancer cell line used as a positive control, we confirm that AREG is important for cell invasion, growth without anchorage, proliferation and apoptosis in mesothelioma cells. Yet, most of these MPM cell lines failed to correctly execute AREG posttranslational processing by metalloprotease ADAM17/tumor necrosis factor-alpha-converting enzyme (TACE) and extracell secretion. The favorable prognostic value of high cytosolic AREG expression in MPM patients could therefore be sustained by default AREG posttranslational processing and release. Thus, the determination of mesothelioma cell AREG content could be further investigated as a prognostic marker for MPM patients and used as a stratification factor in future clinical trials., (© 2022 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.)

Published
2022
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39. High TUBB3 expression, an independent prognostic marker in patients with early non-small cell lung cancer treated by preoperative chemotherapy, is regulated by K-Ras signaling pathway.

Author

Levallet G, Bergot E, Antoine M, Creveuil C, Santos AO, Beau-Faller M, de Fraipont F, Brambilla E, Levallet J, Morin F, Westeel V, Wislez M, Quoix E, Debieuvre D, Dubois F, Rouquette I, Pujol JL, Moro-Sibilot D, Camonis J, and Zalcman G

Subjects
Adult, Aged, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Biomarkers, Tumor genetics, Biomarkers, Tumor metabolism, Carcinoma, Non-Small-Cell Lung mortality, Female, Gene Expression Regulation, Neoplastic, Humans, Lung Neoplasms mortality, Male, Middle Aged, Mutation, Neoadjuvant Therapy, Prognosis, Proto-Oncogene Proteins p21(ras) genetics, Survival Analysis, Treatment Outcome, Tubulin genetics, Carcinoma, Non-Small-Cell Lung drug therapy, Carcinoma, Non-Small-Cell Lung metabolism, Lung Neoplasms drug therapy, Lung Neoplasms metabolism, Proto-Oncogene Proteins p21(ras) metabolism, Signal Transduction, Tubulin metabolism
Abstract

We assessed the prognostic and predictive value of β-tubulin III (TUBB3) expression, as determined by immunohistochemistry, in 412 non-small cell lung cancer (NSCLC) specimens from early-stage patients who received neoadjuvant chemotherapy (paclitaxel- or gemcitabine-based) in a phase III trial (IFCT-0002). We also correlated TUBB3 expression with K-Ras and EGF receptor (EGFR) mutations in a subset of 208 cryopreserved specimens. High TUBB3 protein expression was associated with nonsquamous cell carcinomas (P < 0.001) and K-Ras mutation (P < 0.001). The 127 (30.8%) TUBB3-negative patients derived more than 1 year of overall survival advantage, with more than 84 months median overall survival versus 71.7 months for TUBB3-positive patients [HR, 1.58; 95% confidence interval (CI), 1.11-2.25)]. This prognostic value was confirmed in multivariate analysis (adjusted HR for death, 1.51; 95% CI, 1.04-2.21; P = 0.031) with a bootstrapping validation procedure. TUBB3 expression was associated with nonresponse to chemotherapy (adjusted HR, 1.31; 95% CI, 1.01-1.70; P = 0.044) but had no predictive value (taxane vs. gemcitabine). Taking account of these clinical findings, we further investigated TUBB3 expression in isogenic human bronchial cell lines only differing by K-Ras gene status and assessed the effect of K-Ras short interfering RNA (siRNA) mediated depletion, cell hypoxia, or pharmacologic inhibitors of K-Ras downstream effectors, on TUBB3 protein cell content. siRNA K-Ras knockdown, inhibition of RAF/MEK (MAP-ERK kinase) and phosphoinositide 3-kinase (PI3K)/AKT signaling, and hypoxia were shown to downregulate TUBB3 expression in bronchial cells. This study is the first one to identify K-Ras mutations as determinant of TUBB3 expression, a chemoresistance marker. Our in vitro data deserve studies combining standard chemotherapy with anti-MEK or anti-PI3K drugs in patients with TUBB3-overexpressing tumors., (©2012 AACR)

Published
2012
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40. Expression of the cAMP-phosphodiesterase PDE4D isoforms and age-related changes in follicle-stimulating hormone-stimulated PDE4 activities in immature rat sertoli cells.

Author

Levallet G, Levallet J, Bouraïma-Lelong H, and Bonnamy PJ

Subjects
3',5'-Cyclic-AMP Phosphodiesterases genetics, Animals, Blotting, Western, Cyclic Nucleotide Phosphodiesterases, Type 4, DNA Primers, Electrophoresis, Polyacrylamide Gel, Female, Isoenzymes biosynthesis, Isoenzymes genetics, Kinetics, Male, Phosphodiesterase Inhibitors pharmacology, Protein Isoforms genetics, RNA, Messenger biosynthesis, RNA, Messenger genetics, Rats, Rats, Sprague-Dawley, Reverse Transcriptase Polymerase Chain Reaction, Rolipram pharmacology, Sertoli Cells drug effects, Stimulation, Chemical, Subcellular Fractions metabolism, 3',5'-Cyclic-AMP Phosphodiesterases biosynthesis, Aging physiology, Follicle Stimulating Hormone pharmacology, Sertoli Cells enzymology
Abstract

Major changes in the cAMP-dependent signal transduction pathway triggered by FSH take place during transition of rat Sertoli cells from proliferative to the quiescent/terminally differentiated state. Using Sertoli cell cultures isolated from 10-, 20-, and 30-day-old rats, we recorded a specific increase in PDE4 activity in both the soluble and particulate subcellular fractions of 20-day-old Sertoli cells, which also displayed the highest cAMP response to FSH and the highest FSH-induced increase in PDE4 activity in both subcellular compartments. RT-PCR and immunoblotting experiments showed that almost all the PDE4D isoforms, known as the main cAMP-regulated rolipram-sensitive PDE in Sertoli cells, were expressed throughout the early postpartum period, whereas only the short PDE4D isoforms (PDE4D1 and PDE4D2) were transcriptionally regulated by FSH. Unexpectedly, the immunoblot data also revealed that the soluble PDE4 activities were mainly related to the long PDE4D isoforms and that short PDE4D1 was predominantly particulate. The subcellular distribution and expression of PDE4D proteins were unaffected by the developmental status of the Sertoli cells. Only the expression of short PDE4D1 appeared to be upregulated by FSH and only in 20-day-old Sertoli cells, which suggests phenotype-dependent differential regulation of Pde4d1 mRNA translation. Resensitization of the cAMP response to FSH in 20-day-old Sertoli cells was also associated with the highest FSH-induced transient increase in both soluble and particulate PDE4 activities, which suggests developmental changes in the PKA-mediated upregulation of the catalytic activities of long PDE4D. Such alterations may be involved in the phenotype-dependent alterations in FSH receptor coupling with its associated G proteins in rat Sertoli cells.

Published
2007
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41. Adrenocortical tumorigenesis in transgenic mice expressing the inhibin alpha-subunit promoter/simian virus 40 T-antigen transgene: relationship between ectopic expression of luteinizing hormone receptor and transcription factor GATA-4.

Author

Rahman NA, Kiiveri S, Rivero-Müller A, Levallet J, Vierre S, Kero J, Wilson DB, Heikinheimo M, and Huhtaniemi I

Subjects
Animals, Base Sequence, Blotting, Northern, Cell Line, Tumor, DNA Primers, GATA4 Transcription Factor, In Situ Hybridization, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Molecular Sequence Data, Mutagenesis, Site-Directed, Orchiectomy, Reverse Transcriptase Polymerase Chain Reaction, Simian virus 40 genetics, Adrenal Cortex Neoplasms genetics, Antigens, Polyomavirus Transforming genetics, DNA-Binding Proteins genetics, Gene Expression Regulation, Neoplastic genetics, Inhibins genetics, Receptors, LH genetics, Transcription Factors genetics
Abstract

We have analyzed the ontogeny and putative mechanisms of transregulation of LH receptor (LHR) and transcription factor GATA-4, coexpressed during the adrenocortical tumorigenesis of prepubertally gonadectomized transgenic (TG) mice expressing the inhibin alpha-subunit promoter/simian virus 40 T-antigen (inhalpha/Tag) transgene. The onset of adrenal LHR mRNA and protein expression coincided with that of GATA-4 at the age of 4 months and preceded the appearance of discernible adrenal tumors at about 6 months. In situ hybridization and double-immunohistochemistry demonstrated colocalization of the LHR and GATA-4 messages and proteins in the adrenal cortex. A GATA-4 expression plasmid cotransfected with a murine LHR promoter-driven luciferase reporter plasmid, containing a consensus GATA-binding site, induced a dose-dependent significant transactivation of the LHR promoter in nonsteroidogenic human embryonic kidney 293, steroidogenic murine mLTC-1 Leydig cells and in murine adrenal Y-1 cells. The Calpha1 cells derived from an Inhalpha/Tag adrenal tumor did not show this response, apparently due to their high endogenous GATA-4 expression. However, an additional link between GATA-4 and LHR in Calpha1 cells was provided upon the LH/human chorionic gonadotropin stimulation of LHR promoter activity; mutations or deletion of the consensus GATA-4 binding site of the LHR promoter abolished this transactivation. EMSAs further proved GATA-4 binding to the putative consensus GATA recognition site. Our results demonstrate direct interrelationship between LHR and GATA-4 expression during adrenocortical tumorigenesis of the inhalpha/Tag mice. There is apparently a positive and reciprocal feed-forward amplification link between LHR and GATA-4 expression. This mechanism gradually and in synergy with Tag expression leads to formation of the LH-dependent adrenocortical tumors.

Published
2004
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