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2. Novel partial loss-of-function variants in the tyrosyl-tRNA synthetase 1 (YARS1) gene involved in multisystem disease

Author

Estève, Clothilde, Roman, Céline, DeLeusse, Cécile, Baravalle, Melissa, Bertaux, Karine, Blanc, Frédéric, Bourgeois, Patrice, Bresson, Violaine, Cano, Aline, Coste, Marie-Edith, Delteil, Clémence, Lacoste, Caroline, Loosveld, Marie, De Paula, André Maues, Monnier, Anne-Sophie, Secq, Véronique, Levy, Nicolas, Badens, Catherine, and Fabre, Alexandre

Published
2021
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3. AB004. Basaloid carcinoma of the thymus: experience of the RYTHMIC network over an 8-year period

Author

Piton, Nicolas, primary, Mansuet-Lupo, Audrey, additional, Chalabreysse, Lara, additional, Dubois, Romain, additional, Hofman, Véronique, additional, Le Naoures, Cécile, additional, de Montpréville, Vincent Thomas, additional, De Muret, Anne, additional, Parrens, Marie, additional, Rouquette, Isabelle, additional, Secq, Véronique, additional, Dales, Jean-Philippe, additional, Sizaret, Damien, additional, Missy, Pascale, additional, Tran, Quân, additional, Bazéli, Édith, additional, Marx, Alexander, additional, Girard, Nicolas, additional, Besse, Benjamin, additional, and Molina, Thierry Jo, additional

Published
2023
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4. Transcriptomic Analysis Predicts Survival and Sensitivity to Anticancer Drugs of Patients with a Pancreatic Adenocarcinoma

Author

Duconseil, Pauline, Gilabert, Marine, Gayet, Odile, Loncle, Celine, Moutardier, Vincent, Turrini, Olivier, Calvo, Ezequiel, Ewald, Jacques, Giovannini, Marc, Gasmi, Mohamed, Bories, Erwan, Barthet, Marc, Ouaissi, Mehdi, Goncalves, Anthony, Poizat, Flora, Raoul, Jean Luc, Secq, Veronique, Garcia, Stephane, Viens, Patrice, Iovanna, Juan, and Dusetti, Nelson

Published
2015
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5. Angiographic and histopathological study on bronchial-to-pulmonary vascular anastomoses on explants from patients with cystic fibrosis after bronchial artery embolisation

Author

Habert, Paul, primary, Puech, Basile, additional, Coiffard, Benjamin, additional, Secq, Véronique, additional, Thomas, Pascal, additional, Bec, Romain, additional, Vidal, Vincent, additional, Mancini, Julien, additional, Bermudez, Julien, additional, Reynaud-Gaubert, Martine, additional, and Gaubert, Jean-Yves, additional

Published
2022
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8. Homotypic cell cannibalism, a cell‐death process regulated by the nuclear protein 1, opposes to metastasis in pancreatic cancer

Author

Cano, Carla E, primary, José Sandí, María, additional, Hamidi, Tewfik, additional, Calvo, Ezequiel L, additional, Turrini, Olivier, additional, Bartholin, Laurent, additional, Loncle, Céline, additional, Secq, Véronique, additional, Garcia, Stéphane, additional, Lomberk, Gwen, additional, Kroemer, Guido, additional, Urrutia, Raul, additional, and Iovanna, Juan L, additional

Published
2021
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10. Complex Compound Inheritance of Lethal Lung Developmental Disorders due to Disruption of the TBX-FGF Pathway

Author

Karolak, Justyna A, Vincent, Marie, Deutsch, Gail, Gambin, Tomasz, Cogné, Benjamin, Pichon, Olivier, Vetrini, Francesco, Mefford, Heather C, Dines, Jennifer N, Golden-Grant, Katie, Dipple, Katrina, Freed, Amanda S, Leppig, Kathleen A, Dishop, Megan, Mowat, David, Bennetts, Bruce, Gifford, Andrew J, Weber, Martin A, Lee, Anna F, Boerkoel, Cornelius F, Bartell, Tina M, Ward-Melver, Catherine, Besnard, Thomas, Petit, Florence, Bache, Iben, Tümer, Zeynep, Denis-Musquer, Marie, Joubert, Madeleine, Martinovic, Jelena, Bénéteau, Claire, Molin, Arnaud, Carles, Dominique, André, Gwenaelle, Bieth, Eric, Chassaing, Nicolas, Devisme, Louise, Chalabreysse, Lara, Pasquier, Laurent, Secq, Véronique, Don, Massimiliano, Orsaria, Maria, Missirian, Chantal, Mortreux, Jérémie, Sanlaville, Damien, Pons, Linda, Küry, Sébastien, Bézieau, Stéphane, Liet, Jean-Michel, Joram, Nicolas, Bihouée, Tiphaine, Scott, Daryl A, Brown, Chester W, Scaglia, Fernando, Tsai, Anne Chun-Hui, Grange, Dorothy K, Phillips, John A, Pfotenhauer, Jean P, Jhangiani, Shalini N, Gonzaga-Jauregui, Claudia G, Chung, Wendy K, Schauer, Galen M, Lipson, Mark H, Mercer, Catherine L, van Haeringen, Arie, Liu, Qian, Popek, Edwina, Coban Akdemir, Zeynep H, Lupski, James R, Szafranski, Przemyslaw, Isidor, Bertrand, Le Caignec, Cedric, Stankiewicz, Paweł, Karolak, Justyna A, Vincent, Marie, Deutsch, Gail, Gambin, Tomasz, Cogné, Benjamin, Pichon, Olivier, Vetrini, Francesco, Mefford, Heather C, Dines, Jennifer N, Golden-Grant, Katie, Dipple, Katrina, Freed, Amanda S, Leppig, Kathleen A, Dishop, Megan, Mowat, David, Bennetts, Bruce, Gifford, Andrew J, Weber, Martin A, Lee, Anna F, Boerkoel, Cornelius F, Bartell, Tina M, Ward-Melver, Catherine, Besnard, Thomas, Petit, Florence, Bache, Iben, Tümer, Zeynep, Denis-Musquer, Marie, Joubert, Madeleine, Martinovic, Jelena, Bénéteau, Claire, Molin, Arnaud, Carles, Dominique, André, Gwenaelle, Bieth, Eric, Chassaing, Nicolas, Devisme, Louise, Chalabreysse, Lara, Pasquier, Laurent, Secq, Véronique, Don, Massimiliano, Orsaria, Maria, Missirian, Chantal, Mortreux, Jérémie, Sanlaville, Damien, Pons, Linda, Küry, Sébastien, Bézieau, Stéphane, Liet, Jean-Michel, Joram, Nicolas, Bihouée, Tiphaine, Scott, Daryl A, Brown, Chester W, Scaglia, Fernando, Tsai, Anne Chun-Hui, Grange, Dorothy K, Phillips, John A, Pfotenhauer, Jean P, Jhangiani, Shalini N, Gonzaga-Jauregui, Claudia G, Chung, Wendy K, Schauer, Galen M, Lipson, Mark H, Mercer, Catherine L, van Haeringen, Arie, Liu, Qian, Popek, Edwina, Coban Akdemir, Zeynep H, Lupski, James R, Szafranski, Przemyslaw, Isidor, Bertrand, Le Caignec, Cedric, and Stankiewicz, Paweł

Abstract

Primary defects in lung branching morphogenesis, resulting in neonatal lethal pulmonary hypoplasias, are incompletely understood. To elucidate the pathogenetics of human lung development, we studied a unique collection of samples obtained from deceased individuals with clinically and histopathologically diagnosed interstitial neonatal lung disorders: acinar dysplasia (n = 14), congenital alveolar dysplasia (n = 2), and other lethal lung hypoplasias (n = 10). We identified rare heterozygous copy-number variant deletions or single-nucleotide variants (SNVs) involving TBX4 (n = 8 and n = 2, respectively) or FGF10 (n = 2 and n = 2, respectively) in 16/26 (61%) individuals. In addition to TBX4, the overlapping ∼2 Mb recurrent and nonrecurrent deletions at 17q23.1q23.2 identified in seven individuals with lung hypoplasia also remove a lung-specific enhancer region. Individuals with coding variants involving either TBX4 or FGF10 also harbored at least one non-coding SNV in the predicted lung-specific enhancer region, which was absent in 13 control individuals with the overlapping deletions but without any structural lung anomalies. The occurrence of rare coding variants involving TBX4 or FGF10 with the putative hypomorphic non-coding SNVs implies a complex compound inheritance of these pulmonary hypoplasias. Moreover, they support the importance of TBX4-FGF10-FGFR2 epithelial-mesenchymal signaling in human lung organogenesis and help to explain the histopathological continuum observed in these rare lethal developmental disorders of the lung.

Published
2019

11. Complex Compound Inheritance of Lethal Lung Developmental Disorders Due to Disruption of the TBX-FGF Pathway

Author

Karolak, Justyna A., primary, Vincent, Marie, additional, Deutsch, Gail, additional, Gambin, Tomasz, additional, Cogné, Benjamin, additional, Pichon, Olivier, additional, Vetrini, Francesco, additional, Mefford, Heather C., additional, Dines, Jennifer N., additional, Golden-Grant, Katie, additional, Dipple, Katrina, additional, Freed, Amanda S., additional, Leppig, Kathleen A., additional, Dishop, Megan, additional, Mowat, David, additional, Bennetts, Bruce, additional, Gifford, Andrew J., additional, Weber, Martin A., additional, Lee, Anna F., additional, Boerkoel, Cornelius F., additional, Bartell, Tina M., additional, Ward-Melver, Catherine, additional, Besnard, Thomas, additional, Petit, Florence, additional, Bache, Iben, additional, Tümer, Zeynep, additional, Denis-Musquer, Marie, additional, Joubert, Madeleine, additional, Martinovic, Jelena, additional, Bénéteau, Claire, additional, Molin, Arnaud, additional, Carles, Dominique, additional, André, Gwenaelle, additional, Bieth, Eric, additional, Chassaing, Nicolas, additional, Devisme, Louise, additional, Chalabreysse, Lara, additional, Pasquier, Laurent, additional, Secq, Véronique, additional, Don, Massimiliano, additional, Orsaria, Maria, additional, Missirian, Chantal, additional, Mortreux, Jérémie, additional, Sanlaville, Damien, additional, Pons, Linda, additional, Küry, Sébastien, additional, Bézieau, Stéphane, additional, Liet, Jean-Michel, additional, Joram, Nicolas, additional, Bihouée, Tiphaine, additional, Scott, Daryl A., additional, Brown, Chester W., additional, Scaglia, Fernando, additional, Tsai, Anne Chun-Hui, additional, Grange, Dorothy K., additional, Phillips, John A., additional, Pfotenhauer, Jean P., additional, Jhangiani, Shalini N., additional, Gonzaga-Jauregui, Claudia G., additional, Chung, Wendy K., additional, Schauer, Galen M., additional, Lipson, Mark H., additional, Mercer, Catherine L., additional, van Haeringen, Arie, additional, Liu, Qian, additional, Popek, Edwina, additional, Coban Akdemir, Zeynep H., additional, Lupski, James R., additional, Szafranski, Przemyslaw, additional, Isidor, Bertrand, additional, Le Caignec, Cedric, additional, and Stankiewicz, Paweł, additional

Published
2019
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12. Gene expression profiling of patient‐derived pancreatic cancer xenografts predicts sensitivity to the BET bromodomain inhibitor JQ1: implications for individualized medicine efforts

Author

Bian, Benjamin, Bigonnet, Martin, Gayet, Odile, Loncle, Céline, Maignan, Aurélie, Gilabert, Marine, Moutardier, Vincent, Garcia, Stéphane, Turrini, Olivier, Delpero, Jean-Robert, Giovannini, Marc, Grandval, Philippe, Gasmi, Mohamed, Ouaissi, Mehdi, Secq, Véronique, Poizat, Flora, Nicolle, Rémy, Blum, Yuna, Marisa, Laetitia, Rubis, Marion, Raoul, Jean-Luc, Bradner, James, Qi, Jun, Lomberk, Gwen, Urrutia, Raul, Saúl, Andres, Dusetti, Nelson, Iovanna, Juan, Bidaut, Ghislain, Centre de Recherche en Cancérologie de Marseille (CRCM), Aix Marseille Université (AMU)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Aix-Marseille Université - Faculté de médecine (AMU MED), Aix Marseille Université (AMU), Hôpital Nord [CHU - APHM], Department of Surgical Oncology, Université de la Méditerranée - Aix-Marseille 2, Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC), Génétique Médicale et Génomique Fonctionnelle (GMGF), Aix Marseille Université (AMU)-Assistance Publique - Hôpitaux de Marseille (APHM)- Hôpital de la Timone [CHU - APHM] (TIMONE)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Hôpital de la Timone [CHU - APHM] (TIMONE), Institut Curie [Paris], (le programme) Cartes d'identité des tumeurs (CIT), Ligue Nationales Contre le Cancer (LNCC), Centre de Recherche Saint-Antoine (UMRS893), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Dana-Farber Cancer Institute [Boston], Laboratory of Epigenetics and Chromatin Dynamics, Mayo Clinic, Centre Interdisciplinaire de Nanoscience de Marseille (CINaM), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Aix Marseille Université (AMU), Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU), Institut Curie, Physiologie, Environnement et Génétique pour l'Animal et les Systèmes d'Elevage [Rennes] (PEGASE), AGROCAMPUS OUEST-Institut National de la Recherche Agronomique (INRA), and Centre de Recherche Saint-Antoine (CR Saint-Antoine)

Subjects
Adult, Male, Cell Survival, JQ1, [SDV]Life Sciences [q-bio], Antineoplastic Agents, [SDV.CAN]Life Sciences [q-bio]/Cancer, Chromatin, Epigenetics, Genomics & Functional Genomics, Mice, [SDV.CAN] Life Sciences [q-bio]/Cancer, transcriptomic signature, pancreatic adenocarcinoma, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, Animals, Humans, bromodomains, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Precision Medicine, Cells, Cultured, Research Articles, Aged, Cancer, Aged, 80 and over, Gene Expression Profiling, Azepines, Middle Aged, Triazoles, Chromatin, Pancreatic Neoplasms, [SDV] Life Sciences [q-bio], c-MYC, c‐MYC, Genomics and Functional Genomics, Heterografts, Female, Epigenetics, Research Article
Abstract

International audience; c-MYC controls more than 15% of genes responsible for proliferation , differentiation, and cellular metabolism in pancreatic as well as other cancers making this transcription factor a prime target for treating patients. The transcriptome of 55 patient-derived xenografts show that 30% of them share an exacerbated expression profile of MYC transcriptional targets (MYC-high). This cohort is characterized by a high level of Ki67 staining, a lower differentiation state, and a shorter survival time compared to the MYC-low subgroup. To define classifier expression signature, we selected a group of 10 MYC target transcripts which expression is increased in the MYC-high group and six transcripts increased in the MYC-low group. We validated the ability of these markers panel to identify MYC-high patient-derived xenografts from both: discovery and validation cohorts as well as primary cell cultures from the same patients. We then showed that cells from MYC-high patients are more sensitive to JQ1 treatment compared to MYC-low cells, in monolayer, 3D cultured spheroids and in vivo xenografted tumors, due to cell cycle arrest followed by apoptosis. Therefore, these results provide new markers and potentially novel therapeutic modalities for distinct subgroups of pancreatic tumors and may find application to the future management of these patients within the setting of individualized medicine clinics.

Published
2017

13. LIF Drives Neural Remodeling in Pancreatic Cancer and Offers a New Candidate Biomarker

Author

Bressy, Christian, primary, Lac, Sophie, additional, Nigri, Jérémy, additional, Leca, Julie, additional, Roques, Julie, additional, Lavaut, Marie-Nöelle, additional, Secq, Véronique, additional, Guillaumond, Fabienne, additional, Bui, Thi-Thien, additional, Pietrasz, Daniel, additional, Granjeaud, Samuel, additional, Bachet, Jean-Baptiste, additional, Ouaissi, Mehdi, additional, Iovanna, Juan, additional, Vasseur, Sophie, additional, and Tomasini, Richard, additional

Published
2018
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14. BTN3A is a prognosis marker and a promising target for Vγ9Vδ2 T cells based-immunotherapy in pancreatic ductal adenocarcinoma (PDAC)

Author

Benyamine, Audrey, primary, Loncle, Céline, additional, Foucher, Etienne, additional, Blazquez, Juan-Luis, additional, Castanier, Céline, additional, Chrétien, Anne-Sophie, additional, Modesti, Mauro, additional, Secq, Véronique, additional, Chouaib, Salem, additional, Gironella, Meritxell, additional, Vila-Navarro, Elena, additional, Montalto, Giuseppe, additional, Dagorn, Jean-Charles, additional, Dusetti, Nelson, additional, Iovanna, Juan, additional, and Olive, Daniel, additional

Published
2017
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15. PAP/HIP protein is an obesogenic factor

Author

Secq, Véronique, Mallmann, Cecilia, Gironella, Meritxell, López, Belén, Closa, Daniel, García, Stéphane, Christa, Laurence, Montalto, Giuseppe, Dusetti, Nelson, Iovanna, Juan Lucio, Secq, V, Mallmann, C, Gironella, M, Lopez, B, Closa, D, Garcia, S, Christa, L, Montalto, G, Dusetti, N, and Iovanna, JL

Subjects
Transgenic mice, PAP/HIP, Severe obesity
Abstract

In this article we report the obesogenic role of the acute phase protein PAP/HIP. We found that the transgenic TgPAP/HIP mice develop spontaneous obesity under standard nutritional conditions, with high levels of glucose, leptin, and LDL and low levels of triglycerides and HDL in blood. Accordingly, PAP/HIP-deficient mice are skinny under standard nutritional conditions. We also found that expression of PAP/HIP is induced in intestinal epithelial cells in response to gavage with olive oil and this induction is AG490 sensitive. We demonstrated that incubation of 3T3-L1 preadipocytes with a low concentration as 1ng/ml of recombinant PAP/HIP results in accelerated BrdU incorporation in vitro. PAP/HIP-dependent adipocytes growth is sensitive to the MEK inhibitor U0126. Finally, patients with severe obesity present higher blood levels of PAP/HIP than non-obese control individuals. Altogether our data suggest that PAP/HIP could be a mediator of fat tissue development, released by the intestine and induced by the presence of food into the gut. © 2013 Wiley Periodicals, Inc., Funded by: INSERM.

Published
2014

16. Cancer-associated fibroblast-derived annexin A6+ extracellular vesicles support pancreatic cancer aggressiveness

Author

Leca, Julie, primary, Martinez, Sébastien, additional, Lac, Sophie, additional, Nigri, Jérémy, additional, Secq, Véronique, additional, Rubis, Marion, additional, Bressy, Christian, additional, Sergé, Arnauld, additional, Lavaut, Marie-Noelle, additional, Dusetti, Nelson, additional, Loncle, Céline, additional, Roques, Julie, additional, Pietrasz, Daniel, additional, Bousquet, Corinne, additional, Garcia, Stéphane, additional, Granjeaud, Samuel, additional, Ouaissi, Mehdi, additional, Bachet, Jean Baptiste, additional, Brun, Christine, additional, Iovanna, Juan L., additional, Zimmermann, Pascale, additional, Vasseur, Sophie, additional, and Tomasini, Richard, additional

Published
2016
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20. Single-domain antibodies: a versatile and rich source of binders for breast cancer diagnostic approaches

Author

Even-Desrumeaux, Klervi, Fourquet, Patrick, Secq, Véronique, Baty, Daniel, Chames, Patrick, Chames, Patrick, Centre de Recherche en Cancérologie de Marseille (CRCM), Aix Marseille Université (AMU)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre d'Immunologie de Marseille - Luminy (CIML), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and This work was supported by the ANR (Agence Nationale de Recherche) program 'Nanosciences and Nanotechnologies' under the grant ANR-07-PNANO-051-01 and by the ARC (Association pour la Recherche contre le Cancer).

Subjects
[INFO.INFO-BT] Computer Science [cs]/Biotechnology, [SDV.BIO]Life Sciences [q-bio]/Biotechnology, Single domain antibodies, cancer, diagnostic, biomarkers, beads array, [INFO.INFO-BT]Computer Science [cs]/Biotechnology, [SDV.BIO] Life Sciences [q-bio]/Biotechnology
Abstract

International audience; Noninvasive early detection of breast cancer through the use of biomarkers is urgently needed since the risk of recurrence, morbidity, and mortality is closely related to disease stage at the time of primary surgery. A crucial issue in this approach is the availability of relevant markers and corresponding monoclonal antibodies suitable for the development of effective immunodiagnostic modalities. The identification of such markers from human pathological lesions and the isolation of specific antibodies using conventional approaches remain major challenges. Camelids produce functional antibodies devoid of light chains in which the single N-terminal domain of the heavy chain is fully capable of antigen binding. When produced as an independent domain, these so-called single-domain antibody fragments (sdAbs) or nanobodies have several advantages for biotechnological applications owing to their unique properties of size (13 kDa), stability, solubility, and expression yield. In this work, we have generated phage display libraries from animals immunized with breast cancer biopsies. These libraries were used to isolate sdAbs against known and relevant antigens such as HER2, or several cancer-specific sdAbs against unknown targets. We describe the identification of one these targets, cytokeratin 19, using affinity purification in combination with mass spectrometry. Some of these sdAbs were used in several straightforward diagnostic applications such as immunohistochemical analysis of tumor samples, multiplexed cytometric bead array analysis of crude samples, or an immune enrichment procedure of rare cells. Here, we demonstrate that phage display-based selection of single-domain antibodies is an efficient and high-throughput compatible approach to generate binders with excellent characteristics for the fast development of diagnostic and prognostic modalities.

Published
2012

21. PAP/HIP protein is an obesogenic factor

Author

Secq, Véronique, Mallmann, Cecilia, Gironella, Meritxell, López, Belén, Closa, Daniel, García, Stéphane, Christa, Laurence, Montalto, Giuseppe, Dusetti, Nelson, Iovanna, Juan Lucio, Secq, Véronique, Mallmann, Cecilia, Gironella, Meritxell, López, Belén, Closa, Daniel, García, Stéphane, Christa, Laurence, Montalto, Giuseppe, Dusetti, Nelson, and Iovanna, Juan Lucio

Abstract

In this article we report the obesogenic role of the acute phase protein PAP/HIP. We found that the transgenic TgPAP/HIP mice develop spontaneous obesity under standard nutritional conditions, with high levels of glucose, leptin, and LDL and low levels of triglycerides and HDL in blood. Accordingly, PAP/HIP-deficient mice are skinny under standard nutritional conditions. We also found that expression of PAP/HIP is induced in intestinal epithelial cells in response to gavage with olive oil and this induction is AG490 sensitive. We demonstrated that incubation of 3T3-L1 preadipocytes with a low concentration as 1ng/ml of recombinant PAP/HIP results in accelerated BrdU incorporation in vitro. PAP/HIP-dependent adipocytes growth is sensitive to the MEK inhibitor U0126. Finally, patients with severe obesity present higher blood levels of PAP/HIP than non-obese control individuals. Altogether our data suggest that PAP/HIP could be a mediator of fat tissue development, released by the intestine and induced by the presence of food into the gut. © 2013 Wiley Periodicals, Inc.

Published
2013

22. BTN3A is a prognosis marker and a promising target for Vγ9Vδ2 T cells based-immunotherapy in pancreatic ductal adenocarcinoma (PDAC).

Author

Benyamine, Audrey, Loncle, Céline, Foucher, Etienne, Blazquez, Juan-Luis, Castanier, Céline, Chrétien, Anne-Sophie, Modesti, Mauro, Secq, Véronique, Chouaib, Salem, Gironella, Meritxell, Vila-Navarro, Elena, Montalto, Giuseppe, Dagorn, Jean-Charles, Dusetti, Nelson, Iovanna, Juan, and Olive, Daniel

Subjects
ADENOCARCINOMA, CANCER treatment, IMMUNOTHERAPY, T cells, THERAPEUTICS
Abstract

Vγ9Vδ2 T cells are anti-tumor immune effectors of growing interest in cancer including Pancreatic Ductal Adenocarcinoma (PDAC), an especially aggressive cancer characterized by a hypoxic and nutrient-starved immunosuppressive microenvironment. Since Butyrophilin 3 A (BTN3A) isoforms are critical activating molecules of Vγ9Vδ2 T cells, we set out to study BTN3A expression under both basal and stress conditions in PDAC primary tumors, and in novel patient-derived xenograft and PDAC-derived cell lines. BTN3A2 was shown to be the most abundant isoform in PDAC and was stress-regulated. Vγ9Vδ2 T cells cytolytic functions against PDAC required BTN3A and this activity was strongly enhanced by the agonist anti-BTN3A 20.1 mAb even under conditions of hypoxia. In PDAC primary tumors, we established that BTN3A expression and high plasma levels of soluble BTN3A were strongly associated with a decreased survival. These findings may have important implications in the design of new immunotherapeutic strategies that target BTN3A for treating PDAC. [ABSTRACT FROM PUBLISHER]

Published
2018
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23. BTN3A is a prognosis marker and a promising target for Vγ9Vδ2 T cells based-immunotherapy in pancreatic ductal adenocarcinoma (PDAC)

Author

Juan-Luis Blazquez, Salem Chouaib, Jean-Charles Dagorn, Juan L. Iovanna, Anne-Sophie Chretien, Giuseppe Montalto, Véronique Secq, Audrey Benyamine, Meritxell Gironella, Elena Vila-Navarro, Mauro Modesti, Nelson Dusetti, Céline Castanier, Etienne Foucher, Celine Loncle, Daniel Olive, Vascular research center of Marseille (VRCM), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche en Cancérologie de Marseille (CRCM), Aix Marseille Université (AMU)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche en Cancérologie Nantes-Angers (CRCNA), Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM)-PRES Université Nantes Angers Le Mans (UNAM)-Hôtel-Dieu de Nantes-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hôpital Laennec-Centre National de la Recherche Scientifique (CNRS)-Faculté de Médecine d'Angers-Centre hospitalier universitaire de Nantes (CHU Nantes), École supérieure du professorat et de l'éducation - Aix Marseille (ESPE AMU), Aix Marseille Université (AMU), Vectorologie et transfert de gènes (VTG / UMR8121), Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Centre National de la Recherche Scientifique (CNRS), Stress Cellulaire, Université de la Méditerranée - Aix-Marseille 2-Institut National de la Santé et de la Recherche Médicale (INSERM), Gastrointestinal and Pancreatic oncology, Laboratoire d'Immunologie des Tumeurs, Université de la Méditerranée - Aix-Marseille 2-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC), Modesti, Mauro, Centre Alexis Vautrin (CAV), Immunologie intégrative des tumeurs (UMR 1186), Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Physiopathologie du stress pancréatique, Institut National de la Santé et de la Recherche Médicale (INSERM), Benyamine, Audrey, Loncle, Céline, Foucher, Etienne, Blazquez, Juan-Lui, Castanier, Céline, Chrétien, Anne-Sophie, Secq, Véronique, Chouaib, Salem, Gironella, Meritxell, Vila-Navarro, Elena, Montalto, Giuseppe, Dagorn, Jean-Charle, Dusetti, Nelson, Iovanna, Juan, Olive, Daniel, Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Paoli-Calmettes, and Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Aix Marseille Université (AMU)

Subjects
0301 basic medicine, Oncology, lcsh:Immunologic diseases. Allergy, medicine.medical_specialty, Pancreatic ductal adenocarcinoma, endocrine system diseases, medicine.medical_treatment, [SDV]Life Sciences [q-bio], Immunology, btn3a, pancreatic ductal adenocarcinoma, lcsh:RC254-282, 03 medical and health sciences, 0302 clinical medicine, Immune system, Internal medicine, medicine, Immunology and Allergy, ComputingMilieux_MISCELLANEOUS, business.industry, cd277, Aggressive cancer, Cancer, Prognosis Marker, Immunotherapy, medicine.disease, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, butyrophilin 3 a, digestive system diseases, 3. Good health, [SDV] Life Sciences [q-bio], 030104 developmental biology, 030220 oncology & carcinogenesis, immunotherapy, business, lcsh:RC581-607, Research Article
Abstract

Vγ9Vδ2 T cells are anti-tumor immune effectors of growing interest in cancer including Pancreatic Ductal Adenocarcinoma (PDAC), an especially aggressive cancer characterized by a hypoxic and nutrient-starved immunosuppressive microenvironment. Since Butyrophilin 3 A (BTN3A) isoforms are critical activating molecules of Vγ9Vδ2 T cells, we set out to study BTN3A expression under both basal and stress conditions in PDAC primary tumors, and in novel patient-derived xenograft and PDAC-derived cell lines. BTN3A2 was shown to be the most abundant isoform in PDAC and was stress-regulated. Vγ9Vδ2 T cells cytolytic functions against PDAC required BTN3A and this activity was strongly enhanced by the agonist anti-BTN3A 20.1 mAb even under conditions of hypoxia. In PDAC primary tumors, we established that BTN3A expression and high plasma levels of soluble BTN3A were strongly associated with a decreased survival. These findings may have important implications in the design of new immunotherapeutic strategies that target BTN3A for treating PDAC.

Published
2017

24. [Early breast carcinoma profiling based on quantitative immunocytochemistry can help predict the risk of early distant metastasis].

Author

Taranger-Charpin C, Giusiano S, Secq V, Djemli A, Andrac L, Lavaut MN, Allasia C, and Garcia S

Subjects
Adenocarcinoma pathology, Adult, Aged, Biomarkers, Tumor analysis, Early Diagnosis, Female, Humans, Immunohistochemistry, Middle Aged, Breast Neoplasms pathology, Neoplasm Metastasis diagnosis
Abstract

We examined a series of 667 patients with node-negative breast carcinomas in order to identify prognostic immunohistochemical molecular signatures for the prediction of early metastasis, and potential new therapeutic targets. We used a standardized quantitative immunocytochemical approach with 37 antibodies, based on high-throughput tissue microarrays and image analysis, and analyzed the results with respect to metastatic status after a mean follow-up of 86 months. Complete data were obtained for 586 patients. The predictive value of the markers was first analyzed individually by univariate analysis (log rank test) in 586 node-negative tumors, according to metastatic status during follow-up. Twenty-seven markers had significant prognostic value. ROC curve analysis (logistic regression) was then used to determine the marker combination that best classified the patients with and without metastases. A 15-marker signature (Bcl2, P16, P21, P27, P53, CD34, CA IX, c-kit, FGF-R1, P38, JAK, pSTAT3, CK9, STAT1 and ER) correctly classified 84.8% of the patients (sensitivity 85.5%, specificity 84.6%). When ER, PR and c-erb B2 were excluded from the analysis, a very similar signature, in which CK8-18 replaced ER, correctly classified 83.6% of the patients (sensitivity 84.5%, specificity 83.4%). These results show that quantitative immunoprofiling, independently of ER, PR and c-erb B2 status, can provide a basal-like signature, can properly predict the metastatic risk of node-negative breast carcinomas at diagnostic time. This may be helpful for selecting patients who do not need aggressive adjuvant chemotherapy, and for developing tailored therapies.

Published
2009

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