Search

Your search keyword '"Paillas, Salome"' showing total 11 results
Start Over Author "Paillas, Salome" Language english
11 results on '"Paillas, Salome"'

1. Dietary fibre supplementation enhances radiotherapy tumour control and alleviates intestinal radiation toxicity

Author

Then, Chee Kin, Paillas, Salome, Moomin, Aliu, Misheva, Mariya D., Moir, Rachel A., Hay, Susan M., Bremner, David, Roberts (nee Nellany), Kristine S., Smith, Ellen E., Heidari, Zeynab, Sescu, Daniel, Wang, Xuedan, Suárez-Bonnet, Alejandro, Hay, Nadine, Murdoch, Sarah L., Saito, Ryoichi, Collie-Duguid, Elaina S. R., Richardson, Shirley, Priestnall, Simon L., Wilson, Joan M., Gurumurthy, Mahalakshmi, Royle, Justine S., Samuel, Leslie M., Ramsay, George, Vallis, Katherine A., Foster, Kevin R., McCullagh, James S. O., and Kiltie, Anne E.

Published
2024
Full Text
View/download PDF

9. The Histone Deacetylase Inhibitor Romidepsin Spares Normal Tissues While Acting as an Effective Radiosensitizer in Bladder Tumors in Vivo.

Author

Paillas, Salome, Then, Chee K., Kilgas, Susan, Ruan, Jia-Ling, Thompson, James, Elliott, Amy, Smart, Sean, and Kiltie, Anne E.

Subjects
*HISTONE deacetylase inhibitors, *BLADDER cancer, *CUTANEOUS T-cell lymphoma, *IONIZING radiation, *DNA repair, *TUMOR growth, *PROTEIN metabolism, *RESEARCH, *DNA, *ANIMAL experimentation, *RESEARCH methodology, *HUMAN body, *METABOLISM, *EVALUATION research, *MEDICAL cooperation, *COMPARATIVE studies, *RADIATION-sensitizing agents, *RESEARCH funding, *CELL lines, *PEPTIDES, *ENZYME inhibitors, *PHARMACODYNAMICS, *PHYSIOLOGICAL effects of radiation, BLADDER tumors
Abstract

Purpose: Muscle-invasive bladder cancer has a 40% to 60% 5-year survival rate with radical treatment by surgical removal of the bladder or radiation therapy-based bladder preservation techniques, including concurrent chemoradiation. Elderly patients cannot tolerate current chemoradiation therapy regimens and often receive only radiation therapy, which is less effective. We urgently need effective chemotherapy agents for use with radiation therapy combinations that are nontoxic to normal tissues and tolerated by elderly patients.Methods and Materials: We have identified histone deacetylase (HDAC) inhibitors as promising agents to study. Pan-HDAC inhibition, using panobinostat, is a good strategy for radiosensitization, but more selective agents may be more useful radiosensitizers in a clinical setting, resulting in fewer systemic side effects. Herein, we study the HDAC class I-selective agent romidepsin, which we predict to have fewer off-target effects than panobinostat while maintaining an effective level of tumor radiosensitization.Results: In vitro effects of romidepsin were assessed by clonogenic assay and showed that romidepsin was effective in the nanomolar range in different bladder cancer cells and radiosensitized these cells. The radiosensitizing effect of romidepsin was confirmed in vivo using superficial xenografts. The drug/irradiation combination treatment resulted in significant tumor growth delay but did not increase the severity of acute (3.75 days) intestinal normal tissue toxicity or late toxicity at 29 weeks. Moreover, we showed that romidepsin treatment impaired both homologous recombination and nonhomologous end joining DNA repair pathways, suggesting that the disruption of DNA repair pathways caused by romidepsin is a key mechanism for its radiosensitizing effect in bladder cancer cells.Conclusions: This study demonstrates that romidepsin is an effective radiosensitizer in vitro and in vivo and does not increase the acute and late toxicity after ionizing radiation. Romidepsin is already in clinical use for the cutaneous T-cell lymphoma, but a phase 1 clinical trial of romidepsin as a radiosensitizer could be considered in muscle-invasive bladder cancer. [ABSTRACT FROM AUTHOR]

Published
2020
Full Text
View/download PDF

10. MAPK14/p38α confers irinotecan resistance to TP53-defective cells by inducing survival autophagy.: MAPK14/p38α induces survival autophagy

Author

Paillas, Salome, Causse, Annick, Marzi, Laetitia, De Médina, Philippe, Poirot, Marc, Denis, Vincent, Vezzio-Vie, Nadia, Espert, Lucile, Arzouk, Hayat, Coquelle, Arnaud, Martineau, Pierre, Del Rio, Maguy, Pattingre, Sophie, Gongora, Céline, Institut de recherche en cancérologie de Montpellier (IRCM - U896 Inserm - UM1), Université Montpellier 1 (UM1)-CRLCC Val d'Aurelle - Paul Lamarque-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Centre de Physiopathologie de Toulouse-Purpan (INSERM U563 - CNRS UMR1037), Centre National de la Recherche Scientifique (CNRS)-Centre de lutte contre le cancer (CLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse]-CHU Toulouse [Toulouse]-Institut Claudius Regaud, Institut de Recherche en Infectiologie de Montpellier (IRIM), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), and Funds for this research were provided by INSERM

Subjects
MAPK14/p38. Survival Autophagy. Irinotecan resistance. Colon cancer. Chemotherapy, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.BC]Life Sciences [q-bio]/Cellular Biology
Abstract

International audience; Recently we have shown that the mitogen-activated protein kinase (MAPK) MAPK14/p38α is involved in resistance of colon cancer cells to camptothecin-related drugs. Here we further investigated the cellular mechanisms involved in such drug resistance and showed that, in HCT116 human colorectal adenocarcinoma cells in which TP53 was genetically ablated (HCT116-TP53KO), overexpression of constitutively active MAPK14/p38α decreases cell sensitivity to SN-38 (the active metabolite of irinotecan), inhibits cell proliferation and induces survival-autophagy. Since autophagy is known to facilitate cancer cell resistance to chemotherapy and radiation treatment, we then investigated the relationship between MAPK14/p38α, autophagy and resistance to irinotecan. We demonstrated that induction of autophagy by SN38 is dependent on MAPK14/p38α activation. Finally, we showed that inhibition of MAPK14/p38α or autophagy both sensitizes HCT116-TP53KO cells to drug therapy. Our data proved that the two effects are interrelated, since the role of autophagy in drug resistance required the MAPK14/p38α. Our results highlight the existence of a new mechanism of resistance to camptothecin-related drugs: upon SN38 induction, MAPK14/p38α is activated and triggers survival-promoting autophagy to protect tumor cells against the cytotoxic effects of the drug. Colon cancer cells could thus be sensitized to drug therapy by inhibiting either MAPK14/p38 or autophagy.

Published
2012
Full Text
View/download PDF

11. Targeting the p38 MAPK Pathway Inhibits Irinotecan Resistance in Colon Adenocarcinoma

Author

Paillas, Salome, Bibeau, Frédéric, Denouël, Amélie, Mollevi, Caroline, Causse, Annick, Denis, Vincent, Vezzio-Vié, Nadia, Marzi, Laetitia, Cortijo, Cédric, Ait-Arsa, Imade, Askari, Nadav, Pourquier, Philippe, Martineau, Pierre, Del Rio, Maguy, Gongora, Celine, Boissière, Florence, Vezzio-Vie, N., Institut de recherche en cancérologie de Montpellier (IRCM - U896 Inserm - UM1), Université Montpellier 1 (UM1)-CRLCC Val d'Aurelle - Paul Lamarque-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Département de Pathologie [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), EndoFrance [CHRU Montpellier], Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Institut de Recherche en Cancérologie de Montpellier (IRCM - U1194 Inserm - UM), CRLCC Val d'Aurelle - Paul Lamarque-Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM), Cyclotron Réunion Océan Indien (CYROI), Université de La Réunion (UR)-Centre Hospitalier Universitaire de La Réunion (CHU La Réunion), Sanford-Burnham Medical Research Institute, Signalisation et Mecanismes Moleculaires de l'Apoptose, Université Bordeaux Segalen - Bordeaux 2-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire d'anatomo-pathologie, CRLCC Val d'Aurelle - Paul Lamarque, Unité de biostatistiques, Validation et identification de nouvelles cibles en oncologie (VINCO), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Bergonié [Bordeaux], UNICANCER-UNICANCER-Université Bordeaux Segalen - Bordeaux 2, Centre Régional de Lutte contre le Cancer François Baclesse (CRLC François Baclesse ), Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN), IDvet, Laboratoire d'Informatique, de Modélisation et d'optimisation des Systèmes (LIMOS), Université Blaise Pascal - Clermont-Ferrand 2 (UBP)-Université d'Auvergne - Clermont-Ferrand I (UdA)-Sigma CLERMONT (Sigma CLERMONT)-Centre National de la Recherche Scientifique (CNRS)-Ecole Nationale Supérieure des Mines de St Etienne, CRLCC Val d'Aurelle - Paul Lamarque-Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 1 (UM1), Institut Bergonié [Bordeaux], and UNICANCER-UNICANCER-Université Bordeaux Segalen - Bordeaux 2-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Cancer Research, Pyridines, Colorectal cancer, [SDV]Life Sciences [q-bio], Cell, Leucovorin, Drug resistance, p38 Mitogen-Activated Protein Kinases, MESH: Drug Synergism, Mice, 0302 clinical medicine, Antineoplastic Combined Chemotherapy Protocols, MAPK p38, MESH: Protein Kinase Inhibitors, MESH: Animals, Phosphorylation, ComputingMilieux_MISCELLANEOUS, 0303 health sciences, Imidazoles, Drug Synergism, [SDV.SP]Life Sciences [q-bio]/Pharmaceutical sciences, Immunohistochemistry, MESH: Drug Resistance, Neoplasm, 3. Good health, Isoenzymes, MESH: Antineoplastic Combined Chemotherapy Protocols, medicine.anatomical_structure, Oncology, 030220 oncology & carcinogenesis, Colonic Neoplasms, MESH: Isoenzymes, MESH: Camptothecin, Adenocarcinoma, Female, Fluorouracil, MESH: Imidazoles, medicine.drug, MESH: Xenograft Model Antitumor Assays, MAP Kinase Signaling System, MESH: HCT116 Cells, Mice, Nude, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Biology, Irinotecan, Article, 03 medical and health sciences, Downregulation and upregulation, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], medicine, MESH: Mice, Nude, Animals, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Protein Kinase Inhibitors, MESH: Mice, 030304 developmental biology, MESH: Colonic Neoplasms, MESH: Humans, MESH: Phosphorylation, MESH: MAP Kinase Signaling System, MESH: Adenocarcinoma, MESH: Pyridines, Cancer, MESH: Immunohistochemistry, HCT116 Cells, medicine.disease, Xenograft Model Antitumor Assays, MESH: p38 Mitogen-Activated Protein Kinases, SN38, Drug Resistance, Neoplasm, Immunology, Cancer research, Camptothecin, MESH: Leucovorin, MESH: Female, MESH: Fluorouracil
Abstract

Despite recent advances in the treatment of colon cancer, tumor resistance is a frequent cause of chemotherapy failure. To better elucidate the molecular mechanisms involved in resistance to irinotecan (and its active metabolite SN38), we established SN38-resistant clones derived from HCT-116 and SW48 cell lines. These clones show various levels (6- to 60-fold) of resistance to SN-38 and display enhanced levels of activated MAPK p38 as compared with the corresponding parental cells. Because four different isoforms of p38 have been described, we then studied the effect of p38 overexpression or downregulation of each isoform on cell sensivity to SN38 and found that both α and β isoforms are involved in the development of resistance to SN38. In this line, we show that cell treatment with SB202190, which inhibits p38α and p38β, enhanced the cytotoxic activity of SN38. Moreover, p38 inhibition sensitized tumor cells derived from both SN38-sensitive and -resistant HCT116 cells to irinotecan treatment in xenograft models. Finally, we detected less phosphorylated p38 in primary colon cancer of patients sensitive to irinotecan-based treatment, compared with nonresponder patients. This indicates that enhanced level of phosphorylated p38 could predict the absence of clinical response to irinotecan. Altogether, our results show that the p38 MAPK pathway is involved in irinotecan sensitivity and suggest that phosphorylated p38 expression level could be used as a marker of clinical resistance to irinotecan. They further suggest that targeting the p38 pathway may be a potential strategy to overcome resistance to irinotecan-based chemotherapies in colorectal cancer. Cancer Res; 71(3); 1041–9. ©2010 AACR.

Published
2011
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results