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Alain Puisieux

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https://www.readbyqxmd.com/read/27911856/splicing-factor-ratio-as-an-index-of-epithelial-mesenchymal-transition-and-tumor-aggressiveness-in-breast-cancer
#1
Pietro Fici, Giulia Gallerani, Anne-Pierre Morel, Laura Mercatali, Toni Ibrahim, Emanuela Scarpi, Dino Amadori, Alain Puisieux, Michel Rigaud, Francesco Fabbri
Epithelial-to-mesenchymal transition (EMT) has been shown to be associated with tumor progression and metastasis. During this process in breast cancer, a crucial role is played by alternative splicing systems. To identify a new early prognostic marker of metastasis, we evaluated EMT-related gene expression in breast cell lines, and in primary tumor tissue from 31 patients with early breast cancer, focusing our attention on EMT-related splicing factors ESRP1, ESRP2 and RBFOX2. Results showed that the expression patterns of these genes were indicative of the onset of EMT in in-vitro models, but not in tissue samples...
November 29, 2016: Oncotarget
https://www.readbyqxmd.com/read/27894504/-contribution-and-challenges-of-big-data-in-oncology
#2
REVIEW
Pierre Saintigny, Jean-Philippe Foy, Anthony Ferrari, Philippe Cassier, Alain Viari, Alain Puisieux
Since the first draft of the human genome sequence published in 2001, the cost of sequencing has dramatically decreased. The development of new technologies such as next generation sequencing led to a comprehensive characterization of a large number of tumors of various types as well as to significant advances in precision medicine. Despite the valuable information this technological revolution has allowed to produce, the vast amount of data generated resulted in the emergence of new challenges for the biomedical community, such as data storage, processing and mining...
November 25, 2016: Bulletin du Cancer
https://www.readbyqxmd.com/read/27615180/-cancer-cell-plasticity-and-metastatic-dissemination
#3
Caroline Moyret-Lalle, Roxane Pommier, Charlotte Bouard, Ebticem Nouri, Geoffrey Richard, Alain Puisieux
Metastatic dissemination consists of a sequence of events resulting in the invasion by cancer cells of tissues located away from the primary tumour. This process is highly inefficient, since each event represents an obstacle that only a limited number of cells can overcome. However, two biological phenomena intrinsically linked with tumour development facilitate the dissemination of cancer cells throughout the body and promote the formation of metastases, namely the genetic diversity of cancer cells within a given tumour, which arises from their genetic instability and from successive clonal expansions, and cellular plasticity conveyed to the cells by micro-environmental signals...
August 2016: Médecine Sciences: M/S
https://www.readbyqxmd.com/read/27596438/zeb1-mediated-melanoma-cell-plasticity-enhances-resistance-to-mapk-inhibitors
#4
Geoffrey Richard, Stéphane Dalle, Marie-Ambre Monet, Maud Ligier, Amélie Boespflug, Roxane M Pommier, Arnaud de la Fouchardière, Marie Perier-Muzet, Lauriane Depaepe, Romain Barnault, Garance Tondeur, Stéphane Ansieau, Emilie Thomas, Corine Bertolotto, Robert Ballotti, Samia Mourah, Maxime Battistella, Céleste Lebbé, Luc Thomas, Alain Puisieux, Julie Caramel
Targeted therapies with MAPK inhibitors (MAPKi) are faced with severe problems of resistance in BRAF-mutant melanoma. In parallel to the acquisition of genetic mutations, melanoma cells may also adapt to the drugs through phenotype switching. The ZEB1 transcription factor, a known inducer of EMT and invasiveness, is now considered as a genuine oncogenic factor required for tumor initiation, cancer cell plasticity, and drug resistance in carcinomas. Here, we show that high levels of ZEB1 expression are associated with inherent resistance to MAPKi in BRAF(V)(600)-mutated cell lines and tumors...
October 4, 2016: EMBO Molecular Medicine
https://www.readbyqxmd.com/read/27440268/genomic-copy-number-profiling-using-circulating-free-tumor-dna-highlights-heterogeneity-in-neuroblastoma
#5
Mathieu Chicard, Sandrine Boyault, Leo Colmet Daage, Wilfrid Richer, David Gentien, Gaelle Pierron, Eve Lapouble, Angela Bellini, Nathalie Clement, Isabelle Iacono, Stéphanie Bréjon, Marjorie Carrere, Cécile Reyes, Toby Hocking, Virginie Bernard, Michel Peuchmaur, Nadège Corradini, Cécile Faure-Conter, Carole Coze, Dominique Plantaz, Anne Sophie Defachelles, Estelle Thebaud, Marion Gambart, Frédéric Millot, Dominique Valteau-Couanet, Jean Michon, Alain Puisieux, Olivier Delattre, Valérie Combaret, Gudrun Schleiermacher
PURPOSE: The tumor genomic copy number profile is of prognostic significance in neuroblastoma patients. We have studied the genomic copy number profile of cell-free DNA (cfDNA) and compared this with primary tumor arrayCGH (aCGH) at diagnosis. EXPERIMENTAL DESIGN: In 70 patients, cfDNA genomic copy number profiling was performed using the OncoScan platform. The profiles were classified according to the overall pattern, including numerical chromosome alterations (NCA), segmental chromosome alterations (SCA), and MYCN amplification (MNA)...
July 20, 2016: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/27237323/the-heterodimeric-twist1-e12-complex-drives-the-oncogenic-potential-of-twist1-in-human-mammary-epithelial-cells
#6
Laurent Jacqueroud, Charlotte Bouard, Geoffrey Richard, Léa Payen, Mojgan Devouassoux-Shisheboran, Douglas B Spicer, Julie Caramel, Guillaume Collin, Alain Puisieux, Agnès Tissier, Stéphane Ansieau
The TWIST1 embryonic transcription factor displays biphasic functions during the course of carcinogenesis. It facilitates the escape of cells from oncogene-induced fail-safe programs (senescence, apoptosis) and their consequent neoplastic transformation. Additionally, it promotes the epithelial-to-mesenchymal transition and the initiation of the metastatic spread of cancer cells. Interestingly, cancer cells recurrently remain dependent on TWIST1 for their survival and/or proliferation, making TWIST1 their Achilles' heel...
May 2016: Neoplasia: An International Journal for Oncology Research
https://www.readbyqxmd.com/read/27151200/deciphering-the-molecular-mechanisms-underlying-the-binding-of-the-twist1-e12-complex-to-regulatory-e-box-sequences
#7
Charlotte Bouard, Raphael Terreux, Mylène Honorat, Brigitte Manship, Stéphane Ansieau, Arnaud M Vigneron, Alain Puisieux, Léa Payen
The TWIST1 bHLH transcription factor controls embryonic development and cancer processes. Although molecular and genetic analyses have provided a wealth of data on the role of bHLH transcription factors, very little is known on the molecular mechanisms underlying their binding affinity to the E-box sequence of the promoter. Here, we used an in silico model of the TWIST1/E12 (TE) heterocomplex and performed molecular dynamics (MD) simulations of its binding to specific (TE-box) and modified E-box sequences. We focused on (i) active E-box and inactive E-box sequences, on (ii) modified active E-box sequences, as well as on (iii) two box sequences with modified adjacent bases the AT- and TA-boxes...
June 20, 2016: Nucleic Acids Research
https://www.readbyqxmd.com/read/26867874/influence-of-nucleoshuttling-of-the-atm-protein-in-the-healthy-tissues-response-to-radiation-therapy-toward-a-molecular-classification-of-human-radiosensitivity
#8
Adeline Granzotto, Mohamed Amine Benadjaoud, Guillaume Vogin, Clément Devic, Mélanie L Ferlazzo, Larry Bodgi, Sandrine Pereira, Laurène Sonzogni, Fabien Forcheron, Muriel Viau, Aurélie Etaix, Karim Malek, Laurence Mengue-Bindjeme, Clémence Escoffier, Isabelle Rouvet, Marie-Thérèse Zabot, Aurélie Joubert, Anne Vincent, Nicole Dalla Venezia, Michel Bourguignon, Edme-Philippe Canat, Anne d'Hombres, Estelle Thébaud, Daniel Orbach, Dominique Stoppa-Lyonnet, Abderraouf Radji, Eric Doré, Yoann Pointreau, Céline Bourgier, Pierre Leblond, Anne-Sophie Defachelles, Cyril Lervat, Stéphanie Guey, Loic Feuvret, Françoise Gilsoul, Claire Berger, Coralie Moncharmont, Guy de Laroche, Marie-Virginie Moreau-Claeys, Nicole Chavaudra, Patrick Combemale, Marie-Claude Biston, Claude Malet, Isabelle Martel-Lafay, Cécile Laude, Ngoc-Hanh Hau-Desbat, Amira Ziouéche, Ronan Tanguy, Marie-Pierre Sunyach, Séverine Racadot, Pascal Pommier, Line Claude, Frédéric Baleydier, Bertrand Fleury, Renaud de Crevoisier, Jean-Marc Simon, Pierre Verrelle, Didier Peiffert, Yazid Belkacemi, Jean Bourhis, Eric Lartigau, Christian Carrie, Florent De Vathaire, François Eschwege, Alain Puisieux, Jean-Léon Lagrange, Jacques Balosso, Nicolas Foray
PURPOSE: Whereas post-radiation therapy overreactions (OR) represent a clinical and societal issue, there is still no consensual radiobiological endpoint to predict clinical radiosensitivity. Since 2003, skin biopsy specimens have been collected from patients treated by radiation therapy against different tumor localizations and showing a wide range of OR. Here, we aimed to establish quantitative links between radiobiological factors and OR severity grades that would be relevant to radioresistant and genetic hyperradiosensitive cases...
March 1, 2016: International Journal of Radiation Oncology, Biology, Physics
https://www.readbyqxmd.com/read/26282171/tif1%C3%AE-suppresses-tumor-progression-by-regulating-mitotic-checkpoints-and-chromosomal-stability
#9
Roxane M Pommier, Johann Gout, David F Vincent, Lindsay B Alcaraz, Nicolas Chuvin, Vanessa Arfi, Sylvie Martel, Bastien Kaniewski, Guillaume Devailly, Geneviève Fourel, Pascal Bernard, Caroline Moyret-Lalle, Stéphane Ansieau, Alain Puisieux, Ulrich Valcourt, Stéphanie Sentis, Laurent Bartholin
The transcription accessory factor TIF1γ/TRIM33/RFG7/PTC7/Ectodermin functions as a tumor suppressor that promotes development and cellular differentiation. However, its precise function in cancer has been elusive. In the present study, we report that TIF1γ inactivation causes cells to accumulate chromosomal defects, a hallmark of cancer, due to attenuations in the spindle assembly checkpoint and the post-mitotic checkpoint. TIF1γ deficiency also caused a loss of contact growth inhibition and increased anchorage-independent growth in vitro and in vivo...
October 15, 2015: Cancer Research
https://www.readbyqxmd.com/read/26118872/-quinze-questions-importantes-%C3%A3-se-poser-en-oncologie-en-2015
#10
REVIEW
Jean-Yves Blay, Olivier Tredan, Isabelle Ray-Coquard, Michel Rivoire, Patrick Mehlen, Alain Puisieux, Thomas Bachelot
Cancers can now be classified by multidimensional criteria including tumour site, histology, primary - "driver" - molecular alterations, secondary molecular alterations, characteristics of the immune stroma, and genetic profile of the patient. The development of tools for the characterisation of the cancers, as well as novel molecular and immune therapeutics are evolving at an unprecedented pace. In 2012, a list of future challenges was identified at the occasion of the European Organisation for Research and Treatment of Cancer (EORTC) 50(th) anniversary...
June 2015: Bulletin du Cancer
https://www.readbyqxmd.com/read/26007656/dynamics-of-mbd2-deposition-across-methylated-dna-regions-during-malignant-transformation-of-human-mammary-epithelial-cells
#11
Guillaume Devailly, Mélodie Grandin, Laury Perriaud, Pauline Mathot, Jean-Guy Delcros, Yannick Bidet, Anne-Pierre Morel, Jean-Yves Bignon, Alain Puisieux, Patrick Mehlen, Robert Dante
DNA methylation is thought to induce transcriptional silencing through the combination of two mechanisms: the repulsion of transcriptional activators unable to bind their target sites when methylated, and the recruitment of transcriptional repressors with specific affinity for methylated DNA. The Methyl CpG Binding Domain proteins MeCP2, MBD1 and MBD2 belong to the latter category. Here, we present MBD2 ChIPseq data obtained from the endogenous MBD2 in an isogenic cellular model of oncogenic transformation of human mammary cells...
July 13, 2015: Nucleic Acids Research
https://www.readbyqxmd.com/read/25688109/les-entretiens-jacques-cartier-symposium-4-targeted-cancer-therapies-stakes-and-prospects-for-patients
#12
David G Cox, Alain Puisieux
No abstract text is available yet for this article.
March 2015: Mutagenesis
https://www.readbyqxmd.com/read/25532497/copper-isotope-effect-in-serum-of-cancer-patients-a-pilot-study
#13
Philippe Télouk, Alain Puisieux, Toshiyuki Fujii, Vincent Balter, Victor P Bondanese, Anne-Pierre Morel, Gilles Clapisson, Aline Lamboux, Francis Albarede
The isotope effect describes mass-dependent variations of natural isotope abundances for a particular element. In this pilot study, we measured the (65)Cu/(63)Cu ratios in the serums of 20 breast and 8 colorectal cancer patients, which correspond to, respectively, 90 and 49 samples taken at different times with molecular biomarker documentation. Copper isotope compositions were determined by multiple-collector inductively coupled plasma mass spectrometry (MC-ICP-MS). When compared with the literature data from a control group of 50 healthy blood donors, abundances of Cu isotopes predict mortality in the colorectal cancer group with a probability p = 0...
February 2015: Metallomics: Integrated Biometal Science
https://www.readbyqxmd.com/read/25475555/twist1-is-a-direct-transcriptional-target-of-mycn-and-myc-in-neuroblastoma
#14
Abdelkader Selmi, Maud de Saint-Jean, Anne-Catherine Jallas, Elisabeth Garin, Michael D Hogarty, Jean Bénard, Alain Puisieux, Aurélien Marabelle, Sandrine Valsesia-Wittmann
In neuroblastoma, MYCN amplification is associated with a worse prognosis and is a criterion used in the clinic to provide intensive treatments to children even with localized disease. In correlation with MYCN amplification, upregulation of TWIST1, a transcription factor playing a crucial role in inhibition of apoptosis and differentiation, was previously reported. Clinical data set analysis of MYCN, MYC and TWIST1 expression permits us to confirm that TWIST1 expression is upregulated in MYCN amplified neuroblastoma but also in a subset of neuroblastoma harboring high expression of MYCN or MYC without gene amplification...
February 1, 2015: Cancer Letters
https://www.readbyqxmd.com/read/25474134/mbl-ii-141-a-chromone-derivative-enhances-irinotecan-cpt-11-anticancer-efficiency-in-abcg2-positive-xenografts
#15
Léa Payen, Mylène Honorat, Jérôme Guitton, Charlotte Gauthier, Charlotte Bouard, Florine Lecerf-Schmidt, Basile Peres, Raphaël Terreux, Héloïse Gervot, Catherine Rioufol, Ahcène Boumendjel, Alain Puisieux, Attilio Di Pietro
ABCG2 is responsible for the multidrug resistance (MDR) phenotype, and strongly modulates cancer outcomes. Its high expression at a number of physiological barriers, including blood-brain and intestinal barriers, impacts on drug pharmacokinetics parameters. We characterized MBL-II-141, a specific and potent ABCG2 inhibitor. Combination of 10 mg/kg MBL-II-141 with the anticancer agent CPT-11 completely blocked the growth of 90% freshly implanted ABCG2-positive tumors. Moreover, the same combination slowed the growth of already established tumors...
December 15, 2014: Oncotarget
https://www.readbyqxmd.com/read/25216750/abcg2-a-novel-antigen-to-sort-luminal-progenitors-of-brca1-breast-cancer-cells
#16
Felicia Leccia, Luigi Del Vecchio, Elisabetta Mariotti, Rosa Di Noto, Anne-Pierre Morel, Alain Puisieux, Francesco Salvatore, Stéphane Ansieau
INTRODUCTION: Tumor-initiating cells (TICs), aka "cancer stem cells", are believed to fuel tumors and to sustain therapy resistance and systemic metastasis. Breast cancer is the first human carcinoma in which a subpopulation of cells displaying a specific CD44+/CD24-/low/ESA+ antigenic phenotype was found to have TIC properties. However, CD44+/CD24-/low/ESA+ is not a universal marker phenotype of TICs in all breast cancer subtypes. The aim of this study was to identify novel antigens with which to isolate the TIC population of the basal-A/basal-like breast cancer cell lines...
September 12, 2014: Molecular Cancer
https://www.readbyqxmd.com/read/25137474/retraction-interleukin-17-acts-in-synergy-with-b-cell-activating-factor-to-influence-b-cell-biology-and-the-pathophysiology-of-systemic-lupus-erythematosus
#17
(no author information available yet)
No abstract text is available yet for this article.
September 2014: Nature Immunology
https://www.readbyqxmd.com/read/25114847/epithelial-mesenchymal-transition-transcription-factors-and-mirnas-plastic-surgeons-of-breast-cancer
#18
REVIEW
Caroline Moyret-Lalle, Emmanuelle Ruiz, Alain Puisieux
Growing evidence suggests that breast cancer cell plasticity arises due to a partial reactivation of epithelial-mesenchymal transition (EMT) programs in order to give cells pluripotency, leading to a stemness-like phenotype. A complete EMT would be a dead end program that would render cells unable to fully metastasize to distant organs. Evoking the EMT-mesenchymal-to-epithelial transition (MET) cascade promotes successful colonization of distal target tissues. It is unlikely that direct reprogramming or trans-differentiation without passing through a pluripotent stage would be the preferred mechanism during tumor progression...
August 10, 2014: World Journal of Clinical Oncology
https://www.readbyqxmd.com/read/24875735/oncogenic-roles-of-emt-inducing-transcription-factors
#19
REVIEW
Alain Puisieux, Thomas Brabletz, Julie Caramel
The plasticity of cancer cells underlies their capacity to adapt to the selective pressures they encounter during tumour development. Aberrant reactivation of epithelial-mesenchymal transition (EMT), an essential embryonic process, can promote cancer cell plasticity and fuel both tumour initiation and metastatic spread. Here we discuss the roles of EMT-inducing transcription factors in creating a pro-tumorigenic setting characterized by an intrinsic ability to withstand oncogenic insults through the mitigation of p53-dependent oncosuppressive functions and the gain of stemness-related properties...
June 2014: Nature Cell Biology
https://www.readbyqxmd.com/read/24638100/snail-family-members-unequally-trigger-emt-and-thereby-differ-in-their-ability-to-promote-the-neoplastic-transformation-of-mammary-epithelial-cells
#20
Baptiste Gras, Laurent Jacqueroud, Anne Wierinckx, Christelle Lamblot, Frédérique Fauvet, Joël Lachuer, Alain Puisieux, Stéphane Ansieau
By fostering cell commitment to the epithelial-to-mesenchymal transition (EMT), SNAIL proteins endow cells with motility, thereby favoring the metastatic spread of tumor cells. Whether the phenotypic change additionally facilitates tumor initiation has never been addressed. Here we demonstrate that when a SNAIL protein is ectopically produced in non-transformed mammary epithelial cells, the cells are protected from anoikis and proliferate under low-adherence conditions: a hallmark of cancer cells. The three SNAIL proteins show unequal oncogenic potential, strictly correlating with their ability to promote EMT...
2014: PloS One
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