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8 results on '"MESH: Twist Transcription Factor"'

1. Deregulation of TWIST-1 in the CD34+ compartment represents a novel prognostic factor in chronic myeloid leukemia

Author

Franck E. Nicolini, Sandrine Hayette, Ghassan Hamdan, Sandrine Jeanpierre, Francois-Xavier Mahon, Karen Sagorny, Alain Puisieux, Erika Cosset, Thibault Voeltzel, Charles Dumontet, Véronique Maguer-Satta, Laboratoire de Biophotonique et Pharmacologie - UMR 7213 ( LBP ), Centre National de la Recherche Scientifique ( CNRS ) -Réseau nanophotonique et optique, Université de Strasbourg ( UNISTRA ) -Université de Haute-Alsace (UHA) Mulhouse - Colmar ( Université de Haute-Alsace (UHA) ) -Centre National de la Recherche Scientifique ( CNRS ) -Université de Strasbourg ( UNISTRA ) -Université de Haute-Alsace (UHA) Mulhouse - Colmar ( Université de Haute-Alsace (UHA) ) -Centre National de la Recherche Scientifique ( CNRS ), Université Claude Bernard Lyon 1 ( UCBL ), Université de Lyon, Equipe 11, Centre Léon Bérard [Lyon]-Centre de Recherche en Cancérologie de Lyon ( CRCL ), Université de Lyon-Université de Lyon-Centre Léon Bérard [Lyon]-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ) -Université Claude Bernard Lyon 1 ( UCBL ), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Oncogénèse et progression tumorale, Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 ( UCBL ), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 ( UCBL ), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre de Recherche en Cancérologie de Lyon ( CRCL ), Université de Lyon-Université de Lyon-Centre Léon Bérard [Lyon]-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Laboratoire de Biologie Moléculaire, Hospices Civils de Lyon ( HCL ), Transfert de Genes a Visee Therapeutique Dans les Cellules Souches, Université Bordeaux Segalen - Bordeaux 2-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Equipe 14, Centre de Recherche en Cancérologie de Lyon ( CRCL ), Université de Lyon-Université de Lyon-Centre Léon Bérard [Lyon]-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), equipe 2, Institut Universitaire de France ( IUF ), Ministère de l'Éducation nationale, de l’Enseignement supérieur et de la Recherche ( M.E.N.E.S.R. ) -Ministère de l'Éducation nationale, de l’Enseignement supérieur et de la Recherche ( M.E.N.E.S.R. ) -Centre de Recherche en Cancérologie de Lyon ( CRCL ), Laboratoire de Biophotonique et Pharmacologie - UMR 7213 (LBP), Centre National de la Recherche Scientifique (CNRS)-Réseau nanophotonique et optique, Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA))-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA)), Université Claude Bernard Lyon 1 (UCBL), Centre Léon Bérard [Lyon]-Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hospices Civils de Lyon (HCL), Université Bordeaux Segalen - Bordeaux 2-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Institut Universitaire de France (IUF), and Ministère de l'Education nationale, de l’Enseignement supérieur et de la Recherche (M.E.N.E.S.R.)-Ministère de l'Education nationale, de l’Enseignement supérieur et de la Recherche (M.E.N.E.S.R.)-Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL)

Subjects
MESH : RNA, Messenger, MESH: Piperazines, MESH : Pyrimidines, Antigens, CD34, Drug resistance, MESH : RNA, Small Interfering, Biochemistry, Piperazines, [ SDV.CAN ] Life Sciences [q-bio]/Cancer, 0302 clinical medicine, MESH: Reverse Transcriptase Polymerase Chain Reaction, hemic and lymphatic diseases, MESH: RNA, Small Interfering, MESH: Protein Kinase Inhibitors, RNA, Small Interfering, 0303 health sciences, Reverse Transcriptase Polymerase Chain Reaction, MESH : Reverse Transcriptase Polymerase Chain Reaction, Nuclear Proteins, MESH: Twist Transcription Factor, Myeloid leukemia, MESH: Gene Expression Regulation, Neoplastic, Hematology, MESH: Drug Resistance, Neoplasm, 3. Good health, Gene Expression Regulation, Neoplastic, Leukemia, MESH : Drug Resistance, Neoplasm, 030220 oncology & carcinogenesis, Benzamides, Imatinib Mesylate, MESH : Antigens, CD34, Tyrosine kinase, medicine.drug, MESH: Cell Line, Tumor, MESH : Gene Expression Regulation, Neoplastic, Immunology, [SDV.CAN]Life Sciences [q-bio]/Cancer, Biology, 03 medical and health sciences, Myelogenous, Cell Line, Tumor, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, medicine, Humans, RNA, Messenger, Protein Kinase Inhibitors, MESH: RNA, Messenger, 030304 developmental biology, MESH: Humans, Oncogene, MESH : Cell Line, Tumor, Twist-Related Protein 1, MESH : Twist Transcription Factor, MESH : Humans, MESH : Nuclear Proteins, Imatinib, MESH: Antigens, CD34, Cell Biology, MESH : Protein Kinase Inhibitors, medicine.disease, respiratory tract diseases, Pyrimidines, Imatinib mesylate, MESH: Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Drug Resistance, Neoplasm, MESH: Pyrimidines, MESH : Piperazines, Cancer research, MESH : Leukemia, Myelogenous, Chronic, BCR-ABL Positive, MESH: Nuclear Proteins
Abstract

The mechanisms of resistance to tyrosine kinase inhibitors (TKIs) in chronic myeloid leukemia (CML) often remain obscure. Analysis of patient samples during disease progression revealed the up-regulation of the oncogene TWIST-1, also measured in primary samples from TKI-resistant patients. Moreover, we found that TWIST-1 was overexpressed in CML diagnostic samples of patients who later developed cytogenetic resistance to imatinib, even those without any detectable resistance mechanism. We confirmed the up-regulation of TWIST-1 at both RNA and protein levels in imatinib-resistant cell lines, irrespective of any other resistance mechanism. Analysis with specific small interfering RNA suggested TWIST-1 involvement in the resistance phenotype. Finally, the kinetics of TWIST-1 expression during the individual medical histories of CML patients indicated that TWIST-1 expression is down-regulated by TKIs and up-regulated with TKI resistance. We hypothesize that the overexpression of the TWIST-1 oncogene represents a novel key prognostic factor potentially useful for optimizing CML management in the TKI era.

Published
2011
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2. A Possible Inflammatory Role of Twist1 in Human White Adipocytes

Author

Amanda T. Pettersson, Anne Bouloumié, Mikael Rydén, Peter Arner, Ingrid Dahlman, Niklas Mejhert, Jurga Laurencikiene, Erik Näslund, Simon, Marie Francoise, Department of medicine [Stockholm], Karolinska Institutet [Stockholm]-Karolinska University Hospital [Stockholm], Division of Surgery, Department of Clinical Sciences, Karolinska Institutet [Stockholm]-Danderyds sjukhus = Danderyd University Hospital, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), and Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Male, MESH: Oxidation-Reduction, Small interfering RNA, Endocrinology, Diabetes and Metabolism, Cellular differentiation, Adipocytes, White, Palmitates, Gene Expression, Adipose tissue, White adipose tissue, MESH: Down-Regulation, Mice, chemistry.chemical_compound, 0302 clinical medicine, Genes, Reporter, Adipocyte, MESH: RNA, Small Interfering, Gene expression, MESH: Animals, Carbon Radioisotopes, RNA, Small Interfering, Promoter Regions, Genetic, MESH: Carbon Radioisotopes, Beta oxidation, Chemokine CCL2, 0303 health sciences, MESH: Middle Aged, Nuclear Proteins, MESH: Twist Transcription Factor, Middle Aged, MESH: Adiponectin, Cell biology, 030220 oncology & carcinogenesis, Original Article, Female, Adiponectin, Oxidation-Reduction, Adult, medicine.medical_specialty, MESH: Gene Expression, animal structures, Lipolysis, Down-Regulation, Biology, 03 medical and health sciences, 3T3-L1 Cells, Internal medicine, MESH: Promoter Regions, Genetic, Internal Medicine, medicine, Animals, Humans, MESH: Lipolysis, MESH: Mice, MESH: Chemokine CCL2, 030304 developmental biology, MESH: Humans, Interleukin-6, Tumor Necrosis Factor-alpha, Twist-Related Protein 1, MESH: Genes, Reporter, MESH: Adult, MESH: Palmitates, MESH: Interleukin-6, MESH: 3T3-L1 Cells, MESH: Male, MESH: Adipocytes, White, Metabolism, Endocrinology, chemistry, MESH: Tumor Necrosis Factor-alpha, MESH: Nuclear Proteins, MESH: Female
Abstract

OBJECTIVE Twist1 is a transcription factor that is highly expressed in murine brown and white adipose tissue (WAT) and negatively regulates fatty acid oxidation in mice. The role of twist1 in WAT is not known and was therefore examined. RESEARCH DESIGN AND METHODS The expression of twist1 was determined by quantitative real-time PCR in different tissues and in different cell types within adipose tissue. The effect of twist1 small interfering RNA on fatty acid oxidation, lipolysis, adipokine secretion, and mRNA expression was determined in human adipocytes. The interaction between twist1 and specific promoters in human adipocytes was investigated by chromatin immunoprecipitation (ChIP) and reporter assays. RESULTS Twist1 was highly expressed in human WAT compared with a set of other tissues and found predominantly in adipocytes. Twist1 levels increased during in vitro differentiation of human preadipocytes. Gene silencing of twist1 in human white adipocytes had no effect on lipolysis or glucose transport. Unexpectedly, and in contrast with results in mice, twist1 RNA interference reduced fatty acid oxidation. Furthermore, the expression and secretion of the inflammatory factors tumor necrosis factor-α, interleukin-6, and monocyte chemoattractant protein-1 were downregulated by twist1 silencing. ChIP and reporter assays confirmed twist1 interaction with the promoters of these genes. CONCLUSIONS Twist1 may play a role in inflammation of human WAT because it can regulate the expression and secretion of inflammatory adipokines via direct transcriptional effects in white adipocytes. Furthermore, twist1 may, in contrast to findings in mice, be a positive regulator of fatty acid oxidation in human white adipocytes.

Published
2009
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3. Revisiting the canonical tumour progression model

Author

Anne-Pierre Morel, George W. Hinkal, Stéphane Ansieau, Alain Puisieux, equipe 2, Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Oncogénèse et progression tumorale, Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Léon Bérard [Lyon]-Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Claude Bernard Lyon 1 (UCBL), Centre de Recherche en Cancérologie de Lyon ( CRCL ), Université Claude Bernard Lyon 1 ( UCBL ), Université de Lyon-Université de Lyon-Centre Léon Bérard [Lyon]-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ) -Université Claude Bernard Lyon 1 ( UCBL ), Université de Lyon-Université de Lyon-Centre Léon Bérard [Lyon]-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 ( UCBL ), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Centre Léon Bérard [Lyon]-Centre de Recherche en Cancérologie de Lyon ( CRCL ), and Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS )

Subjects
Pathology, MESH: Oncogenes, MESH : Models, Biological, MESH : Tumor Escape, Metastasis, [ SDV.CAN ] Life Sciences [q-bio]/Cancer, Twist transcription factor, 0302 clinical medicine, Cell Movement, Neoplasms, MESH : Cell Movement, MESH: Neoplasms, Twist, MESH: Models, Theoretical, MESH: Cell Movement, ComputingMilieux_MISCELLANEOUS, 0303 health sciences, MESH: Twist Transcription Factor, General Medicine, MESH : Epithelial-Mesenchymal Transition, Cell Transformation, Neoplastic, 030220 oncology & carcinogenesis, Disease Progression, MESH: Tumor Escape, MESH: Disease Progression, medicine.medical_specialty, Epithelial-Mesenchymal Transition, [SDV.CAN]Life Sciences [q-bio]/Cancer, Biology, Models, Biological, 03 medical and health sciences, Text mining, medicine, Humans, Epithelial–mesenchymal transition, 030304 developmental biology, MESH : Oncogenes, MESH: Humans, business.industry, MESH : Models, Theoretical, Disease progression, Twist-Related Protein 1, MESH : Twist Transcription Factor, MESH : Humans, MESH: Models, Biological, MESH : Cell Transformation, Neoplastic, Cell movement, Oncogenes, MESH : Disease Progression, Models, Theoretical, medicine.disease, MESH : Neoplasms, MESH: Epithelial-Mesenchymal Transition, Tumor Escape, MESH: Cell Transformation, Neoplastic, Cancer research, business
Abstract

International audience

Published
2011
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4. Mutant p53(R175H) upregulates Twist1 expression and promotes epithelial-mesenchymal transition in immortalized prostate cells

Author

Mariana Brait, Yosef Buganim, Camila Avivi, Sandrine Valsesia-Wittmann, Perry Stambolsky, Iris Barshack, David Sidransky, A. Shelly, Varda Rotter, Adi Zundelevich, Alain Puisieux, Ira Kogan-Sakin, Einav Nili Gal-Yam, Naomi Goldfinger, Hilla Solomon, Iris Kamer, Alina Molchadsky, Shalom Madar, Eytan Domany, Yuval Tabach, Department of Molecular Cell Biology [Rehovot], Weizmann Institute of Science [Rehovot, Israël], Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), equipe 2, Centre Léon Bérard [Lyon]-Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), and Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Claude Bernard Lyon 1 (UCBL)

Subjects
Male, Mutant, medicine.disease_cause, Epigenesis, Genetic, Histones, 0302 clinical medicine, Gene expression, MESH: Up-Regulation, MESH: Epigenesis, Genetic, Promoter Regions, Genetic, MESH: Tumor Suppressor Protein p53, Cell Line, Transformed, Polycomb Repressive Complex 1, MESH: Histones, 0303 health sciences, Mutation, Nuclear Proteins, MESH: Twist Transcription Factor, MESH: Amino Acid Substitution, Up-Regulation, MESH: Repressor Proteins, 030220 oncology & carcinogenesis, MESH: Polycomb Repressive Complex 1, Epithelial-Mesenchymal Transition, MESH: Cell Line, Tumor, MESH: Mutation, [SDV.CAN]Life Sciences [q-bio]/Cancer, Biology, 03 medical and health sciences, DU145, Downregulation and upregulation, Cell Line, Tumor, Proto-Oncogene Proteins, MESH: Promoter Regions, Genetic, medicine, Humans, Epithelial–mesenchymal transition, MESH: Cell Line, Transformed, Molecular Biology, 030304 developmental biology, Original Paper, MESH: Humans, Twist-Related Protein 1, Prostatic Neoplasms, Cell Biology, MESH: Male, Repressor Proteins, MESH: Proto-Oncogene Proteins, MESH: Epithelial-Mesenchymal Transition, Amino Acid Substitution, Cell culture, MESH: Prostatic Neoplasms, Cancer cell, Immunology, Cancer research, Tumor Suppressor Protein p53, MESH: Nuclear Proteins
Abstract

International audience; A mutation within one allele of the p53 tumor suppressor gene can inactivate the remaining wild-type allele in a dominant-negative manner and in some cases can exert an additional oncogenic activity, known as mutant p53 'gain of function' (GOF). To study the role of p53 mutations in prostate cancer and to discriminate between the dominant-negative effect and the GOF activity of mutant p53, we measured, using microarrays, the expression profiles of three immortalized prostate epithelial cultures expressing wild-type, inactivated p53 or mutated p53. Analysis of these gene expression profiles showed that both inactivated p53 and p53(R175H) mutant expression resulted in the upregulation of cell cycle progression genes. A second group, which was upregulated exclusively by mutant p53(R175H), was predominantly enriched in developmental genes. This group of genes included the Twist1, a regulator of metastasis and epithelial-mesenchymal transition (EMT). Twist1 levels were also elevated in metastatic prostate cancer-derived cell line DU145, in immortalized lung fibroblasts and in a subset of lung cancer samples, all in a mutant p53-dependent manner. p53(R175H) mutant bearing immortalized epithelial cells showed typical features of EMT, such as higher expression of mesenchymal markers, lower expression of epithelial markers and enhanced invasive properties in vitro. The mechanism by which p53(R175H) mutant induces Twist1 expression involves alleviation of the epigenetic repression. Our data suggest that Twist1 expression might be upregulated following p53 mutation in cancer cells.

Published
2011
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5. [An alternate model of tumoral progression]

Author

Ansieau , Stéphane, Puisieux , Alain, equipe 2, Centre de Recherche en Cancérologie de Lyon ( CRCL ), Université Claude Bernard Lyon 1 ( UCBL ), Université de Lyon-Université de Lyon-Centre Léon Bérard [Lyon]-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ) -Université Claude Bernard Lyon 1 ( UCBL ), Université de Lyon-Université de Lyon-Centre Léon Bérard [Lyon]-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Institut Universitaire de France ( IUF ), Ministère de l'Éducation nationale, de l’Enseignement supérieur et de la Recherche ( M.E.N.E.S.R. ) -Ministère de l'Éducation nationale, de l’Enseignement supérieur et de la Recherche ( M.E.N.E.S.R. ) -Centre de Recherche en Cancérologie de Lyon ( CRCL ), Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Universitaire de France (IUF), and Ministère de l'Education nationale, de l’Enseignement supérieur et de la Recherche (M.E.N.E.S.R.)-Ministère de l'Education nationale, de l’Enseignement supérieur et de la Recherche (M.E.N.E.S.R.)-Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL)

Subjects
MESH : Cell Aging, [SDV.CAN]Life Sciences [q-bio]/Cancer, Apoptosis, MESH : Models, Biological, Environment, Models, Biological, [ SDV.CAN ] Life Sciences [q-bio]/Cancer, Animals, Humans, MESH: Animals, Neoplasm Metastasis, MESH: Environment, Cellular Senescence, MESH: Humans, MESH: Apoptosis, Twist-Related Protein 1, MESH : Humans, MESH : Twist Transcription Factor, MESH: Models, Biological, MESH: Twist Transcription Factor, MESH : Cell Transformation, Neoplastic, MESH: Neoplasm Metastasis, MESH : Environment, Cell Transformation, Neoplastic, MESH: Cell Aging, MESH: Cell Transformation, Neoplastic, MESH : Neoplasm Metastasis, MESH : Animals, MESH : Apoptosis
Abstract

International audience; Tumor development is usually described as the result of successive waves of genetic and epigenetic changes and of Darwinian selections that allow the progressive emergence of cells with proliferation and survival advantages. According to this model of tumoral progression, the acquisition of metastatic properties is perceived as a late stage-induced response to environmentally damaging conditions in the tumor, in particular oxygen and nutriment lack. Analyzing the consequences linked to the reactivation of embryonic programmes leads, for some cancer types, to question the linearity of this model, by showing that the dissemination of cancerous or precancerous cells may begin as early as the lesions convert from a premalignant to a malignant state. We propose to review the main findings that brought about these conclusions and to discuss what consequences they might have.

Published
2011
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6. TWISTing an embryonic transcription factor into an oncoprotein

Author

Stéphane Ansieau, Jérémy Bastid, Anne-Pierre Morel, George W. Hinkal, Alain Puisieux, equipe 2, Centre de Recherche en Cancérologie de Lyon ( CRCL ), Université Claude Bernard Lyon 1 ( UCBL ), Université de Lyon-Université de Lyon-Centre Léon Bérard [Lyon]-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ) -Université Claude Bernard Lyon 1 ( UCBL ), Université de Lyon-Université de Lyon-Centre Léon Bérard [Lyon]-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Oncogénèse et progression tumorale, Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 ( UCBL ), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Cancer Research, Poor prognosis, [SDV.CAN]Life Sciences [q-bio]/Cancer, Biology, medicine.disease_cause, Bioinformatics, [ SDV.CAN ] Life Sciences [q-bio]/Cancer, 03 medical and health sciences, MESH: Oncogene Proteins, 0302 clinical medicine, Genetics, medicine, Animals, Humans, MESH : Embryonic Stem Cells, MESH: Animals, MESH: Embryonic Stem Cells, Twist Protein, Molecular Biology, Transcription factor, Embryonic Stem Cells, 030304 developmental biology, Oncogene Proteins, 0303 health sciences, MESH: Humans, MESH : Oncogene Proteins, Twist-Related Protein 1, MESH : Humans, MESH : Twist Transcription Factor, MESH: Twist Transcription Factor, Embryonic stem cell, 3. Good health, 030220 oncology & carcinogenesis, Cancer research, MESH : Animals, Carcinogenesis
Abstract

International audience; Over the past decade, the reactivation of TWIST embryonic transcription factors has been described as a frequent event and a marker of poor prognosis in an impressive array of human cancers. Growing evidence now supports the premise that these cancers hijack TWIST's embryonic functions, granting oncogenic and metastatic properties. In this review, we report on the history and recent breakthroughs in understanding TWIST protein functions and the emerging role of the associated epithelial-mesenchymal transition (EMT) in tumorigenesis. We then broaden the discussion to address the general contribution of reactivating embryonic programs in cancerogenesis.

Published
2010
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7. The expression of Twist has an impact on survival in human bladder cancer and is influenced by the smoking status

Author

Jean P. Thiery, Hugues Bittard, Marie E. Fondrevelle, Franck Monnien, Hervé Wallerand, Robert E. Reiter, Dominique Chopin, Bernadette Kantelip, Laboratoire d'anatomie pathologique [Besancon], Centre Hospitalier Régional Universitaire [Besançon] ( CHRU Besançon ) -Hôpital Jean Minjoz-Université de Franche-Comté ( UFC ), 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 Néphrologie et Urologie, Centre Hospitalier Régional Universitaire [Besançon] ( CHRU Besançon ) -Hôpital Saint-Jacques, Service d'urologie, andrologie et transplantation rénale, Université Bordeaux Segalen - Bordeaux 2-CHU Bordeaux [Bordeaux]-Groupe hospitalier Pellegrin, Service d'Anatomie pathologique [CHRU Besançon], Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon), Carcinogénèse épithéliale : facteurs prédictifs et pronostiques - UFC (EA 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), and Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Hôpital Saint-Jacques

Subjects
Oncology, Male, Pathology, MESH : Immunohistochemistry, MESH : Aged, Kaplan-Meier Estimate, MESH: Cadherins, [ SDV.CAN ] Life Sciences [q-bio]/Cancer, MESH: Proportional Hazards Models, 0302 clinical medicine, MESH: Aged, 80 and over, MESH: Risk Factors, Risk Factors, MESH : Neoplasm Staging, MESH : Female, MESH: Kaplan-Meiers Estimate, Stage (cooking), MESH: Aged, Aged, 80 and over, 0303 health sciences, MESH: Middle Aged, MESH : Prognosis, Smoking, MESH: Twist Transcription Factor, Nuclear Proteins, Anatomical pathology, MESH: Neoplasm Staging, Middle Aged, Cadherins, Prognosis, Immunohistochemistry, MESH : Risk Factors, 3. Good health, MESH: Urinary Bladder Neoplasms, MESH : Smoking, MESH : Urinary Bladder Neoplasms, 030220 oncology & carcinogenesis, Disease Progression, MESH: Disease Progression, Female, MESH : Cadherins, medicine.medical_specialty, MESH: Smoking, Urology, MESH : Male, [SDV.CAN]Life Sciences [q-bio]/Cancer, MESH: Multivariate Analysis, MESH: Prognosis, 03 medical and health sciences, Internal medicine, medicine, Humans, MESH : Middle Aged, Epithelial–mesenchymal transition, Risk factor, MESH : Aged, 80 and over, 030304 developmental biology, Aged, Neoplasm Staging, Proportional Hazards Models, Bladder cancer, MESH: Humans, Proportional hazards model, business.industry, Twist-Related Protein 1, MESH : Twist Transcription Factor, MESH : Humans, Cancer, MESH : Multivariate Analysis, MESH : Nuclear Proteins, MESH: Immunohistochemistry, MESH : Kaplan-Meiers Estimate, MESH : Disease Progression, medicine.disease, MESH : Proportional Hazards Models, MESH: Male, Urinary Bladder Neoplasms, Multivariate Analysis, business, MESH: Nuclear Proteins, MESH: Female
Abstract

International audience; OBJECTIVES: Twist is considered as transcription factor that regulates epithelial mesenchymal transition (EMT) by at least inhibition of E-cadherin expression. EMT is a key event in the tumor invasion process. The purpose of this study is to investigate the expression of Twist but also those of E- and N-cadherin in human primary bladder tumor and to evaluate its prognostic value. As smoking cigarettes is a strong bladder cancer risk factor, we tried to evaluate the impact of the tobacco status on these molecular abnormalities. MATERIALS AND METHODS: To delineate on the oncogenic role for Twist in human bladder cancer, we evaluated the E- and N-cadherin but also Twist expression (n = 70) by immunohistochemistry. We evaluated the prognostic value of these expressions. Moreover, we tried to correlate these protein expressions to the smoking status of the patients. Overall survival (OS) and progression-free survival (PFS) were evaluated using the Kaplan-Meier method, and multivariate analysis was performed using the Cox proportional hazard analysis. RESULTS: Of the 70 bladder tumors, 28 (40%) cases were positive for Twist expression, 16 (23%) cases were negative for E-cadherin expression, and 12 (17%) were positive for N-cadherin expression. When categorized into negative vs. positive expression, Twist was associated with the stage (P = 0.001), the grade (P < 0.001), the progression (P = 0.02), and the E-cadherin expression (P = 0.01). Moreover, positive Twist expression clearly predicted poorer PFS (P = 0.02). In the multivariate analysis, both positive Twist expression and loss of E-cadherin expression were independent prognostic factors for PFS (P = 0.046 and P = 0.001, respectively) and only loss of E-cadherin expression for the OS (P < 0.001). We also demonstrated that almost 60% (16/28) of patients with Twist-positive expression were current smokers at the time of the diagnosis, corroborating the fact that smoking modulates the expression of EMT markers including Twist. CONCLUSION: Positive Twist expression may be a useful prognostic marker for patients with bladder cancer. Its expression seems to be correlated to the tobacco status of the patients.

Published
2009
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8. Frequent genomic abnormalities at TWIST in human pediatric osteosarcomas

Author

Marie-Pierre Gaub, Robert Quillet, Chantal Kalifa, Claudine Schmitt, Annie Babin-Boilletot, Fabienne Perrin-Schmitt, Natacha Entz-Werle, Marie-Dominique Tabone, Pierre Oudet, Hélène Pacquement, Laurence Brugiere, Jean-Claude Gentet, Perrine Berard-Marec, Corinne Stoetzel, Patrick Lutz, Institut de génétique et biologie moléculaire et cellulaire (IGBMC), Université Louis Pasteur - Strasbourg I-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut Curie [Paris], and Institut Curie

Subjects
Male, Cancer Research, Pathology, MESH: Osteosarcoma, MESH: Genetic Markers, medicine.disease_cause, Mesoderm, 0302 clinical medicine, MESH: Child, Gene duplication, Child, 0303 health sciences, MESH: Mesoderm, Osteosarcoma, MESH: Twist Transcription Factor, Nuclear Proteins, Cell Differentiation, MESH: Transcription Factors, MESH: Bone and Bones, MESH: Bone Neoplasms, 3. Good health, Real-time polymerase chain reaction, Oncology, 030220 oncology & carcinogenesis, MESH: Survival Analysis, Child, Preschool, Female, Sarcoma, MESH: Cell Differentiation, Adult, Genetic Markers, medicine.medical_specialty, MESH: Mutation, Adolescent, Locus (genetics), Bone Neoplasms, Biology, Bone and Bones, 03 medical and health sciences, medicine, Humans, Gene, 030304 developmental biology, MESH: Adolescent, MESH: Humans, MESH: Child, Preschool, Twist-Related Protein 1, Cytogenetics, MESH: Adult, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, medicine.disease, Survival Analysis, MESH: Male, Mutation, Cancer research, Carcinogenesis, MESH: Nuclear Proteins, MESH: Female, Transcription Factors
Abstract

International audience; The identification of genes as markers for chromosome aberrations in specific tumors might facilitate oncogenesis mechanism comprehension, cancer detection, prediction of clinical outcomes, and response to therapy. Previous physiologic and oncologic data identified the TWIST gene as a marker for mesodermal derivative and bone tissue differentiation, but its contribution to bone malignancies has not been investigated. In the present study, search for genomic alterations in high-grade pediatric osteosarcomas was focused on the 7p21 region, and more specifically on the TWIST gene. In a cohort of 74 patients, we observed by allelotyping that 31 of 68 informative tumors were rearranged at the TWIST locus. Among them, analysis by quantitative PCR (QPCR) revealed that, surprisingly, mostly deletions (22/68), but also amplifications (9/68), of the TWIST gene were detected. Furthermore, deletions at TWIST were statistically correlated to other molecular abnormalities, like alterations at the APC or c-kit loci, as well as to clinical features such as a poor outcome. This work shows that the TWIST gene seemed to be involved in high-grade pediatric osteosarcomas and is a new marker with a possible initial predictive value.

Published
2005
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