MED12 Alterations in Both Human Benign and Malignant Uterine Soft Tissue Tumors
The relationship between benign uterine leiomyomas and their malignant counterparts, i.e. leiomyosarcomas and smooth muscle tumors of uncertain malignant potential (STUMP), is still poorly understood. The idea that a leiomyosarcoma could derive from a leiomyoma is still controversial. Recently MED12...
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| Vydáno v: | PloS one Ročník 7; číslo 6; s. e40015 |
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| Hlavní autoři: | , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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United States
Public Library of Science
29.06.2012
Public Library of Science (PLoS) |
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| ISSN: | 1932-6203, 1932-6203 |
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| Abstract | The relationship between benign uterine leiomyomas and their malignant counterparts, i.e. leiomyosarcomas and smooth muscle tumors of uncertain malignant potential (STUMP), is still poorly understood. The idea that a leiomyosarcoma could derive from a leiomyoma is still controversial. Recently MED12 mutations have been reported in uterine leiomyomas. In this study we asked whether such mutations could also be involved in leiomyosarcomas and STUMP oncogenesis. For this purpose we examined 33 uterine mesenchymal tumors by sequencing the hot-spot mutation region of MED12. We determined that MED12 is altered in 66.6% of typical leiomyomas as previously reported but also in 11% of STUMP and 20% of leiomyosarcomas. The mutated allele is predominantly expressed in leiomyomas and STUMP. Interestingly all classical leiomyomas exhibit MED12 protein expression while 40% of atypical leiomyomas, 50% of STUMP and 80% of leiomyosarcomas (among them the two mutated ones) do not express MED12. All these tumors without protein expression exhibit complex genomic profiles. No mutations and no expression loss were identified in an additional series of 38 non-uterine leiomyosarcomas. MED12 mutations are not exclusive to leiomyomas but seem to be specific to uterine malignancies. A previous study has suggested that MED12 mutations in leiomyomas could lead to Wnt/β-catenin pathway activation however our immunohistochemistry results show that there is no association between MED12 status and β-catenin nuclear/cytoplasmic localization. Collectively, our results show that subgroups of benign and malignant tumors share a common genetics. We propose here that MED12 alterations could be implicated in the development of smooth muscle tumor and that its expression could be inhibited in malignant tumors. |
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| AbstractList | The relationship between benign uterine leiomyomas and their malignant counterparts, i.e. leiomyosarcomas and smooth muscle tumors of uncertain malignant potential (STUMP), is still poorly understood. The idea that a leiomyosarcoma could derive from a leiomyoma is still controversial. Recently MED12 mutations have been reported in uterine leiomyomas. In this study we asked whether such mutations could also be involved in leiomyosarcomas and STUMP oncogenesis. For this purpose we examined 33 uterine mesenchymal tumors by sequencing the hot-spot mutation region of MED12. We determined that MED12 is altered in 66.6% of typical leiomyomas as previously reported but also in 11% of STUMP and 20% of leiomyosarcomas. The mutated allele is predominantly expressed in leiomyomas and STUMP. Interestingly all classical leiomyomas exhibit MED12 protein expression while 40% of atypical leiomyomas, 50% of STUMP and 80% of leiomyosarcomas (among them the two mutated ones) do not express MED12. All these tumors without protein expression exhibit complex genomic profiles. No mutations and no expression loss were identified in an additional series of 38 non-uterine leiomyosarcomas. MED12 mutations are not exclusive to leiomyomas but seem to be specific to uterine malignancies. A previous study has suggested that MED12 mutations in leiomyomas could lead to Wnt/β-catenin pathway activation however our immunohistochemistry results show that there is no association between MED12 status and β-catenin nuclear/cytoplasmic localization. Collectively, our results show that subgroups of benign and malignant tumors share a common genetics. We propose here that MED12 alterations could be implicated in the development of smooth muscle tumor and that its expression could be inhibited in malignant tumors. The relationship between benign uterine leiomyomas and their malignant counterparts, i.e. leiomyosarcomas and smooth muscle tumors of uncertain malignant potential (STUMP), is still poorly understood. The idea that a leiomyosarcoma could derive from a leiomyoma is still controversial. Recently MED12 mutations have been reported in uterine leiomyomas. In this study we asked whether such mutations could also be involved in leiomyosarcomas and STUMP oncogenesis. For this purpose we examined 33 uterine mesenchymal tumors by sequencing the hot-spot mutation region of MED12. We determined that MED12 is altered in 66.6% of typical leiomyomas as previously reported but also in 11% of STUMP and 20% of leiomyosarcomas. The mutated allele is predominantly expressed in leiomyomas and STUMP. Interestingly all classical leiomyomas exhibit MED12 protein expression while 40% of atypical leiomyomas, 50% of STUMP and 80% of leiomyosarcomas (among them the two mutated ones) do not express MED12. All these tumors without protein expression exhibit complex genomic profiles. No mutations and no expression loss were identified in an additional series of 38 non-uterine leiomyosarcomas. MED12 mutations are not exclusive to leiomyomas but seem to be specific to uterine malignancies. A previous study has suggested that MED12 mutations in leiomyomas could lead to Wnt/[beta]-catenin pathway activation however our immunohistochemistry results show that there is no association between MED12 status and [beta]-catenin nuclear/cytoplasmic localization. Collectively, our results show that subgroups of benign and malignant tumors share a common genetics. We propose here that MED12 alterations could be implicated in the development of smooth muscle tumor and that its expression could be inhibited in malignant tumors. The relationship between benign uterine leiomyomas and their malignant counterparts, i.e. leiomyosarcomas and smooth muscle tumors of uncertain malignant potential (STUMP), is still poorly understood. The idea that a leiomyosarcoma could derive from a leiomyoma is still controversial. Recently MED12 mutations have been reported in uterine leiomyomas. In this study we asked whether such mutations could also be involved in leiomyosarcomas and STUMP oncogenesis. For this purpose we examined 33 uterine mesenchymal tumors by sequencing the hot-spot mutation region of MED12. We determined that MED12 is altered in 66.6% of typical leiomyomas as previously reported but also in 11% of STUMP and 20% of leiomyosarcomas. The mutated allele is predominantly expressed in leiomyomas and STUMP. Interestingly all classical leiomyomas exhibit MED12 protein expression while 40% of atypical leiomyomas, 50% of STUMP and 80% of leiomyosarcomas (among them the two mutated ones) do not express MED12. All these tumors without protein expression exhibit complex genomic profiles. No mutations and no expression loss were identified in an additional series of 38 non-uterine leiomyosarcomas. MED12 mutations are not exclusive to leiomyomas but seem to be specific to uterine malignancies. A previous study has suggested that MED12 mutations in leiomyomas could lead to Wnt/β-catenin pathway activation however our immunohistochemistry results show that there is no association between MED12 status and β-catenin nuclear/cytoplasmic localization. Collectively, our results show that subgroups of benign and malignant tumors share a common genetics. We propose here that MED12 alterations could be implicated in the development of smooth muscle tumor and that its expression could be inhibited in malignant tumors.The relationship between benign uterine leiomyomas and their malignant counterparts, i.e. leiomyosarcomas and smooth muscle tumors of uncertain malignant potential (STUMP), is still poorly understood. The idea that a leiomyosarcoma could derive from a leiomyoma is still controversial. Recently MED12 mutations have been reported in uterine leiomyomas. In this study we asked whether such mutations could also be involved in leiomyosarcomas and STUMP oncogenesis. For this purpose we examined 33 uterine mesenchymal tumors by sequencing the hot-spot mutation region of MED12. We determined that MED12 is altered in 66.6% of typical leiomyomas as previously reported but also in 11% of STUMP and 20% of leiomyosarcomas. The mutated allele is predominantly expressed in leiomyomas and STUMP. Interestingly all classical leiomyomas exhibit MED12 protein expression while 40% of atypical leiomyomas, 50% of STUMP and 80% of leiomyosarcomas (among them the two mutated ones) do not express MED12. All these tumors without protein expression exhibit complex genomic profiles. No mutations and no expression loss were identified in an additional series of 38 non-uterine leiomyosarcomas. MED12 mutations are not exclusive to leiomyomas but seem to be specific to uterine malignancies. A previous study has suggested that MED12 mutations in leiomyomas could lead to Wnt/β-catenin pathway activation however our immunohistochemistry results show that there is no association between MED12 status and β-catenin nuclear/cytoplasmic localization. Collectively, our results show that subgroups of benign and malignant tumors share a common genetics. We propose here that MED12 alterations could be implicated in the development of smooth muscle tumor and that its expression could be inhibited in malignant tumors. |
| Audience | Academic |
| Author | Ribeiro, Agnès Lagarde, Pauline Coindre, Jean-Michel Neuville, Agnès Velasco, Valérie Floquet, Anne Stoeckle, Eberhard Pérot, Gaëlle Croce, Sabrina MacGrogan, Gaëtan Chibon, Frédéric |
| AuthorAffiliation | 5 Department of Surgery, Institut Bergonié Cancer Institute, Bordeaux, France Ospedale Pediatrico Bambino Gesu', Italy 2 Department of Pathology, Institut Bergonié Cancer Institute, Bordeaux, France 3 Department of Molecular Pathology, Institut Bergonié Cancer Institute, Bordeaux, France 6 Department of Medical Oncology, Institut Bergonié Cancer Institute, Bordeaux, France 4 University Victor Segalen, Bordeaux, France 1 INSERM U916, Institut Bergonié Cancer Institute, Bordeaux, France |
| AuthorAffiliation_xml | – name: 6 Department of Medical Oncology, Institut Bergonié Cancer Institute, Bordeaux, France – name: 1 INSERM U916, Institut Bergonié Cancer Institute, Bordeaux, France – name: 4 University Victor Segalen, Bordeaux, France – name: 2 Department of Pathology, Institut Bergonié Cancer Institute, Bordeaux, France – name: 5 Department of Surgery, Institut Bergonié Cancer Institute, Bordeaux, France – name: 3 Department of Molecular Pathology, Institut Bergonié Cancer Institute, Bordeaux, France – name: Ospedale Pediatrico Bambino Gesu', Italy |
| Author_xml | – sequence: 1 givenname: Gaëlle surname: Pérot fullname: Pérot, Gaëlle – sequence: 2 givenname: Sabrina surname: Croce fullname: Croce, Sabrina – sequence: 3 givenname: Agnès surname: Ribeiro fullname: Ribeiro, Agnès – sequence: 4 givenname: Pauline surname: Lagarde fullname: Lagarde, Pauline – sequence: 5 givenname: Valérie surname: Velasco fullname: Velasco, Valérie – sequence: 6 givenname: Agnès surname: Neuville fullname: Neuville, Agnès – sequence: 7 givenname: Jean-Michel surname: Coindre fullname: Coindre, Jean-Michel – sequence: 8 givenname: Eberhard surname: Stoeckle fullname: Stoeckle, Eberhard – sequence: 9 givenname: Anne surname: Floquet fullname: Floquet, Anne – sequence: 10 givenname: Gaëtan surname: MacGrogan fullname: MacGrogan, Gaëtan – sequence: 11 givenname: Frédéric surname: Chibon fullname: Chibon, Frédéric |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22768200$$D View this record in MEDLINE/PubMed https://hal.science/hal-04933513$$DView record in HAL |
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| ContentType | Journal Article |
| Copyright | COPYRIGHT 2012 Public Library of Science 2012 Pérot et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. Distributed under a Creative Commons Attribution 4.0 International License Pérot et al. 2012 |
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| DocumentTitleAlternate | MED12 Alterations in Uterine Soft Tissue Tumors |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Conceived and designed the experiments: GP SC FC. Performed the experiments: GP AR PL VV. Analyzed the data: GP SC FC. Wrote the paper: GP SC FC. Diagnosis and acquisition of data: SC AN JMC ES AF GM. |
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| SubjectTerms | Alleles Alterations Base Sequence Benign beta Catenin - metabolism Biology Breast cancer Cancer Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - pathology Deoxyribonucleic acid Development and progression DNA DNA Mutational Analysis DNA, Complementary - genetics Female Fibroids Gene expression Gene Expression Regulation, Neoplastic Gene mutation Genetics Genome, Human - genetics Hot spots Humans Immunohistochemistry Leiomyoma - genetics Leiomyoma - pathology Life Sciences Localization Mediator Complex - genetics Mediator Complex - metabolism Medicine Mesenchyme MicroRNAs Molecular Sequence Data Muscles Muscular system Mutation Mutation - genetics Mutation hot spots Pancreatic cancer Pathology Protein Transport RNA polymerase Sequences Smooth muscle Smooth Muscle Tumor - genetics Smooth Muscle Tumor - pathology Soft Tissue Neoplasms - genetics Soft Tissue Neoplasms - pathology Subgroups Tumorigenesis Tumors Uterine cancer Uterine Neoplasms - genetics Uterine Neoplasms - pathology Uterus Wnt protein Wnt Signaling Pathway - genetics β-Catenin |
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| Title | MED12 Alterations in Both Human Benign and Malignant Uterine Soft Tissue Tumors |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/22768200 https://www.proquest.com/docview/1325036098 https://www.proquest.com/docview/1024094398 https://hal.science/hal-04933513 https://pubmed.ncbi.nlm.nih.gov/PMC3386951 https://doaj.org/article/3aeb970673f74ea0b16288fd73cedc24 http://dx.doi.org/10.1371/journal.pone.0040015 |
| Volume | 7 |
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