Targeted genomic analysis of Müllerian adenosarcoma
Müllerian adenosarcoma (MA) is a rare mixed mesenchymal tumour of the female genital tract, composed of malignant stroma and benign‐appearing epithelium. Sarcomatous overgrowth (SO) is the only established histological variable associated with higher stage and shorter survival. Specific molecular or...
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| Published in | The Journal of pathology Vol. 235; no. 1; pp. 37 - 49 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Chichester, UK
John Wiley & Sons, Ltd
01.01.2015
Wiley Subscription Services, Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0022-3417 1096-9896 1096-9896 |
| DOI | 10.1002/path.4442 |
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| Abstract | Müllerian adenosarcoma (MA) is a rare mixed mesenchymal tumour of the female genital tract, composed of malignant stroma and benign‐appearing epithelium. Sarcomatous overgrowth (SO) is the only established histological variable associated with higher stage and shorter survival. Specific molecular or immunohistochemistry (IHC) tools for the diagnosis of MA are lacking. Our goal was to study genomic mutations and copy number variations (CNVs) in MA to understand better its pathobiology, and develop specific diagnostic and prognostic tools. DNA was extracted from 20 samples of MA from 18 subjects (12 without SO and 6 with SO), including two in which areas of both typical MA histology and SO were independently tested. Samples were analysed using a targeted next‐generation sequencing assay interrogating exonic sequences of 275 cancer genes for mutations and CNVs as well as 91 introns across 30 genes for cancer‐associated rearrangements. The mean number of mutations in MA with SO (mean 9.7; range 3–14) did not differ significantly from that in MA without SO (mean 9.6; range 5–16). MA with SO had significantly higher mean numbers of gene‐level CNVs (24.6) compared to MA without SO (5; p = 0.0002). The most frequent amplification involved MDM2 and CDK4 (5/18; 28%), accompanied by focal CDK4 and MDM2 and diffuse HMGA2 expression using immunohistochemistry. MYBL1 amplification was seen in 4/18 (22%), predominantly in SO. Alterations in PIK3CA/AKT/PTEN pathway members were seen in 13/18 (72%). Notably, TP53 mutations were uncommon, present in only two cases with SO. Three out of 18 (17%) had mutations in ATRX, all associated with SO. No chromosomal rearrangements were identified. We have identified a number of recurrent genomic alterations in MA, including some associated with SO. Although further investigation of these findings is needed, confirmation of one or more may lead to new mechanistic insights and novel markers for this often difficult‐to‐diagnose tumour. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd |
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| AbstractList | Müllerian adenosarcoma (MA) is a rare mixed mesenchymal tumour of the female genital tract, composed of malignant stroma and benign‐appearing epithelium. Sarcomatous overgrowth (SO) is the only established histological variable associated with higher stage and shorter survival. Specific molecular or immunohistochemistry (IHC) tools for the diagnosis of MA are lacking. Our goal was to study genomic mutations and copy number variations (CNVs) in MA to understand better its pathobiology, and develop specific diagnostic and prognostic tools. DNA was extracted from 20 samples of MA from 18 subjects (12 without SO and 6 with SO), including two in which areas of both typical MA histology and SO were independently tested. Samples were analysed using a targeted next‐generation sequencing assay interrogating exonic sequences of 275 cancer genes for mutations and CNVs as well as 91 introns across 30 genes for cancer‐associated rearrangements. The mean number of mutations in MA with SO (mean 9.7; range 3–14) did not differ significantly from that in MA without SO (mean 9.6; range 5–16). MA with SO had significantly higher mean numbers of gene‐level CNVs (24.6) compared to MA without SO (5; p = 0.0002). The most frequent amplification involved MDM2 and CDK4 (5/18; 28%), accompanied by focal CDK4 and MDM2 and diffuse HMGA2 expression using immunohistochemistry. MYBL1 amplification was seen in 4/18 (22%), predominantly in SO. Alterations in PIK3CA/AKT/PTEN pathway members were seen in 13/18 (72%). Notably, TP53 mutations were uncommon, present in only two cases with SO. Three out of 18 (17%) had mutations in ATRX, all associated with SO. No chromosomal rearrangements were identified. We have identified a number of recurrent genomic alterations in MA, including some associated with SO. Although further investigation of these findings is needed, confirmation of one or more may lead to new mechanistic insights and novel markers for this often difficult‐to‐diagnose tumour. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd Müllerian adenosarcoma ( MA ) is a rare mixed mesenchymal tumour of the female genital tract, composed of malignant stroma and benign‐appearing epithelium. Sarcomatous overgrowth ( SO ) is the only established histological variable associated with higher stage and shorter survival. Specific molecular or immunohistochemistry ( IHC ) tools for the diagnosis of MA are lacking. Our goal was to study genomic mutations and copy number variations ( CNVs ) in MA to understand better its pathobiology, and develop specific diagnostic and prognostic tools. DNA was extracted from 20 samples of MA from 18 subjects (12 without SO and 6 with SO ), including two in which areas of both typical MA histology and SO were independently tested. Samples were analysed using a targeted next‐generation sequencing assay interrogating exonic sequences of 275 cancer genes for mutations and CNVs as well as 91 introns across 30 genes for cancer‐associated rearrangements. The mean number of mutations in MA with SO (mean 9.7; range 3–14) did not differ significantly from that in MA without SO (mean 9.6; range 5–16). MA with SO had significantly higher mean numbers of gene‐level CNVs (24.6) compared to MA without SO (5; p = 0.0002). The most frequent amplification involved MDM2 and CDK4 (5/18; 28%), accompanied by focal CDK4 and MDM2 and diffuse HMGA2 expression using immunohistochemistry. MYBL1 amplification was seen in 4/18 (22%), predominantly in SO . Alterations in PIK3CA / AKT / PTEN pathway members were seen in 13/18 (72%). Notably, TP53 mutations were uncommon, present in only two cases with SO . Three out of 18 (17%) had mutations in ATRX , all associated with SO . No chromosomal rearrangements were identified. We have identified a number of recurrent genomic alterations in MA , including some associated with SO . Although further investigation of these findings is needed, confirmation of one or more may lead to new mechanistic insights and novel markers for this often difficult‐to‐diagnose tumour. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd Mullerian adenosarcoma (MA) is a rare mixed mesenchymal tumour of the female genital tract, composed of malignant stroma and benign-appearing epithelium. Sarcomatous overgrowth (SO) is the only established histological variable associated with higher stage and shorter survival. Specific molecular or immunohistochemistry (IHC) tools for the diagnosis of MA are lacking. Our goal was to study genomic mutations and copy number variations (CNVs) in MA to understand better its pathobiology, and develop specific diagnostic and prognostic tools. DNA was extracted from 20 samples of MA from 18 subjects (12 without SO and 6 with SO), including two in which areas of both typical MA histology and SO were independently tested. Samples were analysed using a targeted next-generation sequencing assay interrogating exonic sequences of 275 cancer genes for mutations and CNVs as well as 91 introns across 30 genes for cancer-associated rearrangements. The mean number of mutations in MA with SO (mean 9.7; range 3-14) did not differ significantly from that in MA without SO (mean 9.6; range 5-16). MA with SO had significantly higher mean numbers of gene-level CNVs (24.6) compared to MA without SO (5; p = 0.0002). The most frequent amplification involved MDM2 and CDK4 (5/18; 28%), accompanied by focal CDK4 and MDM2 and diffuse HMGA2 expression using immunohistochemistry. MYBL1 amplification was seen in 4/18 (22%), predominantly in SO. Alterations in PIK3CA/AKT/PTEN pathway members were seen in 13/18 (72%). Notably, TP53 mutations were uncommon, present in only two cases with SO. Three out of 18 (17%) had mutations in ATRX, all associated with SO. No chromosomal rearrangements were identified. We have identified a number of recurrent genomic alterations in MA, including some associated with SO. Although further investigation of these findings is needed, confirmation of one or more may lead to new mechanistic insights and novel markers for this often difficult-to-diagnose tumour. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd Müllerian adenosarcoma (MA) is a rare mixed mesenchymal tumour of the female genital tract, composed of malignant stroma and benign-appearing epithelium. Sarcomatous overgrowth (SO) is the only established histological variable associated with higher stage and shorter survival. Specific molecular or immunohistochemistry (IHC) tools for the diagnosis of MA are lacking. Our goal was to study genomic mutations and copy number variations (CNVs) in MA to understand better its pathobiology, and develop specific diagnostic and prognostic tools. DNA was extracted from 20 samples of MA from 18 subjects (12 without SO and 6 with SO), including two in which areas of both typical MA histology and SO were independently tested. Samples were analysed using a targeted next-generation sequencing assay interrogating exonic sequences of 275 cancer genes for mutations and CNVs as well as 91 introns across 30 genes for cancer-associated rearrangements. The mean number of mutations in MA with SO (mean 9.7; range 3-14) did not differ significantly from that in MA without SO (mean 9.6; range 5-16). MA with SO had significantly higher mean numbers of gene-level CNVs (24.6) compared to MA without SO (5; p = 0.0002). The most frequent amplification involved MDM2 and CDK4 (5/18; 28%), accompanied by focal CDK4 and MDM2 and diffuse HMGA2 expression using immunohistochemistry. MYBL1 amplification was seen in 4/18 (22%), predominantly in SO. Alterations in PIK3CA/AKT/PTEN pathway members were seen in 13/18 (72%). Notably, TP53 mutations were uncommon, present in only two cases with SO. Three out of 18 (17%) had mutations in ATRX, all associated with SO. No chromosomal rearrangements were identified. We have identified a number of recurrent genomic alterations in MA, including some associated with SO. Although further investigation of these findings is needed, confirmation of one or more may lead to new mechanistic insights and novel markers for this often difficult-to-diagnose tumour.Müllerian adenosarcoma (MA) is a rare mixed mesenchymal tumour of the female genital tract, composed of malignant stroma and benign-appearing epithelium. Sarcomatous overgrowth (SO) is the only established histological variable associated with higher stage and shorter survival. Specific molecular or immunohistochemistry (IHC) tools for the diagnosis of MA are lacking. Our goal was to study genomic mutations and copy number variations (CNVs) in MA to understand better its pathobiology, and develop specific diagnostic and prognostic tools. DNA was extracted from 20 samples of MA from 18 subjects (12 without SO and 6 with SO), including two in which areas of both typical MA histology and SO were independently tested. Samples were analysed using a targeted next-generation sequencing assay interrogating exonic sequences of 275 cancer genes for mutations and CNVs as well as 91 introns across 30 genes for cancer-associated rearrangements. The mean number of mutations in MA with SO (mean 9.7; range 3-14) did not differ significantly from that in MA without SO (mean 9.6; range 5-16). MA with SO had significantly higher mean numbers of gene-level CNVs (24.6) compared to MA without SO (5; p = 0.0002). The most frequent amplification involved MDM2 and CDK4 (5/18; 28%), accompanied by focal CDK4 and MDM2 and diffuse HMGA2 expression using immunohistochemistry. MYBL1 amplification was seen in 4/18 (22%), predominantly in SO. Alterations in PIK3CA/AKT/PTEN pathway members were seen in 13/18 (72%). Notably, TP53 mutations were uncommon, present in only two cases with SO. Three out of 18 (17%) had mutations in ATRX, all associated with SO. No chromosomal rearrangements were identified. We have identified a number of recurrent genomic alterations in MA, including some associated with SO. Although further investigation of these findings is needed, confirmation of one or more may lead to new mechanistic insights and novel markers for this often difficult-to-diagnose tumour. Müllerian adenosarcoma (MA) is a rare mixed mesenchymal tumour of the female genital tract, composed of malignant stroma and benign-appearing epithelium. Sarcomatous overgrowth (SO) is the only established histological variable associated with higher stage and shorter survival. Specific molecular or immunohistochemistry (IHC) tools for the diagnosis of MA are lacking. Our goal was to study genomic mutations and copy number variations (CNVs) in MA to understand better its pathobiology, and develop specific diagnostic and prognostic tools. DNA was extracted from 20 samples of MA from 18 subjects (12 without SO and 6 with SO), including two in which areas of both typical MA histology and SO were independently tested. Samples were analysed using a targeted next-generation sequencing assay interrogating exonic sequences of 275 cancer genes for mutations and CNVs as well as 91 introns across 30 genes for cancer-associated rearrangements. The mean number of mutations in MA with SO (mean 9.7; range 3-14) did not differ significantly from that in MA without SO (mean 9.6; range 5-16). MA with SO had significantly higher mean numbers of gene-level CNVs (24.6) compared to MA without SO (5; p = 0.0002). The most frequent amplification involved MDM2 and CDK4 (5/18; 28%), accompanied by focal CDK4 and MDM2 and diffuse HMGA2 expression using immunohistochemistry. MYBL1 amplification was seen in 4/18 (22%), predominantly in SO. Alterations in PIK3CA/AKT/PTEN pathway members were seen in 13/18 (72%). Notably, TP53 mutations were uncommon, present in only two cases with SO. Three out of 18 (17%) had mutations in ATRX, all associated with SO. No chromosomal rearrangements were identified. We have identified a number of recurrent genomic alterations in MA, including some associated with SO. Although further investigation of these findings is needed, confirmation of one or more may lead to new mechanistic insights and novel markers for this often difficult-to-diagnose tumour. |
| Author | Dal Cin, P Garcia, Elizabeth Jia, Yonghui Quade, Bradley J Kuo, Frank Howitt, Brooke E MacConaill, Laura Yuan, Liping Lindeman, Neal Sholl, Lynette M Nucci, Marisa R |
| Author_xml | – sequence: 1 givenname: Brooke E surname: Howitt fullname: Howitt, Brooke E email: bhowitt@partners.org organization: Women's and Perinatal Pathology Division, Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, MA, Boston, USA – sequence: 2 givenname: Lynette M surname: Sholl fullname: Sholl, Lynette M organization: Center for Advanced Molecular Diagnostics, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA, USA – sequence: 3 givenname: P surname: Dal Cin fullname: Dal Cin, P organization: Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, MA, Boston, USA – sequence: 4 givenname: Yonghui surname: Jia fullname: Jia, Yonghui organization: Center for Advanced Molecular Diagnostics, Brigham and Women's Hospital, and Harvard Medical School, MA, Boston, USA – sequence: 5 givenname: Liping surname: Yuan fullname: Yuan, Liping organization: Women's and Perinatal Pathology Division, Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, MA, Boston, USA – sequence: 6 givenname: Laura surname: MacConaill fullname: MacConaill, Laura organization: Center for Advanced Molecular Diagnostics, Brigham and Women's Hospital, and Harvard Medical School, MA, Boston, USA – sequence: 7 givenname: Neal surname: Lindeman fullname: Lindeman, Neal organization: Center for Advanced Molecular Diagnostics, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA, USA – sequence: 8 givenname: Frank surname: Kuo fullname: Kuo, Frank organization: Center for Advanced Molecular Diagnostics, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA, USA – sequence: 9 givenname: Elizabeth surname: Garcia fullname: Garcia, Elizabeth organization: Center for Advanced Molecular Diagnostics, Brigham and Women's Hospital, and Harvard Medical School, MA, Boston, USA – sequence: 10 givenname: Marisa R surname: Nucci fullname: Nucci, Marisa R organization: Women's and Perinatal Pathology Division, Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, MA, Boston, USA – sequence: 11 givenname: Bradley J surname: Quade fullname: Quade, Bradley J organization: Women's and Perinatal Pathology Division, Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, MA, Boston, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25231023$$D View this record in MEDLINE/PubMed |
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| Copyright | Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. Copyright © 2015 Pathological Society of Great Britain and Ireland |
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| Issue | 1 |
| Keywords | adenosarcoma MDM2 HMGA2 Müllerian MYBL1 sarcomagenesis |
| Language | English |
| License | Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c4572-72c62b56f3e77317b7cf17f07f37f4d06cb06838add1046cf17bc06360d800b93 |
| Notes | istex:47545304165284B00B048D499BCD4DB9B56BB924 ark:/67375/WNG-FQW3N8S8-J Presented in part on 4 March 2014 at the 103rd USCAP meeting in San Diego, California. FigureS1. MDM2 amplification by FISH analysis using probes for MDM2 (red) and chromosome 12 centromere (green).FileS1. Complete list of genes interrogated in the assay.FileS2. Complete list of SNVs identified in MAs in this study.FileS3. Complete list of CNVs identified in MAs in this study. ArticleID:PATH4442 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
| PMID | 25231023 |
| PQID | 1634957570 |
| PQPubID | 1006392 |
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| PublicationCentury | 2000 |
| PublicationDate | January 2015 |
| PublicationDateYYYYMMDD | 2015-01-01 |
| PublicationDate_xml | – month: 01 year: 2015 text: January 2015 |
| PublicationDecade | 2010 |
| PublicationPlace | Chichester, UK |
| PublicationPlace_xml | – name: Chichester, UK – name: England – name: Bognor Regis |
| PublicationTitle | The Journal of pathology |
| PublicationTitleAlternate | J. Pathol |
| PublicationYear | 2015 |
| Publisher | John Wiley & Sons, Ltd Wiley Subscription Services, Inc |
| Publisher_xml | – name: John Wiley & Sons, Ltd – name: Wiley Subscription Services, Inc |
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DAXX/ATRX, MEN1, and mTOR pathway genes are frequently altered in pancreatic neuroendocrine tumors. Science 2011; 331: 1199-1203. Gallardo A, Prat J. Mullerian adenosarcoma: a clinicopathologic and immunohistochemical study of 55 cases challenging the existence of adenofibroma. Am J Surg Pathol 2009; 33: 278-288. Van der Auwera GA, Carneiro MO, Hartl C, et al. From FastQ data to high-confidence variant calls: the Genome Analysis Toolkit best practices pipeline. Curr Protoc Bioinform 2013; 43: 11.10.1-11.10.33. Bol S, Wanschura S, Thode B, et al. An endometrial polyp with a rearrangement of HMGI-C underlying a complex cytogenetic rearrangement involving chromosomes 2 and 12. Cancer Genet Cytogenet 1996; 90: 88-90. Blom R, Guerrieri C. Adenosarcoma of the uterus: a clinicopathologic, DNA flow cytometric, p53 and mdm-2 analysis of 11 cases. Int J Gynecol Cancer 1999; 9: 37-43. Abeler VM, Nenodovic M. Diagnostic immunohistochemistry in uterine sarcomas: a study of 397 cases. 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Expression of CD10 in malignant Müllerian mixed tumors and adenosarcomas: an immunohistochemical study. Mod Pathol 2002; 15: 923-930. de Wilde RF, Heaphy CM, Maitra A, et al. Loss of ATRX or DAXX expression and concomitant acquisition of the alternative lengthening of telomeres phenotype are late events in a small subset of Men-1 syndrome pancreatic neuroendocrine tumors. Mod Pathol 2012; 25: 1033-1039. Dal Cin P, Timmerman D, Van den Berghe I, et al. Genomic changes in endometrial polyps associated with tamoxifen show no evidence for its action as an external carcinogen. Cancer Res 1998; 58: 2278-2281. Marinoni I, Kurrer AS, Vassella E, et al. Loss of DAXX and ATRX are associated with chromosome instability and reduced survival of patients with pancreatic neuroendocrine tumors. Gastroenterology 2014; 146: 453-460.e455. Dal Cin P, Turc-Carel C, Sandberg AA. Consistent involvement of band 12q14 in two different translocations in three lipomas from the same patient. Cancer Genet Cytogenet 1988; 31: 237-240. Spencer DH, Sehn JK, Abel HJ, et al. Comparison of clinical targeted next-generation sequence data from formalin-fixed and fresh-frozen tissue specimens. J Mol Diagn 2013; 15: 623-633. Wu G, Diaz AK, Paugh BS, et al. The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma. Nature Genet 2014; 46: 444-450. Clement PB, Scully RE. Mullerian adenosarcoma of the uterus. A clinicopathologic analysis of ten cases of a distinctive type of Mullerian mixed tumor. Cancer 1974; 34: 1138-1149. Medeiros F, Erickson-Johnson MR, Keeney GL, et al. Frequency and characterization of HMGA2 and HMGA1 rearrangements in mesenchymal tumors of the lower genital tract. Genes Chromosomes Cancer 2007; 46: 981-990. Tesfaye A, Di Cello F, Hillion J, et al. The high-mobility group A1 gene up-regulates cyclooxygenase 2 expression in uterine tumorigenesis. Cancer Res 2007; 67: 3998-4004. Sprogoe-Jakobsen S, Holund B. Immunohistochemistry (Ki-67 and p53) as a tool in determining malignancy in smooth muscle neoplasms (exemplified by a myxoid leiomyosarcoma of the uterus). APMIS 1996; 104: 705-708. Jiao Y, Killela PJ, Reitman ZJ, et al. Frequent ATRX, CIC, FUBP1 and IDH1 mutations refine the classification of malignant gliomas. Oncotarget 2012; 3: 709-722. Anderson SE, Nonaka D, Chuai S, et al. p53, epidermal growth factor, and platelet-derived growth factor in uterine leiomyosarcoma and leiomyomas. Int J Gynecol Cancer 2006; 16: 849-853. Soslow RA, Ali A, Oliva E. Mullerian adenosarcomas: an immunophenotypic analysis of 35 cases. Am J Surg Pathol 2008; 32: 1013-1021. Auerbach HE, LiVolsi VA, Merino MJ. Malignant mixed Mullerian tumors of the uterus. An immunohistochemical study. Int J Gynecol Pathol 1988; 7: 123-130. Nucci MR, Weremowicz S, Neskey DM, et al. Chromosomal translocation t(8;12) induces aberrant HMGIC expression in aggressive angiomyxoma of the vulva. Genes Chromosomes Cancer 2001; 32: 172-176. Krivak TC, Seidman JD, McBroom JW, et al. Uterine adenosarcoma with sarcomatous overgrowth versus uterine carcinosarcoma: comparison of treatment and survival. Gynecol Oncol 2001; 83: 89-94. Dal Cin P, Vanni R, Marras S, et al. Four cytogenetic subgroups can be identified in endometrial polyps. Cancer Res 1995; 55: 1565-1568. Walter TA, Fan SX, Medchill MT, et al. inv(12)(p11.2q13) in an endometrial polyp. Cancer Genet Cytogenet 1989; 41: 99-103. Boo LM, Lin HH, Chung V, et al. High mobility group A2 potentiates genotoxic stress in part through the modulation of basal and DNA damage-dependent phosphatidylinositol 3-kinase-related protein kinase activation. Cancer Res 2005; 65:6622-6630. Tallini G, Vanni R, Manfioletti G, et al. HMGI-C and HMGI(Y) immunoreactivity correlates with cytogenetic abnormalities in lipomas, pulmonary chondroid hamartomas, endometrial polyps, and uterine leiomyomas and is compatible with rearrangement of the HMGI-C and HMGI(Y) genes. Lab Invest 2000; 80:359-369. Dal Cin P, Van Den Berghe H, Brosens I. Involvement of 6p in an endometrial polyp. Cancer Genet Cytogenet 1991; 51: 279-280. Medeiros F, Araujo AR, Erickson-Johnson MR, et al. HMGA1 and HMGA2 rearrangements in mass-forming endometriosis. Genes Chromosomes Cancer. 2010; 49: 630-634. Ramkissoon LA, Horowitz PM, Craig JM, et al. Genomic analysis of diffuse pediatric low-grade gliomas identifies recurrent oncogenic truncating rearrangements in the transcription factor MYBL1. Proc Natl Acad Sci U S A 2013; 110: 8188-8193. Ito M, Barys L, O'Reilly T, et al. Comprehensive mapping of p53 pathway alterations reveals an apparent role for both SNP309 and MDM2 amplification in sarcomagenesis. Clin Cancer Res 2011; 17: 416-426. McCluggage WG. Mullerian adenosarcoma of the female genital tract. Adv Anat Pathol 2010; 17: 122-129. Zaloudek CJ, Norris HJ. Adenofibroma and adenosarcoma of the uterus: a clinicopathologic study of 35 cases. Cancer 1981; 48: 354-366. Eichhorn JH, Young RH, Clement PB, et al. Mesodermal (Müllerian) adenosarcoma of the ovary: a clinicopathologic analysis of 40 cases and a review of the literature. Am J Surg Pathol 2002; 26: 1243-1258. Taylor NP, Zighelboim I, Huettner PC, et al. DNA mismatch repair and TP53 defects are early events in uterine carcinosarcoma tumorigenesis. Mod Pathol 2006; 19: 1333-1338. Chen Z, Hong B, Drozd-Borysiuk E, et al. Molecular cytogenetic characterization of a case of Müllerian adenosarcoma. Cancer Genet Cytogenet 2004; 148: 129-132. Dal Cin P, Wanschura S, Kazmierczak B, et al. Amplification and expression of the HMGIC gene in a benign endometrial polyp. Genes Chromosomes Cancer 1998; 22:95-99. Amant F, Schurmans K, Steenkiste E, et al. Immunohistochemical determination of estrogen and progesterone receptor positivity in uterine adenosarcoma. Gynecol Oncol 2004; 93: 680-685. McKenna A, Hanna M, Banks E, et al. The Genome Analysis Toolkit: a MapReduce framework for analyzing next-generation DNA sequencing data. Genome Res 2010; 20: 1297-1303. Maekawa Y, Tsukumo S, Chiba S, et al. Delta1-Notch3 interactions bias the functional differentiation of activated CD4+ T cells. Immunity 2003; 19: 549-559. Garcia EP, Kuo F, Jia Y, Zepf D, et al. Development and clinical validation 1989; 41 1993; 8 1993; 68 2002; 15 2013; 1 2007; 105 2010; 17 1991; 51 1981; 48 2005; 65 2008; 32 2003; 19 1988; 31 2011; 17 1996; 104 1992; 11 2010; 20 2013; 15 1996; 60 1979; 3 2013; 110 2012; 25 2007; 67 1998; 58 1991; 3 1974; 34 2004; 148 2013; 43 1995; 59 2006; 16 1995; 55 2011; 30 2006; 19 2014; 46 1996; 90 1997; 181 1994; 83 2011; 331 1998; 22 1999; 9 2009; 33 1990; 21 2002; 26 2001; 83 2010; 49 2012; 3 2004; 93 2004; 14 2013; 31 1988; 7 2011; 43 2000; 80 2014 2013; 131 2005; 99 2007; 46 2014; 146 2001; 32 e_1_2_7_3_1 e_1_2_7_9_1 e_1_2_7_7_1 e_1_2_7_19_1 e_1_2_7_60_1 e_1_2_7_17_1 e_1_2_7_15_1 e_1_2_7_41_1 e_1_2_7_13_1 e_1_2_7_43_1 e_1_2_7_11_1 e_1_2_7_45_1 e_1_2_7_47_1 e_1_2_7_26_1 e_1_2_7_49_1 e_1_2_7_28_1 Dal Cin P (e_1_2_7_46_1) 1998; 58 e_1_2_7_50_1 e_1_2_7_25_1 e_1_2_7_31_1 e_1_2_7_52_1 e_1_2_7_23_1 e_1_2_7_33_1 e_1_2_7_54_1 e_1_2_7_21_1 e_1_2_7_56_1 e_1_2_7_37_1 e_1_2_7_58_1 e_1_2_7_39_1 Garcia EP (e_1_2_7_22_1) 2013; 15 e_1_2_7_6_1 e_1_2_7_4_1 e_1_2_7_8_1 e_1_2_7_18_1 e_1_2_7_16_1 e_1_2_7_40_1 e_1_2_7_2_1 e_1_2_7_14_1 e_1_2_7_42_1 e_1_2_7_12_1 e_1_2_7_44_1 e_1_2_7_10_1 e_1_2_7_27_1 e_1_2_7_29_1 Liu FS (e_1_2_7_35_1) 1994; 83 e_1_2_7_51_1 e_1_2_7_30_1 e_1_2_7_53_1 e_1_2_7_24_1 e_1_2_7_32_1 e_1_2_7_55_1 e_1_2_7_34_1 e_1_2_7_57_1 Kurman R (e_1_2_7_5_1) 2014 e_1_2_7_20_1 e_1_2_7_36_1 e_1_2_7_59_1 e_1_2_7_38_1 Dal Cin P (e_1_2_7_48_1) 1995; 55 |
| References_xml | – reference: Van der Auwera GA, Carneiro MO, Hartl C, et al. From FastQ data to high-confidence variant calls: the Genome Analysis Toolkit best practices pipeline. Curr Protoc Bioinform 2013; 43: 11.10.1-11.10.33. – reference: Kobayashi H, Uekuri C, Akasaka J, et al. The biology of uterine sarcomas: a review and update. Mol Clin Oncol 2013; 1: 599-609. – reference: Ito M, Barys L, O'Reilly T, et al. Comprehensive mapping of p53 pathway alterations reveals an apparent role for both SNP309 and MDM2 amplification in sarcomagenesis. Clin Cancer Res 2011; 17: 416-426. – reference: Nucci MR, Weremowicz S, Neskey DM, et al. Chromosomal translocation t(8;12) induces aberrant HMGIC expression in aggressive angiomyxoma of the vulva. Genes Chromosomes Cancer 2001; 32: 172-176. – reference: Speleman F, Dal Cin P, Van Roy N, et al. Is t(6;20)(p21;q13) a characteristic chromosome change in endometrial polyps? Genes Chromosomes Cancer 1991; 3: 318-319. – reference: Maekawa Y, Tsukumo S, Chiba S, et al. Delta1-Notch3 interactions bias the functional differentiation of activated CD4+ T cells. Immunity 2003; 19: 549-559. – reference: Kurman R, Carcangiu ML, Young RH (Eds). World Health Organization Classification of Tumours of Female Reproductive Organs. IARC Press: Lyon, 2014. – reference: Chen Z, Hong B, Drozd-Borysiuk E, et al. Molecular cytogenetic characterization of a case of Müllerian adenosarcoma. Cancer Genet Cytogenet 2004; 148: 129-132. – reference: Anderson SE, Nonaka D, Chuai S, et al. p53, epidermal growth factor, and platelet-derived growth factor in uterine leiomyosarcoma and leiomyomas. Int J Gynecol Cancer 2006; 16: 849-853. – reference: Taylor NP, Zighelboim I, Huettner PC, et al. DNA mismatch repair and TP53 defects are early events in uterine carcinosarcoma tumorigenesis. Mod Pathol 2006; 19: 1333-1338. – reference: Clement PB, Scully RE. Mullerian adenosarcoma of the uterus: a clinicopathologic analysis of 100 cases with a review of the literature. Hum Pathol 1990; 21: 363-381. – reference: Tesfaye A, Di Cello F, Hillion J, et al. The high-mobility group A1 gene up-regulates cyclooxygenase 2 expression in uterine tumorigenesis. Cancer Res 2007; 67: 3998-4004. – reference: Dal Cin P, Wanschura S, Kazmierczak B, et al. Amplification and expression of the HMGIC gene in a benign endometrial polyp. Genes Chromosomes Cancer 1998; 22:95-99. – reference: Dal Cin P, Vanni R, Marras S, et al. Four cytogenetic subgroups can be identified in endometrial polyps. Cancer Res 1995; 55: 1565-1568. – reference: Dal Cin P, Kools P, De Jonge I, et al. Rearrangement of 12q14-15 in pulmonary chondroid hamartoma. Genes Chromosomes Cancer 1993; 8: 131-133. – reference: Clement PB, Scully RE. Mullerian adenosarcoma of the uterus. A clinicopathologic analysis of ten cases of a distinctive type of Mullerian mixed tumor. Cancer 1974; 34: 1138-1149. – reference: Bol S, Wanschura S, Thode B, et al. An endometrial polyp with a rearrangement of HMGI-C underlying a complex cytogenetic rearrangement involving chromosomes 2 and 12. Cancer Genet Cytogenet 1996; 90: 88-90. – reference: Abeler VM, Nenodovic M. Diagnostic immunohistochemistry in uterine sarcomas: a study of 397 cases. Int J Gynecol Pathol 2011; 30: 236-243. – reference: McCluggage WG. Mullerian adenosarcoma of the female genital tract. Adv Anat Pathol 2010; 17: 122-129. – reference: Zaloudek CJ, Norris HJ. Adenofibroma and adenosarcoma of the uterus: a clinicopathologic study of 35 cases. Cancer 1981; 48: 354-366. – reference: Auerbach HE, LiVolsi VA, Merino MJ. Malignant mixed Mullerian tumors of the uterus. An immunohistochemical study. Int J Gynecol Pathol 1988; 7: 123-130. – reference: Marinoni I, Kurrer AS, Vassella E, et al. Loss of DAXX and ATRX are associated with chromosome instability and reduced survival of patients with pancreatic neuroendocrine tumors. Gastroenterology 2014; 146: 453-460.e455. – reference: Krivak TC, Seidman JD, McBroom JW, et al. Uterine adenosarcoma with sarcomatous overgrowth versus uterine carcinosarcoma: comparison of treatment and survival. Gynecol Oncol 2001; 83: 89-94. – reference: Bernard B, Clarke BA, Malowany JI, et al. Uterine adenosarcomas: a dual-institution update on staging, prognosis and survival. Gynecol Oncol 2013; 131: 634-639. – reference: Dal Cin P, Turc-Carel C, Sandberg AA. Consistent involvement of band 12q14 in two different translocations in three lipomas from the same patient. Cancer Genet Cytogenet 1988; 31: 237-240. – reference: Jiao Y, Killela PJ, Reitman ZJ, et al. Frequent ATRX, CIC, FUBP1 and IDH1 mutations refine the classification of malignant gliomas. Oncotarget 2012; 3: 709-722. – reference: Spencer DH, Sehn JK, Abel HJ, et al. Comparison of clinical targeted next-generation sequence data from formalin-fixed and fresh-frozen tissue specimens. J Mol Diagn 2013; 15: 623-633. – reference: Walter TA, Fan SX, Medchill MT, et al. inv(12)(p11.2q13) in an endometrial polyp. Cancer Genet Cytogenet 1989; 41: 99-103. – reference: Boo LM, Lin HH, Chung V, et al. High mobility group A2 potentiates genotoxic stress in part through the modulation of basal and DNA damage-dependent phosphatidylinositol 3-kinase-related protein kinase activation. Cancer Res 2005; 65:6622-6630. – reference: Ramkissoon LA, Horowitz PM, Craig JM, et al. Genomic analysis of diffuse pediatric low-grade gliomas identifies recurrent oncogenic truncating rearrangements in the transcription factor MYBL1. Proc Natl Acad Sci U S A 2013; 110: 8188-8193. – reference: Wu G, Diaz AK, Paugh BS, et al. The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma. Nature Genet 2014; 46: 444-450. – reference: Blom R, Guerrieri C. Adenosarcoma of the uterus: a clinicopathologic, DNA flow cytometric, p53 and mdm-2 analysis of 11 cases. Int J Gynecol Cancer 1999; 9: 37-43. – reference: Fox H, Harilal KR, Youell A. Müllerian adenosarcoma of the uterine body: a report of nine cases. Histopathology 1979; 3: 167-180. – reference: Tallini G, Vanni R, Manfioletti G, et al. HMGI-C and HMGI(Y) immunoreactivity correlates with cytogenetic abnormalities in lipomas, pulmonary chondroid hamartomas, endometrial polyps, and uterine leiomyomas and is compatible with rearrangement of the HMGI-C and HMGI(Y) genes. Lab Invest 2000; 80:359-369. – reference: McKenna A, Hanna M, Banks E, et al. The Genome Analysis Toolkit: a MapReduce framework for analyzing next-generation DNA sequencing data. Genome Res 2010; 20: 1297-1303. – reference: Swisher EM, Gown AM, Skelly M, et al. The expression of epidermal growth factor receptor, Her-2/Neu, p53, and Ki-67 antigen in uterine malignant mixed mesodermal tumors and adenosarcoma. Gynecol Oncol 1996; 60: 81-88. – reference: Dal Cin P, Van Den Berghe H, Brosens I. Involvement of 6p in an endometrial polyp. Cancer Genet Cytogenet 1991; 51: 279-280. – reference: Gollard R, Kosty M, Bordin G, et al. Two unusual presentations of Müllerian adenosarcoma: case reports, literature review, and treatment considerations. Gynecol Oncol 1995; 59: 412-422. – reference: Medeiros F, Erickson-Johnson MR, Keeney GL, et al. Frequency and characterization of HMGA2 and HMGA1 rearrangements in mesenchymal tumors of the lower genital tract. Genes Chromosomes Cancer 2007; 46: 981-990. – reference: Cibulskis K, Lawrence MS, Carter SL, et al. Sensitive detection of somatic point mutations in impure and heterogeneous cancer samples. Nature Biotechnol 2013; 31: 213-219. – reference: Liu FS, Kohler MF, Marks JR, et al. Mutation and overexpression of the p53 tumor suppressor gene frequently occurs in uterine and ovarian sarcomas. Obstet Gynecol 1994; 83: 118-124. – reference: Van Mieghem T, Abeler VM, Moerman P, et al. CD10, estrogen and progesterone receptor expression in ovarian adenosarcoma. Gynecol Oncol 2005; 99: 493-496. – reference: Dei Tos AP, Doglioni C, Piccinin S, et al. Molecular abnormalities of the p53 pathway in dedifferentiated liposarcoma. J Pathol 1997; 181: 8-13. – reference: Mikami Y, Hata S, Kiyokawa T, et al. Expression of CD10 in malignant Müllerian mixed tumors and adenosarcomas: an immunohistochemical study. Mod Pathol 2002; 15: 923-930. – reference: Garcia EP, Kuo F, Jia Y, Zepf D, et al. Development and clinical validation of a targeted next-generation sequencing platform for the detection of somatic mutations, indels, rearrangements, and copy-number alterations in human tumors. J Mol Diagn 2013; 15: 872. – reference: Sprogoe-Jakobsen S, Holund B. Immunohistochemistry (Ki-67 and p53) as a tool in determining malignancy in smooth muscle neoplasms (exemplified by a myxoid leiomyosarcoma of the uterus). APMIS 1996; 104: 705-708. – reference: Manoharan M, Azmi MA, Soosay G, et al. Mullerian adenosarcoma of uterine cervix: report of three cases and review of literature. Gynecol Oncol 2007; 105: 256-260. – reference: Kaku T, Silverberg SG, Major FJ, et al. Adenosarcoma of the uterus: a gynecologic oncology group clinicopathologic study of 31 cases. Int J Gynecol Pathol 1992; 11: 75-88. – reference: Amant F, Steenkiste E, Schurmans K, et al. Immunohistochemical expression of CD10 antigen in uterine adenosarcoma. Int J Gynecol Cancer 2004; 14: 1118-1121. – reference: Gallardo A, Prat J. Mullerian adenosarcoma: a clinicopathologic and immunohistochemical study of 55 cases challenging the existence of adenofibroma. Am J Surg Pathol 2009; 33: 278-288. – reference: Dal Cin P, Timmerman D, Van den Berghe I, et al. 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| SubjectTerms | adenosarcoma Adenosarcoma - genetics Adenosarcoma - pathology Adult Aged Aged, 80 and over DNA Copy Number Variations - genetics Female Genetic Predisposition to Disease Genome-Wide Association Study Genomics - methods HMGA2 Humans Immunohistochemistry - methods MDM2 Middle Aged Mutation - genetics MYBL1 Müllerian sarcomagenesis Young Adult |
| Title | Targeted genomic analysis of Müllerian adenosarcoma |
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