ARID1A and TERT promoter mutations in dedifferentiated meningioma
Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanis...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Abedalthagafi, Malak S. [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2015transfer abstract |
|---|
| Schlagwörter: |
|---|
| Umfang: |
6 |
|---|
| Übergeordnetes Werk: |
Enthalten in: 0488: Assessment of aortic regurgitation severity: a cardiac magnetic resonance and echocardiographic comparison study - Mohty, Dania ELSEVIER, 2016, Amsterdam [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:208 ; year:2015 ; number:6 ; pages:345-350 ; extent:6 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.cancergen.2015.03.005 |
|---|
| Katalog-ID: |
ELV034576185 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | ELV034576185 | ||
| 003 | DE-627 | ||
| 005 | 20230625201248.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 180603s2015 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.cancergen.2015.03.005 |2 doi | |
| 028 | 5 | 2 | |a GBVA2015011000030.pica |
| 035 | |a (DE-627)ELV034576185 | ||
| 035 | |a (ELSEVIER)S2210-7762(15)00036-8 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | |a 610 | |
| 082 | 0 | 4 | |a 610 |q DE-600 |
| 082 | 0 | 4 | |a 610 |q VZ |
| 082 | 0 | 4 | |a 380 |q VZ |
| 084 | |a 55.82 |2 bkl | ||
| 100 | 1 | |a Abedalthagafi, Malak S. |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a ARID1A and TERT promoter mutations in dedifferentiated meningioma |
| 264 | 1 | |c 2015transfer abstract | |
| 300 | |a 6 | ||
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression. | ||
| 520 | |a Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression. | ||
| 650 | 7 | |a anaplastic |2 Elsevier | |
| 650 | 7 | |a SWI/SNF complex |2 Elsevier | |
| 650 | 7 | |a intratumoral heterogeneity |2 Elsevier | |
| 650 | 7 | |a chromatin remodeling |2 Elsevier | |
| 650 | 7 | |a Meningioma |2 Elsevier | |
| 700 | 1 | |a Bi, Wenya Linda |4 oth | |
| 700 | 1 | |a Merrill, Parker H. |4 oth | |
| 700 | 1 | |a Gibson, William J. |4 oth | |
| 700 | 1 | |a Rose, Matthew F. |4 oth | |
| 700 | 1 | |a Du, Ziming |4 oth | |
| 700 | 1 | |a Francis, Joshua M. |4 oth | |
| 700 | 1 | |a Du, Rose |4 oth | |
| 700 | 1 | |a Dunn, Ian F. |4 oth | |
| 700 | 1 | |a Ligon, Azra H. |4 oth | |
| 700 | 1 | |a Beroukhim, Rameen |4 oth | |
| 700 | 1 | |a Santagata, Sandro |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier Science |a Mohty, Dania ELSEVIER |t 0488: Assessment of aortic regurgitation severity: a cardiac magnetic resonance and echocardiographic comparison study |d 2016 |g Amsterdam [u.a.] |w (DE-627)ELV019379730 |
| 773 | 1 | 8 | |g volume:208 |g year:2015 |g number:6 |g pages:345-350 |g extent:6 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.cancergen.2015.03.005 |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a GBV_ELV | ||
| 912 | |a SYSFLAG_U | ||
| 936 | b | k | |a 55.82 |j Güterverkehr |q VZ |
| 951 | |a AR | ||
| 952 | |d 208 |j 2015 |e 6 |h 345-350 |g 6 | ||
| 953 | |2 045F |a 610 | ||
| author_variant |
m s a ms msa |
|---|---|
| matchkey_str |
abedalthagafimalaksbiwenyalindamerrillpa:2015----:rdantrpooemttosneifrn |
| hierarchy_sort_str |
2015transfer abstract |
| bklnumber |
55.82 |
| publishDate |
2015 |
| allfields |
10.1016/j.cancergen.2015.03.005 doi GBVA2015011000030.pica (DE-627)ELV034576185 (ELSEVIER)S2210-7762(15)00036-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 380 VZ 55.82 bkl Abedalthagafi, Malak S. verfasserin aut ARID1A and TERT promoter mutations in dedifferentiated meningioma 2015transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression. Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression. anaplastic Elsevier SWI/SNF complex Elsevier intratumoral heterogeneity Elsevier chromatin remodeling Elsevier Meningioma Elsevier Bi, Wenya Linda oth Merrill, Parker H. oth Gibson, William J. oth Rose, Matthew F. oth Du, Ziming oth Francis, Joshua M. oth Du, Rose oth Dunn, Ian F. oth Ligon, Azra H. oth Beroukhim, Rameen oth Santagata, Sandro oth Enthalten in Elsevier Science Mohty, Dania ELSEVIER 0488: Assessment of aortic regurgitation severity: a cardiac magnetic resonance and echocardiographic comparison study 2016 Amsterdam [u.a.] (DE-627)ELV019379730 volume:208 year:2015 number:6 pages:345-350 extent:6 https://doi.org/10.1016/j.cancergen.2015.03.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 55.82 Güterverkehr VZ AR 208 2015 6 345-350 6 045F 610 |
| spelling |
10.1016/j.cancergen.2015.03.005 doi GBVA2015011000030.pica (DE-627)ELV034576185 (ELSEVIER)S2210-7762(15)00036-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 380 VZ 55.82 bkl Abedalthagafi, Malak S. verfasserin aut ARID1A and TERT promoter mutations in dedifferentiated meningioma 2015transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression. Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression. anaplastic Elsevier SWI/SNF complex Elsevier intratumoral heterogeneity Elsevier chromatin remodeling Elsevier Meningioma Elsevier Bi, Wenya Linda oth Merrill, Parker H. oth Gibson, William J. oth Rose, Matthew F. oth Du, Ziming oth Francis, Joshua M. oth Du, Rose oth Dunn, Ian F. oth Ligon, Azra H. oth Beroukhim, Rameen oth Santagata, Sandro oth Enthalten in Elsevier Science Mohty, Dania ELSEVIER 0488: Assessment of aortic regurgitation severity: a cardiac magnetic resonance and echocardiographic comparison study 2016 Amsterdam [u.a.] (DE-627)ELV019379730 volume:208 year:2015 number:6 pages:345-350 extent:6 https://doi.org/10.1016/j.cancergen.2015.03.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 55.82 Güterverkehr VZ AR 208 2015 6 345-350 6 045F 610 |
| allfields_unstemmed |
10.1016/j.cancergen.2015.03.005 doi GBVA2015011000030.pica (DE-627)ELV034576185 (ELSEVIER)S2210-7762(15)00036-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 380 VZ 55.82 bkl Abedalthagafi, Malak S. verfasserin aut ARID1A and TERT promoter mutations in dedifferentiated meningioma 2015transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression. Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression. anaplastic Elsevier SWI/SNF complex Elsevier intratumoral heterogeneity Elsevier chromatin remodeling Elsevier Meningioma Elsevier Bi, Wenya Linda oth Merrill, Parker H. oth Gibson, William J. oth Rose, Matthew F. oth Du, Ziming oth Francis, Joshua M. oth Du, Rose oth Dunn, Ian F. oth Ligon, Azra H. oth Beroukhim, Rameen oth Santagata, Sandro oth Enthalten in Elsevier Science Mohty, Dania ELSEVIER 0488: Assessment of aortic regurgitation severity: a cardiac magnetic resonance and echocardiographic comparison study 2016 Amsterdam [u.a.] (DE-627)ELV019379730 volume:208 year:2015 number:6 pages:345-350 extent:6 https://doi.org/10.1016/j.cancergen.2015.03.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 55.82 Güterverkehr VZ AR 208 2015 6 345-350 6 045F 610 |
| allfieldsGer |
10.1016/j.cancergen.2015.03.005 doi GBVA2015011000030.pica (DE-627)ELV034576185 (ELSEVIER)S2210-7762(15)00036-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 380 VZ 55.82 bkl Abedalthagafi, Malak S. verfasserin aut ARID1A and TERT promoter mutations in dedifferentiated meningioma 2015transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression. Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression. anaplastic Elsevier SWI/SNF complex Elsevier intratumoral heterogeneity Elsevier chromatin remodeling Elsevier Meningioma Elsevier Bi, Wenya Linda oth Merrill, Parker H. oth Gibson, William J. oth Rose, Matthew F. oth Du, Ziming oth Francis, Joshua M. oth Du, Rose oth Dunn, Ian F. oth Ligon, Azra H. oth Beroukhim, Rameen oth Santagata, Sandro oth Enthalten in Elsevier Science Mohty, Dania ELSEVIER 0488: Assessment of aortic regurgitation severity: a cardiac magnetic resonance and echocardiographic comparison study 2016 Amsterdam [u.a.] (DE-627)ELV019379730 volume:208 year:2015 number:6 pages:345-350 extent:6 https://doi.org/10.1016/j.cancergen.2015.03.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 55.82 Güterverkehr VZ AR 208 2015 6 345-350 6 045F 610 |
| allfieldsSound |
10.1016/j.cancergen.2015.03.005 doi GBVA2015011000030.pica (DE-627)ELV034576185 (ELSEVIER)S2210-7762(15)00036-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 380 VZ 55.82 bkl Abedalthagafi, Malak S. verfasserin aut ARID1A and TERT promoter mutations in dedifferentiated meningioma 2015transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression. Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression. anaplastic Elsevier SWI/SNF complex Elsevier intratumoral heterogeneity Elsevier chromatin remodeling Elsevier Meningioma Elsevier Bi, Wenya Linda oth Merrill, Parker H. oth Gibson, William J. oth Rose, Matthew F. oth Du, Ziming oth Francis, Joshua M. oth Du, Rose oth Dunn, Ian F. oth Ligon, Azra H. oth Beroukhim, Rameen oth Santagata, Sandro oth Enthalten in Elsevier Science Mohty, Dania ELSEVIER 0488: Assessment of aortic regurgitation severity: a cardiac magnetic resonance and echocardiographic comparison study 2016 Amsterdam [u.a.] (DE-627)ELV019379730 volume:208 year:2015 number:6 pages:345-350 extent:6 https://doi.org/10.1016/j.cancergen.2015.03.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 55.82 Güterverkehr VZ AR 208 2015 6 345-350 6 045F 610 |
| language |
English |
| source |
Enthalten in 0488: Assessment of aortic regurgitation severity: a cardiac magnetic resonance and echocardiographic comparison study Amsterdam [u.a.] volume:208 year:2015 number:6 pages:345-350 extent:6 |
| sourceStr |
Enthalten in 0488: Assessment of aortic regurgitation severity: a cardiac magnetic resonance and echocardiographic comparison study Amsterdam [u.a.] volume:208 year:2015 number:6 pages:345-350 extent:6 |
| format_phy_str_mv |
Article |
| bklname |
Güterverkehr |
| institution |
findex.gbv.de |
| topic_facet |
anaplastic SWI/SNF complex intratumoral heterogeneity chromatin remodeling Meningioma |
| dewey-raw |
610 |
| isfreeaccess_bool |
false |
| container_title |
0488: Assessment of aortic regurgitation severity: a cardiac magnetic resonance and echocardiographic comparison study |
| authorswithroles_txt_mv |
Abedalthagafi, Malak S. @@aut@@ Bi, Wenya Linda @@oth@@ Merrill, Parker H. @@oth@@ Gibson, William J. @@oth@@ Rose, Matthew F. @@oth@@ Du, Ziming @@oth@@ Francis, Joshua M. @@oth@@ Du, Rose @@oth@@ Dunn, Ian F. @@oth@@ Ligon, Azra H. @@oth@@ Beroukhim, Rameen @@oth@@ Santagata, Sandro @@oth@@ |
| publishDateDaySort_date |
2015-01-01T00:00:00Z |
| hierarchy_top_id |
ELV019379730 |
| dewey-sort |
3610 |
| id |
ELV034576185 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV034576185</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625201248.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2015 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.cancergen.2015.03.005</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2015011000030.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV034576185</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S2210-7762(15)00036-8</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">380</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">55.82</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Abedalthagafi, Malak S.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">ARID1A and TERT promoter mutations in dedifferentiated meningioma</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2015transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">6</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">anaplastic</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">SWI/SNF complex</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">intratumoral heterogeneity</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">chromatin remodeling</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Meningioma</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bi, Wenya Linda</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Merrill, Parker H.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Gibson, William J.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Rose, Matthew F.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Du, Ziming</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Francis, Joshua M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Du, Rose</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dunn, Ian F.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ligon, Azra H.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Beroukhim, Rameen</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Santagata, Sandro</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Mohty, Dania ELSEVIER</subfield><subfield code="t">0488: Assessment of aortic regurgitation severity: a cardiac magnetic resonance and echocardiographic comparison study</subfield><subfield code="d">2016</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV019379730</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:208</subfield><subfield code="g">year:2015</subfield><subfield code="g">number:6</subfield><subfield code="g">pages:345-350</subfield><subfield code="g">extent:6</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.cancergen.2015.03.005</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">55.82</subfield><subfield code="j">Güterverkehr</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">208</subfield><subfield code="j">2015</subfield><subfield code="e">6</subfield><subfield code="h">345-350</subfield><subfield code="g">6</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| author |
Abedalthagafi, Malak S. |
| spellingShingle |
Abedalthagafi, Malak S. ddc 610 ddc 380 bkl 55.82 Elsevier anaplastic Elsevier SWI/SNF complex Elsevier intratumoral heterogeneity Elsevier chromatin remodeling Elsevier Meningioma ARID1A and TERT promoter mutations in dedifferentiated meningioma |
| authorStr |
Abedalthagafi, Malak S. |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV019379730 |
| format |
electronic Article |
| dewey-ones |
610 - Medicine & health 380 - Commerce, communications & transportation |
| delete_txt_mv |
keep |
| author_role |
aut |
| collection |
elsevier |
| remote_str |
true |
| illustrated |
Not Illustrated |
| topic_title |
610 610 DE-600 610 VZ 380 VZ 55.82 bkl ARID1A and TERT promoter mutations in dedifferentiated meningioma anaplastic Elsevier SWI/SNF complex Elsevier intratumoral heterogeneity Elsevier chromatin remodeling Elsevier Meningioma Elsevier |
| topic |
ddc 610 ddc 380 bkl 55.82 Elsevier anaplastic Elsevier SWI/SNF complex Elsevier intratumoral heterogeneity Elsevier chromatin remodeling Elsevier Meningioma |
| topic_unstemmed |
ddc 610 ddc 380 bkl 55.82 Elsevier anaplastic Elsevier SWI/SNF complex Elsevier intratumoral heterogeneity Elsevier chromatin remodeling Elsevier Meningioma |
| topic_browse |
ddc 610 ddc 380 bkl 55.82 Elsevier anaplastic Elsevier SWI/SNF complex Elsevier intratumoral heterogeneity Elsevier chromatin remodeling Elsevier Meningioma |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
w l b wl wlb p h m ph phm w j g wj wjg m f r mf mfr z d zd j m f jm jmf r d rd i f d if ifd a h l ah ahl r b rb s s ss |
| hierarchy_parent_title |
0488: Assessment of aortic regurgitation severity: a cardiac magnetic resonance and echocardiographic comparison study |
| hierarchy_parent_id |
ELV019379730 |
| dewey-tens |
610 - Medicine & health 380 - Commerce, communications & transportation |
| hierarchy_top_title |
0488: Assessment of aortic regurgitation severity: a cardiac magnetic resonance and echocardiographic comparison study |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)ELV019379730 |
| title |
ARID1A and TERT promoter mutations in dedifferentiated meningioma |
| ctrlnum |
(DE-627)ELV034576185 (ELSEVIER)S2210-7762(15)00036-8 |
| title_full |
ARID1A and TERT promoter mutations in dedifferentiated meningioma |
| author_sort |
Abedalthagafi, Malak S. |
| journal |
0488: Assessment of aortic regurgitation severity: a cardiac magnetic resonance and echocardiographic comparison study |
| journalStr |
0488: Assessment of aortic regurgitation severity: a cardiac magnetic resonance and echocardiographic comparison study |
| lang_code |
eng |
| isOA_bool |
false |
| dewey-hundreds |
600 - Technology 300 - Social sciences |
| recordtype |
marc |
| publishDateSort |
2015 |
| contenttype_str_mv |
zzz |
| container_start_page |
345 |
| author_browse |
Abedalthagafi, Malak S. |
| container_volume |
208 |
| physical |
6 |
| class |
610 610 DE-600 610 VZ 380 VZ 55.82 bkl |
| format_se |
Elektronische Aufsätze |
| author-letter |
Abedalthagafi, Malak S. |
| doi_str_mv |
10.1016/j.cancergen.2015.03.005 |
| dewey-full |
610 380 |
| title_sort |
arid1a and tert promoter mutations in dedifferentiated meningioma |
| title_auth |
ARID1A and TERT promoter mutations in dedifferentiated meningioma |
| abstract |
Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression. |
| abstractGer |
Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression. |
| abstract_unstemmed |
Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U |
| container_issue |
6 |
| title_short |
ARID1A and TERT promoter mutations in dedifferentiated meningioma |
| url |
https://doi.org/10.1016/j.cancergen.2015.03.005 |
| remote_bool |
true |
| author2 |
Bi, Wenya Linda Merrill, Parker H. Gibson, William J. Rose, Matthew F. Du, Ziming Francis, Joshua M. Du, Rose Dunn, Ian F. Ligon, Azra H. Beroukhim, Rameen Santagata, Sandro |
| author2Str |
Bi, Wenya Linda Merrill, Parker H. Gibson, William J. Rose, Matthew F. Du, Ziming Francis, Joshua M. Du, Rose Dunn, Ian F. Ligon, Azra H. Beroukhim, Rameen Santagata, Sandro |
| ppnlink |
ELV019379730 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth oth oth oth oth oth oth oth |
| doi_str |
10.1016/j.cancergen.2015.03.005 |
| up_date |
2024-07-06T21:27:48.140Z |
| _version_ |
1803866622542217216 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV034576185</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625201248.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2015 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.cancergen.2015.03.005</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2015011000030.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV034576185</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S2210-7762(15)00036-8</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">380</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">55.82</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Abedalthagafi, Malak S.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">ARID1A and TERT promoter mutations in dedifferentiated meningioma</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2015transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">6</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Unlike patients with World Health Organization (WHO) grade I meningiomas, which are considered benign, patients with WHO grade III meningiomas have very high mortality rates. The principles underlying tumor progression in meningioma are largely unknown, yet a detailed understanding of these mechanisms will be required for effective management of patients with these high grade lethal tumors. We present a case of an intraventricular meningioma that at first presentation displayed remarkable morphologic heterogeneity—composed of distinct regions independently fulfilling histopathologic criteria for WHO grade I, II, and III designations. The lowest grade regions had classic meningothelial features, while the highest grade regions were markedly dedifferentiated. Whereas progression in meningiomas is generally observed during recurrence following radiation and systemic medical therapies, the current case offers us a snapshot of histologic progression and intratumoral heterogeneity in a native pretreatment context. Using whole exome sequencing and high resolution array-based comparative genomic hybridization, we observed marked genetic heterogeneity between the various areas. Notably, in the higher grade regions we found increased aneuploidy with progressive loss of heterozygosity, the emergence of mutations in the TERT promoter, and compromise of ARID1A. These findings provide new insights into intratumoral heterogeneity in the evolution of malignant phenotypes in anaplastic meningiomas and potential pathways of malignant progression.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">anaplastic</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">SWI/SNF complex</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">intratumoral heterogeneity</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">chromatin remodeling</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Meningioma</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bi, Wenya Linda</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Merrill, Parker H.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Gibson, William J.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Rose, Matthew F.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Du, Ziming</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Francis, Joshua M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Du, Rose</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dunn, Ian F.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ligon, Azra H.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Beroukhim, Rameen</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Santagata, Sandro</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Mohty, Dania ELSEVIER</subfield><subfield code="t">0488: Assessment of aortic regurgitation severity: a cardiac magnetic resonance and echocardiographic comparison study</subfield><subfield code="d">2016</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV019379730</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:208</subfield><subfield code="g">year:2015</subfield><subfield code="g">number:6</subfield><subfield code="g">pages:345-350</subfield><subfield code="g">extent:6</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.cancergen.2015.03.005</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">55.82</subfield><subfield code="j">Güterverkehr</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">208</subfield><subfield code="j">2015</subfield><subfield code="e">6</subfield><subfield code="h">345-350</subfield><subfield code="g">6</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| score |
7.400609 |