Loss of ARID1A expression is associated with DNA mismatch repair protein deficiency and favorable prognosis in advanced stage surgically resected esophageal adenocarcinoma
Esophageal adenocarcinoma often presents at an advanced stage and has a dismal prognosis. Current prognostic markers have limited utility. ARID1A is implicated as a tumor suppressor gene in esophageal adenocarcinoma. Loss of ARID1A expression correlates with DNA mismatch repair (MMR) protein deficie...
Ausführliche Beschreibung
Autor*in: |
Lowenthal, Brett M. [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2019transfer abstract |
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Umfang: |
10 |
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Übergeordnetes Werk: |
Enthalten in: Chronic Total Occlusion – Percutaneous Coronary Intervention (CTO-PCI) Experience in a Single, Multi-operator Australian Centre: Need for dedicated CTO-PCI programs - BoganaShanmugam, Vimalraj ELSEVIER, 2016, New York, NY [u.a.] |
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Übergeordnetes Werk: |
volume:94 ; year:2019 ; pages:1-10 ; extent:10 |
Links: |
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DOI / URN: |
10.1016/j.humpath.2019.09.004 |
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Katalog-ID: |
ELV048798428 |
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245 | 1 | 0 | |a Loss of ARID1A expression is associated with DNA mismatch repair protein deficiency and favorable prognosis in advanced stage surgically resected esophageal adenocarcinoma |
264 | 1 | |c 2019transfer abstract | |
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520 | |a Esophageal adenocarcinoma often presents at an advanced stage and has a dismal prognosis. Current prognostic markers have limited utility. ARID1A is implicated as a tumor suppressor gene in esophageal adenocarcinoma. Loss of ARID1A expression correlates with DNA mismatch repair (MMR) protein deficiency in other tumors. We hypothesized that ARID1A loss is associated with prognosis and DNA MMR protein deficiency in esophageal adenocarcinoma. Tissue microarrays representing 316 surgically resected esophageal adenocarcinomas without neoadjuvant treatment were evaluated for ARID1A and MMR proteins by immunohistochemistry. Loss of ARID1A expression (ARID1A-loss) was detected in 41 of 316 (13%) adenocarcinomas. MMR deficiency was identified in 5% (17/316) but was detected more frequently in ARID1A-loss adenocarcinomas (13/41, 32%) than in ARID1A-retained adenocarcinomas (4/275, 1%; P < .001). Morphologically, ARID1A-loss adenocarcinomas frequently demonstrated peritumoral lymphoid aggregates (90%) and tumor infiltrating lymphocytes (51%). In patients with locally advanced or metastatic disease (stages III or IV, N = 169), patients with ARID1A-loss adenocarcinomas (N = 22) had longer overall survival than patients with ARID1A-retained adenocarcinomas (median [month]: 26 vs. 16, P = .010). In these patients, ARID1A-loss correlated with a 56% reduction in mortality independent of other prognostic factors (P = .007). In summary, loss of ARID1A expression is associated with DNA MMR protein deficiency in esophageal adenocarcinoma. Furthermore, ARID1A loss is independently associated with a more favorable prognosis for patients with locally advanced or metastatic esophageal adenocarcinomas. | ||
520 | |a Esophageal adenocarcinoma often presents at an advanced stage and has a dismal prognosis. Current prognostic markers have limited utility. ARID1A is implicated as a tumor suppressor gene in esophageal adenocarcinoma. Loss of ARID1A expression correlates with DNA mismatch repair (MMR) protein deficiency in other tumors. We hypothesized that ARID1A loss is associated with prognosis and DNA MMR protein deficiency in esophageal adenocarcinoma. Tissue microarrays representing 316 surgically resected esophageal adenocarcinomas without neoadjuvant treatment were evaluated for ARID1A and MMR proteins by immunohistochemistry. Loss of ARID1A expression (ARID1A-loss) was detected in 41 of 316 (13%) adenocarcinomas. MMR deficiency was identified in 5% (17/316) but was detected more frequently in ARID1A-loss adenocarcinomas (13/41, 32%) than in ARID1A-retained adenocarcinomas (4/275, 1%; P < .001). Morphologically, ARID1A-loss adenocarcinomas frequently demonstrated peritumoral lymphoid aggregates (90%) and tumor infiltrating lymphocytes (51%). In patients with locally advanced or metastatic disease (stages III or IV, N = 169), patients with ARID1A-loss adenocarcinomas (N = 22) had longer overall survival than patients with ARID1A-retained adenocarcinomas (median [month]: 26 vs. 16, P = .010). In these patients, ARID1A-loss correlated with a 56% reduction in mortality independent of other prognostic factors (P = .007). In summary, loss of ARID1A expression is associated with DNA MMR protein deficiency in esophageal adenocarcinoma. Furthermore, ARID1A loss is independently associated with a more favorable prognosis for patients with locally advanced or metastatic esophageal adenocarcinomas. | ||
700 | 1 | |a Nason, Katie S. |4 oth | |
700 | 1 | |a Pennathur, Arjun |4 oth | |
700 | 1 | |a Luketich, James D. |4 oth | |
700 | 1 | |a Pai, Reetesh K. |4 oth | |
700 | 1 | |a Davison, Jon M. |4 oth | |
700 | 1 | |a Ma, Changqing |4 oth | |
773 | 0 | 8 | |i Enthalten in |n Elsevier |a BoganaShanmugam, Vimalraj ELSEVIER |t Chronic Total Occlusion – Percutaneous Coronary Intervention (CTO-PCI) Experience in a Single, Multi-operator Australian Centre: Need for dedicated CTO-PCI programs |d 2016 |g New York, NY [u.a.] |w (DE-627)ELV019059760 |
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10.1016/j.humpath.2019.09.004 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000840.pica (DE-627)ELV048798428 (ELSEVIER)S0046-8177(19)30169-8 DE-627 ger DE-627 rakwb eng 610 VZ 550 VZ 38.48 bkl 38.90 bkl 42.94 bkl Lowenthal, Brett M. verfasserin aut Loss of ARID1A expression is associated with DNA mismatch repair protein deficiency and favorable prognosis in advanced stage surgically resected esophageal adenocarcinoma 2019transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Esophageal adenocarcinoma often presents at an advanced stage and has a dismal prognosis. Current prognostic markers have limited utility. ARID1A is implicated as a tumor suppressor gene in esophageal adenocarcinoma. Loss of ARID1A expression correlates with DNA mismatch repair (MMR) protein deficiency in other tumors. We hypothesized that ARID1A loss is associated with prognosis and DNA MMR protein deficiency in esophageal adenocarcinoma. Tissue microarrays representing 316 surgically resected esophageal adenocarcinomas without neoadjuvant treatment were evaluated for ARID1A and MMR proteins by immunohistochemistry. Loss of ARID1A expression (ARID1A-loss) was detected in 41 of 316 (13%) adenocarcinomas. MMR deficiency was identified in 5% (17/316) but was detected more frequently in ARID1A-loss adenocarcinomas (13/41, 32%) than in ARID1A-retained adenocarcinomas (4/275, 1%; P < .001). Morphologically, ARID1A-loss adenocarcinomas frequently demonstrated peritumoral lymphoid aggregates (90%) and tumor infiltrating lymphocytes (51%). In patients with locally advanced or metastatic disease (stages III or IV, N = 169), patients with ARID1A-loss adenocarcinomas (N = 22) had longer overall survival than patients with ARID1A-retained adenocarcinomas (median [month]: 26 vs. 16, P = .010). In these patients, ARID1A-loss correlated with a 56% reduction in mortality independent of other prognostic factors (P = .007). In summary, loss of ARID1A expression is associated with DNA MMR protein deficiency in esophageal adenocarcinoma. Furthermore, ARID1A loss is independently associated with a more favorable prognosis for patients with locally advanced or metastatic esophageal adenocarcinomas. Esophageal adenocarcinoma often presents at an advanced stage and has a dismal prognosis. Current prognostic markers have limited utility. ARID1A is implicated as a tumor suppressor gene in esophageal adenocarcinoma. Loss of ARID1A expression correlates with DNA mismatch repair (MMR) protein deficiency in other tumors. We hypothesized that ARID1A loss is associated with prognosis and DNA MMR protein deficiency in esophageal adenocarcinoma. Tissue microarrays representing 316 surgically resected esophageal adenocarcinomas without neoadjuvant treatment were evaluated for ARID1A and MMR proteins by immunohistochemistry. Loss of ARID1A expression (ARID1A-loss) was detected in 41 of 316 (13%) adenocarcinomas. MMR deficiency was identified in 5% (17/316) but was detected more frequently in ARID1A-loss adenocarcinomas (13/41, 32%) than in ARID1A-retained adenocarcinomas (4/275, 1%; P < .001). Morphologically, ARID1A-loss adenocarcinomas frequently demonstrated peritumoral lymphoid aggregates (90%) and tumor infiltrating lymphocytes (51%). In patients with locally advanced or metastatic disease (stages III or IV, N = 169), patients with ARID1A-loss adenocarcinomas (N = 22) had longer overall survival than patients with ARID1A-retained adenocarcinomas (median [month]: 26 vs. 16, P = .010). In these patients, ARID1A-loss correlated with a 56% reduction in mortality independent of other prognostic factors (P = .007). In summary, loss of ARID1A expression is associated with DNA MMR protein deficiency in esophageal adenocarcinoma. Furthermore, ARID1A loss is independently associated with a more favorable prognosis for patients with locally advanced or metastatic esophageal adenocarcinomas. Nason, Katie S. oth Pennathur, Arjun oth Luketich, James D. oth Pai, Reetesh K. oth Davison, Jon M. oth Ma, Changqing oth Enthalten in Elsevier BoganaShanmugam, Vimalraj ELSEVIER Chronic Total Occlusion – Percutaneous Coronary Intervention (CTO-PCI) Experience in a Single, Multi-operator Australian Centre: Need for dedicated CTO-PCI programs 2016 New York, NY [u.a.] (DE-627)ELV019059760 volume:94 year:2019 pages:1-10 extent:10 https://doi.org/10.1016/j.humpath.2019.09.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO GBV_ILN_60 38.48 Marine Geologie VZ 38.90 Ozeanologie Ozeanographie VZ 42.94 Meeresbiologie VZ AR 94 2019 1-10 10 |
spelling |
10.1016/j.humpath.2019.09.004 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000840.pica (DE-627)ELV048798428 (ELSEVIER)S0046-8177(19)30169-8 DE-627 ger DE-627 rakwb eng 610 VZ 550 VZ 38.48 bkl 38.90 bkl 42.94 bkl Lowenthal, Brett M. verfasserin aut Loss of ARID1A expression is associated with DNA mismatch repair protein deficiency and favorable prognosis in advanced stage surgically resected esophageal adenocarcinoma 2019transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Esophageal adenocarcinoma often presents at an advanced stage and has a dismal prognosis. Current prognostic markers have limited utility. ARID1A is implicated as a tumor suppressor gene in esophageal adenocarcinoma. Loss of ARID1A expression correlates with DNA mismatch repair (MMR) protein deficiency in other tumors. We hypothesized that ARID1A loss is associated with prognosis and DNA MMR protein deficiency in esophageal adenocarcinoma. Tissue microarrays representing 316 surgically resected esophageal adenocarcinomas without neoadjuvant treatment were evaluated for ARID1A and MMR proteins by immunohistochemistry. Loss of ARID1A expression (ARID1A-loss) was detected in 41 of 316 (13%) adenocarcinomas. MMR deficiency was identified in 5% (17/316) but was detected more frequently in ARID1A-loss adenocarcinomas (13/41, 32%) than in ARID1A-retained adenocarcinomas (4/275, 1%; P < .001). Morphologically, ARID1A-loss adenocarcinomas frequently demonstrated peritumoral lymphoid aggregates (90%) and tumor infiltrating lymphocytes (51%). In patients with locally advanced or metastatic disease (stages III or IV, N = 169), patients with ARID1A-loss adenocarcinomas (N = 22) had longer overall survival than patients with ARID1A-retained adenocarcinomas (median [month]: 26 vs. 16, P = .010). In these patients, ARID1A-loss correlated with a 56% reduction in mortality independent of other prognostic factors (P = .007). In summary, loss of ARID1A expression is associated with DNA MMR protein deficiency in esophageal adenocarcinoma. Furthermore, ARID1A loss is independently associated with a more favorable prognosis for patients with locally advanced or metastatic esophageal adenocarcinomas. Esophageal adenocarcinoma often presents at an advanced stage and has a dismal prognosis. Current prognostic markers have limited utility. ARID1A is implicated as a tumor suppressor gene in esophageal adenocarcinoma. Loss of ARID1A expression correlates with DNA mismatch repair (MMR) protein deficiency in other tumors. We hypothesized that ARID1A loss is associated with prognosis and DNA MMR protein deficiency in esophageal adenocarcinoma. Tissue microarrays representing 316 surgically resected esophageal adenocarcinomas without neoadjuvant treatment were evaluated for ARID1A and MMR proteins by immunohistochemistry. Loss of ARID1A expression (ARID1A-loss) was detected in 41 of 316 (13%) adenocarcinomas. MMR deficiency was identified in 5% (17/316) but was detected more frequently in ARID1A-loss adenocarcinomas (13/41, 32%) than in ARID1A-retained adenocarcinomas (4/275, 1%; P < .001). Morphologically, ARID1A-loss adenocarcinomas frequently demonstrated peritumoral lymphoid aggregates (90%) and tumor infiltrating lymphocytes (51%). In patients with locally advanced or metastatic disease (stages III or IV, N = 169), patients with ARID1A-loss adenocarcinomas (N = 22) had longer overall survival than patients with ARID1A-retained adenocarcinomas (median [month]: 26 vs. 16, P = .010). In these patients, ARID1A-loss correlated with a 56% reduction in mortality independent of other prognostic factors (P = .007). In summary, loss of ARID1A expression is associated with DNA MMR protein deficiency in esophageal adenocarcinoma. Furthermore, ARID1A loss is independently associated with a more favorable prognosis for patients with locally advanced or metastatic esophageal adenocarcinomas. Nason, Katie S. oth Pennathur, Arjun oth Luketich, James D. oth Pai, Reetesh K. oth Davison, Jon M. oth Ma, Changqing oth Enthalten in Elsevier BoganaShanmugam, Vimalraj ELSEVIER Chronic Total Occlusion – Percutaneous Coronary Intervention (CTO-PCI) Experience in a Single, Multi-operator Australian Centre: Need for dedicated CTO-PCI programs 2016 New York, NY [u.a.] (DE-627)ELV019059760 volume:94 year:2019 pages:1-10 extent:10 https://doi.org/10.1016/j.humpath.2019.09.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO GBV_ILN_60 38.48 Marine Geologie VZ 38.90 Ozeanologie Ozeanographie VZ 42.94 Meeresbiologie VZ AR 94 2019 1-10 10 |
allfields_unstemmed |
10.1016/j.humpath.2019.09.004 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000840.pica (DE-627)ELV048798428 (ELSEVIER)S0046-8177(19)30169-8 DE-627 ger DE-627 rakwb eng 610 VZ 550 VZ 38.48 bkl 38.90 bkl 42.94 bkl Lowenthal, Brett M. verfasserin aut Loss of ARID1A expression is associated with DNA mismatch repair protein deficiency and favorable prognosis in advanced stage surgically resected esophageal adenocarcinoma 2019transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Esophageal adenocarcinoma often presents at an advanced stage and has a dismal prognosis. Current prognostic markers have limited utility. ARID1A is implicated as a tumor suppressor gene in esophageal adenocarcinoma. Loss of ARID1A expression correlates with DNA mismatch repair (MMR) protein deficiency in other tumors. We hypothesized that ARID1A loss is associated with prognosis and DNA MMR protein deficiency in esophageal adenocarcinoma. Tissue microarrays representing 316 surgically resected esophageal adenocarcinomas without neoadjuvant treatment were evaluated for ARID1A and MMR proteins by immunohistochemistry. Loss of ARID1A expression (ARID1A-loss) was detected in 41 of 316 (13%) adenocarcinomas. MMR deficiency was identified in 5% (17/316) but was detected more frequently in ARID1A-loss adenocarcinomas (13/41, 32%) than in ARID1A-retained adenocarcinomas (4/275, 1%; P < .001). Morphologically, ARID1A-loss adenocarcinomas frequently demonstrated peritumoral lymphoid aggregates (90%) and tumor infiltrating lymphocytes (51%). In patients with locally advanced or metastatic disease (stages III or IV, N = 169), patients with ARID1A-loss adenocarcinomas (N = 22) had longer overall survival than patients with ARID1A-retained adenocarcinomas (median [month]: 26 vs. 16, P = .010). In these patients, ARID1A-loss correlated with a 56% reduction in mortality independent of other prognostic factors (P = .007). In summary, loss of ARID1A expression is associated with DNA MMR protein deficiency in esophageal adenocarcinoma. Furthermore, ARID1A loss is independently associated with a more favorable prognosis for patients with locally advanced or metastatic esophageal adenocarcinomas. Esophageal adenocarcinoma often presents at an advanced stage and has a dismal prognosis. Current prognostic markers have limited utility. ARID1A is implicated as a tumor suppressor gene in esophageal adenocarcinoma. Loss of ARID1A expression correlates with DNA mismatch repair (MMR) protein deficiency in other tumors. We hypothesized that ARID1A loss is associated with prognosis and DNA MMR protein deficiency in esophageal adenocarcinoma. Tissue microarrays representing 316 surgically resected esophageal adenocarcinomas without neoadjuvant treatment were evaluated for ARID1A and MMR proteins by immunohistochemistry. Loss of ARID1A expression (ARID1A-loss) was detected in 41 of 316 (13%) adenocarcinomas. MMR deficiency was identified in 5% (17/316) but was detected more frequently in ARID1A-loss adenocarcinomas (13/41, 32%) than in ARID1A-retained adenocarcinomas (4/275, 1%; P < .001). Morphologically, ARID1A-loss adenocarcinomas frequently demonstrated peritumoral lymphoid aggregates (90%) and tumor infiltrating lymphocytes (51%). In patients with locally advanced or metastatic disease (stages III or IV, N = 169), patients with ARID1A-loss adenocarcinomas (N = 22) had longer overall survival than patients with ARID1A-retained adenocarcinomas (median [month]: 26 vs. 16, P = .010). In these patients, ARID1A-loss correlated with a 56% reduction in mortality independent of other prognostic factors (P = .007). In summary, loss of ARID1A expression is associated with DNA MMR protein deficiency in esophageal adenocarcinoma. Furthermore, ARID1A loss is independently associated with a more favorable prognosis for patients with locally advanced or metastatic esophageal adenocarcinomas. Nason, Katie S. oth Pennathur, Arjun oth Luketich, James D. oth Pai, Reetesh K. oth Davison, Jon M. oth Ma, Changqing oth Enthalten in Elsevier BoganaShanmugam, Vimalraj ELSEVIER Chronic Total Occlusion – Percutaneous Coronary Intervention (CTO-PCI) Experience in a Single, Multi-operator Australian Centre: Need for dedicated CTO-PCI programs 2016 New York, NY [u.a.] (DE-627)ELV019059760 volume:94 year:2019 pages:1-10 extent:10 https://doi.org/10.1016/j.humpath.2019.09.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO GBV_ILN_60 38.48 Marine Geologie VZ 38.90 Ozeanologie Ozeanographie VZ 42.94 Meeresbiologie VZ AR 94 2019 1-10 10 |
allfieldsGer |
10.1016/j.humpath.2019.09.004 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000840.pica (DE-627)ELV048798428 (ELSEVIER)S0046-8177(19)30169-8 DE-627 ger DE-627 rakwb eng 610 VZ 550 VZ 38.48 bkl 38.90 bkl 42.94 bkl Lowenthal, Brett M. verfasserin aut Loss of ARID1A expression is associated with DNA mismatch repair protein deficiency and favorable prognosis in advanced stage surgically resected esophageal adenocarcinoma 2019transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Esophageal adenocarcinoma often presents at an advanced stage and has a dismal prognosis. Current prognostic markers have limited utility. ARID1A is implicated as a tumor suppressor gene in esophageal adenocarcinoma. Loss of ARID1A expression correlates with DNA mismatch repair (MMR) protein deficiency in other tumors. We hypothesized that ARID1A loss is associated with prognosis and DNA MMR protein deficiency in esophageal adenocarcinoma. Tissue microarrays representing 316 surgically resected esophageal adenocarcinomas without neoadjuvant treatment were evaluated for ARID1A and MMR proteins by immunohistochemistry. Loss of ARID1A expression (ARID1A-loss) was detected in 41 of 316 (13%) adenocarcinomas. MMR deficiency was identified in 5% (17/316) but was detected more frequently in ARID1A-loss adenocarcinomas (13/41, 32%) than in ARID1A-retained adenocarcinomas (4/275, 1%; P < .001). Morphologically, ARID1A-loss adenocarcinomas frequently demonstrated peritumoral lymphoid aggregates (90%) and tumor infiltrating lymphocytes (51%). In patients with locally advanced or metastatic disease (stages III or IV, N = 169), patients with ARID1A-loss adenocarcinomas (N = 22) had longer overall survival than patients with ARID1A-retained adenocarcinomas (median [month]: 26 vs. 16, P = .010). In these patients, ARID1A-loss correlated with a 56% reduction in mortality independent of other prognostic factors (P = .007). In summary, loss of ARID1A expression is associated with DNA MMR protein deficiency in esophageal adenocarcinoma. Furthermore, ARID1A loss is independently associated with a more favorable prognosis for patients with locally advanced or metastatic esophageal adenocarcinomas. Esophageal adenocarcinoma often presents at an advanced stage and has a dismal prognosis. Current prognostic markers have limited utility. ARID1A is implicated as a tumor suppressor gene in esophageal adenocarcinoma. Loss of ARID1A expression correlates with DNA mismatch repair (MMR) protein deficiency in other tumors. We hypothesized that ARID1A loss is associated with prognosis and DNA MMR protein deficiency in esophageal adenocarcinoma. Tissue microarrays representing 316 surgically resected esophageal adenocarcinomas without neoadjuvant treatment were evaluated for ARID1A and MMR proteins by immunohistochemistry. Loss of ARID1A expression (ARID1A-loss) was detected in 41 of 316 (13%) adenocarcinomas. MMR deficiency was identified in 5% (17/316) but was detected more frequently in ARID1A-loss adenocarcinomas (13/41, 32%) than in ARID1A-retained adenocarcinomas (4/275, 1%; P < .001). Morphologically, ARID1A-loss adenocarcinomas frequently demonstrated peritumoral lymphoid aggregates (90%) and tumor infiltrating lymphocytes (51%). In patients with locally advanced or metastatic disease (stages III or IV, N = 169), patients with ARID1A-loss adenocarcinomas (N = 22) had longer overall survival than patients with ARID1A-retained adenocarcinomas (median [month]: 26 vs. 16, P = .010). In these patients, ARID1A-loss correlated with a 56% reduction in mortality independent of other prognostic factors (P = .007). In summary, loss of ARID1A expression is associated with DNA MMR protein deficiency in esophageal adenocarcinoma. Furthermore, ARID1A loss is independently associated with a more favorable prognosis for patients with locally advanced or metastatic esophageal adenocarcinomas. Nason, Katie S. oth Pennathur, Arjun oth Luketich, James D. oth Pai, Reetesh K. oth Davison, Jon M. oth Ma, Changqing oth Enthalten in Elsevier BoganaShanmugam, Vimalraj ELSEVIER Chronic Total Occlusion – Percutaneous Coronary Intervention (CTO-PCI) Experience in a Single, Multi-operator Australian Centre: Need for dedicated CTO-PCI programs 2016 New York, NY [u.a.] (DE-627)ELV019059760 volume:94 year:2019 pages:1-10 extent:10 https://doi.org/10.1016/j.humpath.2019.09.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO GBV_ILN_60 38.48 Marine Geologie VZ 38.90 Ozeanologie Ozeanographie VZ 42.94 Meeresbiologie VZ AR 94 2019 1-10 10 |
allfieldsSound |
10.1016/j.humpath.2019.09.004 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000840.pica (DE-627)ELV048798428 (ELSEVIER)S0046-8177(19)30169-8 DE-627 ger DE-627 rakwb eng 610 VZ 550 VZ 38.48 bkl 38.90 bkl 42.94 bkl Lowenthal, Brett M. verfasserin aut Loss of ARID1A expression is associated with DNA mismatch repair protein deficiency and favorable prognosis in advanced stage surgically resected esophageal adenocarcinoma 2019transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Esophageal adenocarcinoma often presents at an advanced stage and has a dismal prognosis. Current prognostic markers have limited utility. ARID1A is implicated as a tumor suppressor gene in esophageal adenocarcinoma. Loss of ARID1A expression correlates with DNA mismatch repair (MMR) protein deficiency in other tumors. We hypothesized that ARID1A loss is associated with prognosis and DNA MMR protein deficiency in esophageal adenocarcinoma. Tissue microarrays representing 316 surgically resected esophageal adenocarcinomas without neoadjuvant treatment were evaluated for ARID1A and MMR proteins by immunohistochemistry. Loss of ARID1A expression (ARID1A-loss) was detected in 41 of 316 (13%) adenocarcinomas. MMR deficiency was identified in 5% (17/316) but was detected more frequently in ARID1A-loss adenocarcinomas (13/41, 32%) than in ARID1A-retained adenocarcinomas (4/275, 1%; P < .001). Morphologically, ARID1A-loss adenocarcinomas frequently demonstrated peritumoral lymphoid aggregates (90%) and tumor infiltrating lymphocytes (51%). In patients with locally advanced or metastatic disease (stages III or IV, N = 169), patients with ARID1A-loss adenocarcinomas (N = 22) had longer overall survival than patients with ARID1A-retained adenocarcinomas (median [month]: 26 vs. 16, P = .010). In these patients, ARID1A-loss correlated with a 56% reduction in mortality independent of other prognostic factors (P = .007). In summary, loss of ARID1A expression is associated with DNA MMR protein deficiency in esophageal adenocarcinoma. Furthermore, ARID1A loss is independently associated with a more favorable prognosis for patients with locally advanced or metastatic esophageal adenocarcinomas. Esophageal adenocarcinoma often presents at an advanced stage and has a dismal prognosis. Current prognostic markers have limited utility. ARID1A is implicated as a tumor suppressor gene in esophageal adenocarcinoma. Loss of ARID1A expression correlates with DNA mismatch repair (MMR) protein deficiency in other tumors. We hypothesized that ARID1A loss is associated with prognosis and DNA MMR protein deficiency in esophageal adenocarcinoma. Tissue microarrays representing 316 surgically resected esophageal adenocarcinomas without neoadjuvant treatment were evaluated for ARID1A and MMR proteins by immunohistochemistry. Loss of ARID1A expression (ARID1A-loss) was detected in 41 of 316 (13%) adenocarcinomas. MMR deficiency was identified in 5% (17/316) but was detected more frequently in ARID1A-loss adenocarcinomas (13/41, 32%) than in ARID1A-retained adenocarcinomas (4/275, 1%; P < .001). Morphologically, ARID1A-loss adenocarcinomas frequently demonstrated peritumoral lymphoid aggregates (90%) and tumor infiltrating lymphocytes (51%). In patients with locally advanced or metastatic disease (stages III or IV, N = 169), patients with ARID1A-loss adenocarcinomas (N = 22) had longer overall survival than patients with ARID1A-retained adenocarcinomas (median [month]: 26 vs. 16, P = .010). In these patients, ARID1A-loss correlated with a 56% reduction in mortality independent of other prognostic factors (P = .007). In summary, loss of ARID1A expression is associated with DNA MMR protein deficiency in esophageal adenocarcinoma. Furthermore, ARID1A loss is independently associated with a more favorable prognosis for patients with locally advanced or metastatic esophageal adenocarcinomas. Nason, Katie S. oth Pennathur, Arjun oth Luketich, James D. oth Pai, Reetesh K. oth Davison, Jon M. oth Ma, Changqing oth Enthalten in Elsevier BoganaShanmugam, Vimalraj ELSEVIER Chronic Total Occlusion – Percutaneous Coronary Intervention (CTO-PCI) Experience in a Single, Multi-operator Australian Centre: Need for dedicated CTO-PCI programs 2016 New York, NY [u.a.] (DE-627)ELV019059760 volume:94 year:2019 pages:1-10 extent:10 https://doi.org/10.1016/j.humpath.2019.09.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO GBV_ILN_60 38.48 Marine Geologie VZ 38.90 Ozeanologie Ozeanographie VZ 42.94 Meeresbiologie VZ AR 94 2019 1-10 10 |
language |
English |
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Enthalten in Chronic Total Occlusion – Percutaneous Coronary Intervention (CTO-PCI) Experience in a Single, Multi-operator Australian Centre: Need for dedicated CTO-PCI programs New York, NY [u.a.] volume:94 year:2019 pages:1-10 extent:10 |
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Loss of ARID1A expression is associated with DNA mismatch repair protein deficiency and favorable prognosis in advanced stage surgically resected esophageal adenocarcinoma |
abstract |
Esophageal adenocarcinoma often presents at an advanced stage and has a dismal prognosis. Current prognostic markers have limited utility. ARID1A is implicated as a tumor suppressor gene in esophageal adenocarcinoma. Loss of ARID1A expression correlates with DNA mismatch repair (MMR) protein deficiency in other tumors. We hypothesized that ARID1A loss is associated with prognosis and DNA MMR protein deficiency in esophageal adenocarcinoma. Tissue microarrays representing 316 surgically resected esophageal adenocarcinomas without neoadjuvant treatment were evaluated for ARID1A and MMR proteins by immunohistochemistry. Loss of ARID1A expression (ARID1A-loss) was detected in 41 of 316 (13%) adenocarcinomas. MMR deficiency was identified in 5% (17/316) but was detected more frequently in ARID1A-loss adenocarcinomas (13/41, 32%) than in ARID1A-retained adenocarcinomas (4/275, 1%; P < .001). Morphologically, ARID1A-loss adenocarcinomas frequently demonstrated peritumoral lymphoid aggregates (90%) and tumor infiltrating lymphocytes (51%). In patients with locally advanced or metastatic disease (stages III or IV, N = 169), patients with ARID1A-loss adenocarcinomas (N = 22) had longer overall survival than patients with ARID1A-retained adenocarcinomas (median [month]: 26 vs. 16, P = .010). In these patients, ARID1A-loss correlated with a 56% reduction in mortality independent of other prognostic factors (P = .007). In summary, loss of ARID1A expression is associated with DNA MMR protein deficiency in esophageal adenocarcinoma. Furthermore, ARID1A loss is independently associated with a more favorable prognosis for patients with locally advanced or metastatic esophageal adenocarcinomas. |
abstractGer |
Esophageal adenocarcinoma often presents at an advanced stage and has a dismal prognosis. Current prognostic markers have limited utility. ARID1A is implicated as a tumor suppressor gene in esophageal adenocarcinoma. Loss of ARID1A expression correlates with DNA mismatch repair (MMR) protein deficiency in other tumors. We hypothesized that ARID1A loss is associated with prognosis and DNA MMR protein deficiency in esophageal adenocarcinoma. Tissue microarrays representing 316 surgically resected esophageal adenocarcinomas without neoadjuvant treatment were evaluated for ARID1A and MMR proteins by immunohistochemistry. Loss of ARID1A expression (ARID1A-loss) was detected in 41 of 316 (13%) adenocarcinomas. MMR deficiency was identified in 5% (17/316) but was detected more frequently in ARID1A-loss adenocarcinomas (13/41, 32%) than in ARID1A-retained adenocarcinomas (4/275, 1%; P < .001). Morphologically, ARID1A-loss adenocarcinomas frequently demonstrated peritumoral lymphoid aggregates (90%) and tumor infiltrating lymphocytes (51%). In patients with locally advanced or metastatic disease (stages III or IV, N = 169), patients with ARID1A-loss adenocarcinomas (N = 22) had longer overall survival than patients with ARID1A-retained adenocarcinomas (median [month]: 26 vs. 16, P = .010). In these patients, ARID1A-loss correlated with a 56% reduction in mortality independent of other prognostic factors (P = .007). In summary, loss of ARID1A expression is associated with DNA MMR protein deficiency in esophageal adenocarcinoma. Furthermore, ARID1A loss is independently associated with a more favorable prognosis for patients with locally advanced or metastatic esophageal adenocarcinomas. |
abstract_unstemmed |
Esophageal adenocarcinoma often presents at an advanced stage and has a dismal prognosis. Current prognostic markers have limited utility. ARID1A is implicated as a tumor suppressor gene in esophageal adenocarcinoma. Loss of ARID1A expression correlates with DNA mismatch repair (MMR) protein deficiency in other tumors. We hypothesized that ARID1A loss is associated with prognosis and DNA MMR protein deficiency in esophageal adenocarcinoma. Tissue microarrays representing 316 surgically resected esophageal adenocarcinomas without neoadjuvant treatment were evaluated for ARID1A and MMR proteins by immunohistochemistry. Loss of ARID1A expression (ARID1A-loss) was detected in 41 of 316 (13%) adenocarcinomas. MMR deficiency was identified in 5% (17/316) but was detected more frequently in ARID1A-loss adenocarcinomas (13/41, 32%) than in ARID1A-retained adenocarcinomas (4/275, 1%; P < .001). Morphologically, ARID1A-loss adenocarcinomas frequently demonstrated peritumoral lymphoid aggregates (90%) and tumor infiltrating lymphocytes (51%). In patients with locally advanced or metastatic disease (stages III or IV, N = 169), patients with ARID1A-loss adenocarcinomas (N = 22) had longer overall survival than patients with ARID1A-retained adenocarcinomas (median [month]: 26 vs. 16, P = .010). In these patients, ARID1A-loss correlated with a 56% reduction in mortality independent of other prognostic factors (P = .007). In summary, loss of ARID1A expression is associated with DNA MMR protein deficiency in esophageal adenocarcinoma. Furthermore, ARID1A loss is independently associated with a more favorable prognosis for patients with locally advanced or metastatic esophageal adenocarcinomas. |
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Loss of ARID1A expression correlates with DNA mismatch repair (MMR) protein deficiency in other tumors. We hypothesized that ARID1A loss is associated with prognosis and DNA MMR protein deficiency in esophageal adenocarcinoma. Tissue microarrays representing 316 surgically resected esophageal adenocarcinomas without neoadjuvant treatment were evaluated for ARID1A and MMR proteins by immunohistochemistry. Loss of ARID1A expression (ARID1A-loss) was detected in 41 of 316 (13%) adenocarcinomas. MMR deficiency was identified in 5% (17/316) but was detected more frequently in ARID1A-loss adenocarcinomas (13/41, 32%) than in ARID1A-retained adenocarcinomas (4/275, 1%; P < .001). Morphologically, ARID1A-loss adenocarcinomas frequently demonstrated peritumoral lymphoid aggregates (90%) and tumor infiltrating lymphocytes (51%). In patients with locally advanced or metastatic disease (stages III or IV, N = 169), patients with ARID1A-loss adenocarcinomas (N = 22) had longer overall survival than patients with ARID1A-retained adenocarcinomas (median [month]: 26 vs. 16, P = .010). In these patients, ARID1A-loss correlated with a 56% reduction in mortality independent of other prognostic factors (P = .007). In summary, loss of ARID1A expression is associated with DNA MMR protein deficiency in esophageal adenocarcinoma. 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