Activin a Receptor Type 2A Mutation Affects the Tumor Biology of Microsatellite Instability-High Gastric Cancer
Background Activin A receptor type 2A (ACVR2A) is one of the most frequently mutated genes in microsatellite instability-high (MSI-H) gastric cancer. However, the clinical relevance of the ACVR2A mutation in MSI-H gastric cancer patients remains unclear. The aims of this study were to explore the ef...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Yuza, Kizuki [verfasserIn] Nagahashi, Masayuki [verfasserIn] Ichikawa, Hiroshi [verfasserIn] Hanyu, Takaaki [verfasserIn] Nakajima, Masato [verfasserIn] Shimada, Yoshifumi [verfasserIn] Ishikawa, Takashi [verfasserIn] Sakata, Jun [verfasserIn] Takeuchi, Shiho [verfasserIn] Okuda, Shujiro [verfasserIn] Matsuda, Yasunobu [verfasserIn] Abe, Manabu [verfasserIn] Sakimura, Kenji [verfasserIn] Takabe, Kazuaki [verfasserIn] Wakai, Toshifumi [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2021 |
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| Schlagwörter: |
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| Anmerkung: |
© The Society for Surgery of the Alimentary Tract 2021 |
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| Übergeordnetes Werk: |
Enthalten in: Journal of gastrointestinal surgery - New York, NY : Springer, 1997, 25(2021), 9 vom: 08. Jan., Seite 2231-2241 |
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| Übergeordnetes Werk: |
volume:25 ; year:2021 ; number:9 ; day:08 ; month:01 ; pages:2231-2241 |
| Links: |
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| DOI / URN: |
10.1007/s11605-020-04889-9 |
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| Katalog-ID: |
SPR045194238 |
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| 245 | 1 | 0 | |a Activin a Receptor Type 2A Mutation Affects the Tumor Biology of Microsatellite Instability-High Gastric Cancer |
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| 520 | |a Background Activin A receptor type 2A (ACVR2A) is one of the most frequently mutated genes in microsatellite instability-high (MSI-H) gastric cancer. However, the clinical relevance of the ACVR2A mutation in MSI-H gastric cancer patients remains unclear. The aims of this study were to explore the effect of ACVR2A mutation on the tumor behavior and to identify the clinicopathological characteristics of gastric cancer patients with ACVR2A mutations. Methods An in vitro study was performed to investigate the biological role of ACVR2A via CRISPR/Cas9-mediated ACVR2A knockout MKN74 human gastric cancer cells. One hundred twenty-four patients with gastric cancer were retrospectively analyzed, and relations between MSI status, ACVR2A mutations, and clinicopathological factors were evaluated. Results ACVR2A knockout cells showed less aggressive tumor biology than mock-transfected cells, displaying reduced proliferation, migration, and invasion (P < 0.05). MSI mutations were found in 10% (13/124) of gastric cancer patients, and ACVR2A mutations were found in 8.1% (10/124) of patients. All ACVR2A mutations were accompanied by MSI. The 5-year overall survival rates of ACVR2A wild-type patients and ACVR2A-mutated patients were 57% and 90%, respectively (P = 0.048). Multivariate analysis revealed that older age (P = 0.015), distant metastasis (P < 0.001), and ACVR2A wild-type status (P = 0.040) were independent prognostic factors for overall survival. Conclusions Our study demonstrated that gastric cancer patients with ACVR2A mutation have a significantly better prognosis than those without. Dysfunction of ACVR2A in MKN74 human gastric cancer cells caused less aggressive tumor biology, indicating the importance of ACVR2A in the progression of MSI-H tumors. | ||
| 650 | 4 | |a Activin receptors |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Stomach neoplasms |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Microsatellite instability |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Transforming growth factor-β |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a CRISPR-Cas systems |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Nagahashi, Masayuki |e verfasserin |4 aut | |
| 700 | 1 | |a Ichikawa, Hiroshi |e verfasserin |4 aut | |
| 700 | 1 | |a Hanyu, Takaaki |e verfasserin |4 aut | |
| 700 | 1 | |a Nakajima, Masato |e verfasserin |4 aut | |
| 700 | 1 | |a Shimada, Yoshifumi |e verfasserin |4 aut | |
| 700 | 1 | |a Ishikawa, Takashi |e verfasserin |4 aut | |
| 700 | 1 | |a Sakata, Jun |e verfasserin |4 aut | |
| 700 | 1 | |a Takeuchi, Shiho |e verfasserin |4 aut | |
| 700 | 1 | |a Okuda, Shujiro |e verfasserin |4 aut | |
| 700 | 1 | |a Matsuda, Yasunobu |e verfasserin |4 aut | |
| 700 | 1 | |a Abe, Manabu |e verfasserin |4 aut | |
| 700 | 1 | |a Sakimura, Kenji |e verfasserin |4 aut | |
| 700 | 1 | |a Takabe, Kazuaki |e verfasserin |4 aut | |
| 700 | 1 | |a Wakai, Toshifumi |e verfasserin |4 aut | |
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10.1007/s11605-020-04889-9 doi (DE-627)SPR045194238 (SPR)s11605-020-04889-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.87 bkl Yuza, Kizuki verfasserin aut Activin a Receptor Type 2A Mutation Affects the Tumor Biology of Microsatellite Instability-High Gastric Cancer 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Society for Surgery of the Alimentary Tract 2021 Background Activin A receptor type 2A (ACVR2A) is one of the most frequently mutated genes in microsatellite instability-high (MSI-H) gastric cancer. However, the clinical relevance of the ACVR2A mutation in MSI-H gastric cancer patients remains unclear. The aims of this study were to explore the effect of ACVR2A mutation on the tumor behavior and to identify the clinicopathological characteristics of gastric cancer patients with ACVR2A mutations. Methods An in vitro study was performed to investigate the biological role of ACVR2A via CRISPR/Cas9-mediated ACVR2A knockout MKN74 human gastric cancer cells. One hundred twenty-four patients with gastric cancer were retrospectively analyzed, and relations between MSI status, ACVR2A mutations, and clinicopathological factors were evaluated. Results ACVR2A knockout cells showed less aggressive tumor biology than mock-transfected cells, displaying reduced proliferation, migration, and invasion (P < 0.05). MSI mutations were found in 10% (13/124) of gastric cancer patients, and ACVR2A mutations were found in 8.1% (10/124) of patients. All ACVR2A mutations were accompanied by MSI. The 5-year overall survival rates of ACVR2A wild-type patients and ACVR2A-mutated patients were 57% and 90%, respectively (P = 0.048). Multivariate analysis revealed that older age (P = 0.015), distant metastasis (P < 0.001), and ACVR2A wild-type status (P = 0.040) were independent prognostic factors for overall survival. Conclusions Our study demonstrated that gastric cancer patients with ACVR2A mutation have a significantly better prognosis than those without. Dysfunction of ACVR2A in MKN74 human gastric cancer cells caused less aggressive tumor biology, indicating the importance of ACVR2A in the progression of MSI-H tumors. Activin receptors (dpeaa)DE-He213 Stomach neoplasms (dpeaa)DE-He213 Microsatellite instability (dpeaa)DE-He213 Transforming growth factor-β (dpeaa)DE-He213 CRISPR-Cas systems (dpeaa)DE-He213 Nagahashi, Masayuki verfasserin aut Ichikawa, Hiroshi verfasserin aut Hanyu, Takaaki verfasserin aut Nakajima, Masato verfasserin aut Shimada, Yoshifumi verfasserin aut Ishikawa, Takashi verfasserin aut Sakata, Jun verfasserin aut Takeuchi, Shiho verfasserin aut Okuda, Shujiro verfasserin aut Matsuda, Yasunobu verfasserin aut Abe, Manabu verfasserin aut Sakimura, Kenji verfasserin aut Takabe, Kazuaki verfasserin aut Wakai, Toshifumi verfasserin aut Enthalten in Journal of gastrointestinal surgery New York, NY : Springer, 1997 25(2021), 9 vom: 08. Jan., Seite 2231-2241 (DE-627)334375053 (DE-600)2057634-1 1873-4626 nnns volume:25 year:2021 number:9 day:08 month:01 pages:2231-2241 https://dx.doi.org/10.1007/s11605-020-04889-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.87 ASE AR 25 2021 9 08 01 2231-2241 |
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10.1007/s11605-020-04889-9 doi (DE-627)SPR045194238 (SPR)s11605-020-04889-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.87 bkl Yuza, Kizuki verfasserin aut Activin a Receptor Type 2A Mutation Affects the Tumor Biology of Microsatellite Instability-High Gastric Cancer 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Society for Surgery of the Alimentary Tract 2021 Background Activin A receptor type 2A (ACVR2A) is one of the most frequently mutated genes in microsatellite instability-high (MSI-H) gastric cancer. However, the clinical relevance of the ACVR2A mutation in MSI-H gastric cancer patients remains unclear. The aims of this study were to explore the effect of ACVR2A mutation on the tumor behavior and to identify the clinicopathological characteristics of gastric cancer patients with ACVR2A mutations. Methods An in vitro study was performed to investigate the biological role of ACVR2A via CRISPR/Cas9-mediated ACVR2A knockout MKN74 human gastric cancer cells. One hundred twenty-four patients with gastric cancer were retrospectively analyzed, and relations between MSI status, ACVR2A mutations, and clinicopathological factors were evaluated. Results ACVR2A knockout cells showed less aggressive tumor biology than mock-transfected cells, displaying reduced proliferation, migration, and invasion (P < 0.05). MSI mutations were found in 10% (13/124) of gastric cancer patients, and ACVR2A mutations were found in 8.1% (10/124) of patients. All ACVR2A mutations were accompanied by MSI. The 5-year overall survival rates of ACVR2A wild-type patients and ACVR2A-mutated patients were 57% and 90%, respectively (P = 0.048). Multivariate analysis revealed that older age (P = 0.015), distant metastasis (P < 0.001), and ACVR2A wild-type status (P = 0.040) were independent prognostic factors for overall survival. Conclusions Our study demonstrated that gastric cancer patients with ACVR2A mutation have a significantly better prognosis than those without. Dysfunction of ACVR2A in MKN74 human gastric cancer cells caused less aggressive tumor biology, indicating the importance of ACVR2A in the progression of MSI-H tumors. Activin receptors (dpeaa)DE-He213 Stomach neoplasms (dpeaa)DE-He213 Microsatellite instability (dpeaa)DE-He213 Transforming growth factor-β (dpeaa)DE-He213 CRISPR-Cas systems (dpeaa)DE-He213 Nagahashi, Masayuki verfasserin aut Ichikawa, Hiroshi verfasserin aut Hanyu, Takaaki verfasserin aut Nakajima, Masato verfasserin aut Shimada, Yoshifumi verfasserin aut Ishikawa, Takashi verfasserin aut Sakata, Jun verfasserin aut Takeuchi, Shiho verfasserin aut Okuda, Shujiro verfasserin aut Matsuda, Yasunobu verfasserin aut Abe, Manabu verfasserin aut Sakimura, Kenji verfasserin aut Takabe, Kazuaki verfasserin aut Wakai, Toshifumi verfasserin aut Enthalten in Journal of gastrointestinal surgery New York, NY : Springer, 1997 25(2021), 9 vom: 08. Jan., Seite 2231-2241 (DE-627)334375053 (DE-600)2057634-1 1873-4626 nnns volume:25 year:2021 number:9 day:08 month:01 pages:2231-2241 https://dx.doi.org/10.1007/s11605-020-04889-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.87 ASE AR 25 2021 9 08 01 2231-2241 |
| allfields_unstemmed |
10.1007/s11605-020-04889-9 doi (DE-627)SPR045194238 (SPR)s11605-020-04889-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.87 bkl Yuza, Kizuki verfasserin aut Activin a Receptor Type 2A Mutation Affects the Tumor Biology of Microsatellite Instability-High Gastric Cancer 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Society for Surgery of the Alimentary Tract 2021 Background Activin A receptor type 2A (ACVR2A) is one of the most frequently mutated genes in microsatellite instability-high (MSI-H) gastric cancer. However, the clinical relevance of the ACVR2A mutation in MSI-H gastric cancer patients remains unclear. The aims of this study were to explore the effect of ACVR2A mutation on the tumor behavior and to identify the clinicopathological characteristics of gastric cancer patients with ACVR2A mutations. Methods An in vitro study was performed to investigate the biological role of ACVR2A via CRISPR/Cas9-mediated ACVR2A knockout MKN74 human gastric cancer cells. One hundred twenty-four patients with gastric cancer were retrospectively analyzed, and relations between MSI status, ACVR2A mutations, and clinicopathological factors were evaluated. Results ACVR2A knockout cells showed less aggressive tumor biology than mock-transfected cells, displaying reduced proliferation, migration, and invasion (P < 0.05). MSI mutations were found in 10% (13/124) of gastric cancer patients, and ACVR2A mutations were found in 8.1% (10/124) of patients. All ACVR2A mutations were accompanied by MSI. The 5-year overall survival rates of ACVR2A wild-type patients and ACVR2A-mutated patients were 57% and 90%, respectively (P = 0.048). Multivariate analysis revealed that older age (P = 0.015), distant metastasis (P < 0.001), and ACVR2A wild-type status (P = 0.040) were independent prognostic factors for overall survival. Conclusions Our study demonstrated that gastric cancer patients with ACVR2A mutation have a significantly better prognosis than those without. Dysfunction of ACVR2A in MKN74 human gastric cancer cells caused less aggressive tumor biology, indicating the importance of ACVR2A in the progression of MSI-H tumors. Activin receptors (dpeaa)DE-He213 Stomach neoplasms (dpeaa)DE-He213 Microsatellite instability (dpeaa)DE-He213 Transforming growth factor-β (dpeaa)DE-He213 CRISPR-Cas systems (dpeaa)DE-He213 Nagahashi, Masayuki verfasserin aut Ichikawa, Hiroshi verfasserin aut Hanyu, Takaaki verfasserin aut Nakajima, Masato verfasserin aut Shimada, Yoshifumi verfasserin aut Ishikawa, Takashi verfasserin aut Sakata, Jun verfasserin aut Takeuchi, Shiho verfasserin aut Okuda, Shujiro verfasserin aut Matsuda, Yasunobu verfasserin aut Abe, Manabu verfasserin aut Sakimura, Kenji verfasserin aut Takabe, Kazuaki verfasserin aut Wakai, Toshifumi verfasserin aut Enthalten in Journal of gastrointestinal surgery New York, NY : Springer, 1997 25(2021), 9 vom: 08. Jan., Seite 2231-2241 (DE-627)334375053 (DE-600)2057634-1 1873-4626 nnns volume:25 year:2021 number:9 day:08 month:01 pages:2231-2241 https://dx.doi.org/10.1007/s11605-020-04889-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.87 ASE AR 25 2021 9 08 01 2231-2241 |
| allfieldsGer |
10.1007/s11605-020-04889-9 doi (DE-627)SPR045194238 (SPR)s11605-020-04889-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.87 bkl Yuza, Kizuki verfasserin aut Activin a Receptor Type 2A Mutation Affects the Tumor Biology of Microsatellite Instability-High Gastric Cancer 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Society for Surgery of the Alimentary Tract 2021 Background Activin A receptor type 2A (ACVR2A) is one of the most frequently mutated genes in microsatellite instability-high (MSI-H) gastric cancer. However, the clinical relevance of the ACVR2A mutation in MSI-H gastric cancer patients remains unclear. The aims of this study were to explore the effect of ACVR2A mutation on the tumor behavior and to identify the clinicopathological characteristics of gastric cancer patients with ACVR2A mutations. Methods An in vitro study was performed to investigate the biological role of ACVR2A via CRISPR/Cas9-mediated ACVR2A knockout MKN74 human gastric cancer cells. One hundred twenty-four patients with gastric cancer were retrospectively analyzed, and relations between MSI status, ACVR2A mutations, and clinicopathological factors were evaluated. Results ACVR2A knockout cells showed less aggressive tumor biology than mock-transfected cells, displaying reduced proliferation, migration, and invasion (P < 0.05). MSI mutations were found in 10% (13/124) of gastric cancer patients, and ACVR2A mutations were found in 8.1% (10/124) of patients. All ACVR2A mutations were accompanied by MSI. The 5-year overall survival rates of ACVR2A wild-type patients and ACVR2A-mutated patients were 57% and 90%, respectively (P = 0.048). Multivariate analysis revealed that older age (P = 0.015), distant metastasis (P < 0.001), and ACVR2A wild-type status (P = 0.040) were independent prognostic factors for overall survival. Conclusions Our study demonstrated that gastric cancer patients with ACVR2A mutation have a significantly better prognosis than those without. Dysfunction of ACVR2A in MKN74 human gastric cancer cells caused less aggressive tumor biology, indicating the importance of ACVR2A in the progression of MSI-H tumors. Activin receptors (dpeaa)DE-He213 Stomach neoplasms (dpeaa)DE-He213 Microsatellite instability (dpeaa)DE-He213 Transforming growth factor-β (dpeaa)DE-He213 CRISPR-Cas systems (dpeaa)DE-He213 Nagahashi, Masayuki verfasserin aut Ichikawa, Hiroshi verfasserin aut Hanyu, Takaaki verfasserin aut Nakajima, Masato verfasserin aut Shimada, Yoshifumi verfasserin aut Ishikawa, Takashi verfasserin aut Sakata, Jun verfasserin aut Takeuchi, Shiho verfasserin aut Okuda, Shujiro verfasserin aut Matsuda, Yasunobu verfasserin aut Abe, Manabu verfasserin aut Sakimura, Kenji verfasserin aut Takabe, Kazuaki verfasserin aut Wakai, Toshifumi verfasserin aut Enthalten in Journal of gastrointestinal surgery New York, NY : Springer, 1997 25(2021), 9 vom: 08. Jan., Seite 2231-2241 (DE-627)334375053 (DE-600)2057634-1 1873-4626 nnns volume:25 year:2021 number:9 day:08 month:01 pages:2231-2241 https://dx.doi.org/10.1007/s11605-020-04889-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.87 ASE AR 25 2021 9 08 01 2231-2241 |
| allfieldsSound |
10.1007/s11605-020-04889-9 doi (DE-627)SPR045194238 (SPR)s11605-020-04889-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.87 bkl Yuza, Kizuki verfasserin aut Activin a Receptor Type 2A Mutation Affects the Tumor Biology of Microsatellite Instability-High Gastric Cancer 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Society for Surgery of the Alimentary Tract 2021 Background Activin A receptor type 2A (ACVR2A) is one of the most frequently mutated genes in microsatellite instability-high (MSI-H) gastric cancer. However, the clinical relevance of the ACVR2A mutation in MSI-H gastric cancer patients remains unclear. The aims of this study were to explore the effect of ACVR2A mutation on the tumor behavior and to identify the clinicopathological characteristics of gastric cancer patients with ACVR2A mutations. Methods An in vitro study was performed to investigate the biological role of ACVR2A via CRISPR/Cas9-mediated ACVR2A knockout MKN74 human gastric cancer cells. One hundred twenty-four patients with gastric cancer were retrospectively analyzed, and relations between MSI status, ACVR2A mutations, and clinicopathological factors were evaluated. Results ACVR2A knockout cells showed less aggressive tumor biology than mock-transfected cells, displaying reduced proliferation, migration, and invasion (P < 0.05). MSI mutations were found in 10% (13/124) of gastric cancer patients, and ACVR2A mutations were found in 8.1% (10/124) of patients. All ACVR2A mutations were accompanied by MSI. The 5-year overall survival rates of ACVR2A wild-type patients and ACVR2A-mutated patients were 57% and 90%, respectively (P = 0.048). Multivariate analysis revealed that older age (P = 0.015), distant metastasis (P < 0.001), and ACVR2A wild-type status (P = 0.040) were independent prognostic factors for overall survival. Conclusions Our study demonstrated that gastric cancer patients with ACVR2A mutation have a significantly better prognosis than those without. Dysfunction of ACVR2A in MKN74 human gastric cancer cells caused less aggressive tumor biology, indicating the importance of ACVR2A in the progression of MSI-H tumors. Activin receptors (dpeaa)DE-He213 Stomach neoplasms (dpeaa)DE-He213 Microsatellite instability (dpeaa)DE-He213 Transforming growth factor-β (dpeaa)DE-He213 CRISPR-Cas systems (dpeaa)DE-He213 Nagahashi, Masayuki verfasserin aut Ichikawa, Hiroshi verfasserin aut Hanyu, Takaaki verfasserin aut Nakajima, Masato verfasserin aut Shimada, Yoshifumi verfasserin aut Ishikawa, Takashi verfasserin aut Sakata, Jun verfasserin aut Takeuchi, Shiho verfasserin aut Okuda, Shujiro verfasserin aut Matsuda, Yasunobu verfasserin aut Abe, Manabu verfasserin aut Sakimura, Kenji verfasserin aut Takabe, Kazuaki verfasserin aut Wakai, Toshifumi verfasserin aut Enthalten in Journal of gastrointestinal surgery New York, NY : Springer, 1997 25(2021), 9 vom: 08. Jan., Seite 2231-2241 (DE-627)334375053 (DE-600)2057634-1 1873-4626 nnns volume:25 year:2021 number:9 day:08 month:01 pages:2231-2241 https://dx.doi.org/10.1007/s11605-020-04889-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.87 ASE AR 25 2021 9 08 01 2231-2241 |
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Enthalten in Journal of gastrointestinal surgery 25(2021), 9 vom: 08. Jan., Seite 2231-2241 volume:25 year:2021 number:9 day:08 month:01 pages:2231-2241 |
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Activin receptors Stomach neoplasms Microsatellite instability Transforming growth factor-β CRISPR-Cas systems |
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Yuza, Kizuki @@aut@@ Nagahashi, Masayuki @@aut@@ Ichikawa, Hiroshi @@aut@@ Hanyu, Takaaki @@aut@@ Nakajima, Masato @@aut@@ Shimada, Yoshifumi @@aut@@ Ishikawa, Takashi @@aut@@ Sakata, Jun @@aut@@ Takeuchi, Shiho @@aut@@ Okuda, Shujiro @@aut@@ Matsuda, Yasunobu @@aut@@ Abe, Manabu @@aut@@ Sakimura, Kenji @@aut@@ Takabe, Kazuaki @@aut@@ Wakai, Toshifumi @@aut@@ |
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2021-01-08T00:00:00Z |
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However, the clinical relevance of the ACVR2A mutation in MSI-H gastric cancer patients remains unclear. The aims of this study were to explore the effect of ACVR2A mutation on the tumor behavior and to identify the clinicopathological characteristics of gastric cancer patients with ACVR2A mutations. Methods An in vitro study was performed to investigate the biological role of ACVR2A via CRISPR/Cas9-mediated ACVR2A knockout MKN74 human gastric cancer cells. One hundred twenty-four patients with gastric cancer were retrospectively analyzed, and relations between MSI status, ACVR2A mutations, and clinicopathological factors were evaluated. Results ACVR2A knockout cells showed less aggressive tumor biology than mock-transfected cells, displaying reduced proliferation, migration, and invasion (P < 0.05). MSI mutations were found in 10% (13/124) of gastric cancer patients, and ACVR2A mutations were found in 8.1% (10/124) of patients. All ACVR2A mutations were accompanied by MSI. 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| author |
Yuza, Kizuki |
| spellingShingle |
Yuza, Kizuki ddc 610 bkl 44.87 misc Activin receptors misc Stomach neoplasms misc Microsatellite instability misc Transforming growth factor-β misc CRISPR-Cas systems Activin a Receptor Type 2A Mutation Affects the Tumor Biology of Microsatellite Instability-High Gastric Cancer |
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Yuza, Kizuki |
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610 - Medicine & health |
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1873-4626 |
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610 ASE 44.87 bkl Activin a Receptor Type 2A Mutation Affects the Tumor Biology of Microsatellite Instability-High Gastric Cancer Activin receptors (dpeaa)DE-He213 Stomach neoplasms (dpeaa)DE-He213 Microsatellite instability (dpeaa)DE-He213 Transforming growth factor-β (dpeaa)DE-He213 CRISPR-Cas systems (dpeaa)DE-He213 |
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ddc 610 bkl 44.87 misc Activin receptors misc Stomach neoplasms misc Microsatellite instability misc Transforming growth factor-β misc CRISPR-Cas systems |
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ddc 610 bkl 44.87 misc Activin receptors misc Stomach neoplasms misc Microsatellite instability misc Transforming growth factor-β misc CRISPR-Cas systems |
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ddc 610 bkl 44.87 misc Activin receptors misc Stomach neoplasms misc Microsatellite instability misc Transforming growth factor-β misc CRISPR-Cas systems |
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Journal of gastrointestinal surgery |
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610 - Medicine & health |
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Journal of gastrointestinal surgery |
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Activin a Receptor Type 2A Mutation Affects the Tumor Biology of Microsatellite Instability-High Gastric Cancer |
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(DE-627)SPR045194238 (SPR)s11605-020-04889-9-e |
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Activin a Receptor Type 2A Mutation Affects the Tumor Biology of Microsatellite Instability-High Gastric Cancer |
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Yuza, Kizuki |
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Journal of gastrointestinal surgery |
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Journal of gastrointestinal surgery |
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eng |
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600 - Technology |
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Yuza, Kizuki Nagahashi, Masayuki Ichikawa, Hiroshi Hanyu, Takaaki Nakajima, Masato Shimada, Yoshifumi Ishikawa, Takashi Sakata, Jun Takeuchi, Shiho Okuda, Shujiro Matsuda, Yasunobu Abe, Manabu Sakimura, Kenji Takabe, Kazuaki Wakai, Toshifumi |
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Elektronische Aufsätze |
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Yuza, Kizuki |
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10.1007/s11605-020-04889-9 |
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610 |
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verfasserin |
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activin a receptor type 2a mutation affects the tumor biology of microsatellite instability-high gastric cancer |
| title_auth |
Activin a Receptor Type 2A Mutation Affects the Tumor Biology of Microsatellite Instability-High Gastric Cancer |
| abstract |
Background Activin A receptor type 2A (ACVR2A) is one of the most frequently mutated genes in microsatellite instability-high (MSI-H) gastric cancer. However, the clinical relevance of the ACVR2A mutation in MSI-H gastric cancer patients remains unclear. The aims of this study were to explore the effect of ACVR2A mutation on the tumor behavior and to identify the clinicopathological characteristics of gastric cancer patients with ACVR2A mutations. Methods An in vitro study was performed to investigate the biological role of ACVR2A via CRISPR/Cas9-mediated ACVR2A knockout MKN74 human gastric cancer cells. One hundred twenty-four patients with gastric cancer were retrospectively analyzed, and relations between MSI status, ACVR2A mutations, and clinicopathological factors were evaluated. Results ACVR2A knockout cells showed less aggressive tumor biology than mock-transfected cells, displaying reduced proliferation, migration, and invasion (P < 0.05). MSI mutations were found in 10% (13/124) of gastric cancer patients, and ACVR2A mutations were found in 8.1% (10/124) of patients. All ACVR2A mutations were accompanied by MSI. The 5-year overall survival rates of ACVR2A wild-type patients and ACVR2A-mutated patients were 57% and 90%, respectively (P = 0.048). Multivariate analysis revealed that older age (P = 0.015), distant metastasis (P < 0.001), and ACVR2A wild-type status (P = 0.040) were independent prognostic factors for overall survival. Conclusions Our study demonstrated that gastric cancer patients with ACVR2A mutation have a significantly better prognosis than those without. Dysfunction of ACVR2A in MKN74 human gastric cancer cells caused less aggressive tumor biology, indicating the importance of ACVR2A in the progression of MSI-H tumors. © The Society for Surgery of the Alimentary Tract 2021 |
| abstractGer |
Background Activin A receptor type 2A (ACVR2A) is one of the most frequently mutated genes in microsatellite instability-high (MSI-H) gastric cancer. However, the clinical relevance of the ACVR2A mutation in MSI-H gastric cancer patients remains unclear. The aims of this study were to explore the effect of ACVR2A mutation on the tumor behavior and to identify the clinicopathological characteristics of gastric cancer patients with ACVR2A mutations. Methods An in vitro study was performed to investigate the biological role of ACVR2A via CRISPR/Cas9-mediated ACVR2A knockout MKN74 human gastric cancer cells. One hundred twenty-four patients with gastric cancer were retrospectively analyzed, and relations between MSI status, ACVR2A mutations, and clinicopathological factors were evaluated. Results ACVR2A knockout cells showed less aggressive tumor biology than mock-transfected cells, displaying reduced proliferation, migration, and invasion (P < 0.05). MSI mutations were found in 10% (13/124) of gastric cancer patients, and ACVR2A mutations were found in 8.1% (10/124) of patients. All ACVR2A mutations were accompanied by MSI. The 5-year overall survival rates of ACVR2A wild-type patients and ACVR2A-mutated patients were 57% and 90%, respectively (P = 0.048). Multivariate analysis revealed that older age (P = 0.015), distant metastasis (P < 0.001), and ACVR2A wild-type status (P = 0.040) were independent prognostic factors for overall survival. Conclusions Our study demonstrated that gastric cancer patients with ACVR2A mutation have a significantly better prognosis than those without. Dysfunction of ACVR2A in MKN74 human gastric cancer cells caused less aggressive tumor biology, indicating the importance of ACVR2A in the progression of MSI-H tumors. © The Society for Surgery of the Alimentary Tract 2021 |
| abstract_unstemmed |
Background Activin A receptor type 2A (ACVR2A) is one of the most frequently mutated genes in microsatellite instability-high (MSI-H) gastric cancer. However, the clinical relevance of the ACVR2A mutation in MSI-H gastric cancer patients remains unclear. The aims of this study were to explore the effect of ACVR2A mutation on the tumor behavior and to identify the clinicopathological characteristics of gastric cancer patients with ACVR2A mutations. Methods An in vitro study was performed to investigate the biological role of ACVR2A via CRISPR/Cas9-mediated ACVR2A knockout MKN74 human gastric cancer cells. One hundred twenty-four patients with gastric cancer were retrospectively analyzed, and relations between MSI status, ACVR2A mutations, and clinicopathological factors were evaluated. Results ACVR2A knockout cells showed less aggressive tumor biology than mock-transfected cells, displaying reduced proliferation, migration, and invasion (P < 0.05). MSI mutations were found in 10% (13/124) of gastric cancer patients, and ACVR2A mutations were found in 8.1% (10/124) of patients. All ACVR2A mutations were accompanied by MSI. The 5-year overall survival rates of ACVR2A wild-type patients and ACVR2A-mutated patients were 57% and 90%, respectively (P = 0.048). Multivariate analysis revealed that older age (P = 0.015), distant metastasis (P < 0.001), and ACVR2A wild-type status (P = 0.040) were independent prognostic factors for overall survival. Conclusions Our study demonstrated that gastric cancer patients with ACVR2A mutation have a significantly better prognosis than those without. Dysfunction of ACVR2A in MKN74 human gastric cancer cells caused less aggressive tumor biology, indicating the importance of ACVR2A in the progression of MSI-H tumors. © The Society for Surgery of the Alimentary Tract 2021 |
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Activin a Receptor Type 2A Mutation Affects the Tumor Biology of Microsatellite Instability-High Gastric Cancer |
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https://dx.doi.org/10.1007/s11605-020-04889-9 |
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Nagahashi, Masayuki Ichikawa, Hiroshi Hanyu, Takaaki Nakajima, Masato Shimada, Yoshifumi Ishikawa, Takashi Sakata, Jun Takeuchi, Shiho Okuda, Shujiro Matsuda, Yasunobu Abe, Manabu Sakimura, Kenji Takabe, Kazuaki Wakai, Toshifumi |
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Nagahashi, Masayuki Ichikawa, Hiroshi Hanyu, Takaaki Nakajima, Masato Shimada, Yoshifumi Ishikawa, Takashi Sakata, Jun Takeuchi, Shiho Okuda, Shujiro Matsuda, Yasunobu Abe, Manabu Sakimura, Kenji Takabe, Kazuaki Wakai, Toshifumi |
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10.1007/s11605-020-04889-9 |
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2024-07-03T14:23:14.843Z |
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| score |
7.3974285 |