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Molecular Aberrations Associated with Seizure Control in Diffuse Astrocytic and Oligodendroglial Tumors
Diffuse astrocytic and oligodendroglial tumors are frequently associated with symptomatic epilepsy, and predictive seizure control is important for the improvement of patient quality of life. To elucidate the factors related to drug resistance of brain tumor-associated epilepsy from a pathological p...
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Published in: | Neurologia medico-chirurgica 2020, Vol.60(3), pp.147-155 |
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creator | SUZUKI, Hime MIKUNI, Nobuhiro SUGITA, Shintaro AOYAMA, Tomoyuki YOKOYAMA, Rintaro SUZUKI, Yuto ENATSU, Rei AKIYAMA, Yukinori MIKAMI, Takeshi WANIBUCHI, Masahiko HASEGAWA, Tadashi |
description | Diffuse astrocytic and oligodendroglial tumors are frequently associated with symptomatic epilepsy, and predictive seizure control is important for the improvement of patient quality of life. To elucidate the factors related to drug resistance of brain tumor-associated epilepsy from a pathological perspective. From January 2012 to October 2017, 36 patients diagnosed with diffuse astrocytic or oligodendroglial tumors were included. Assessment for seizure control was performed according to the Engel classification of seizures. Patient clinical, radiological, and pathological data were stratified based on the following 16 variables: age, sex, location of tumor, existence of the preoperative seizure, extent of resection, administration of temozolomide, radiation therapy, recurrence, Karnofsky performance scale, isocitrate dehydrogenase 1, 1p/19q co-deletion, Olig2, platelet-derived growth factor receptor alpha, p53, ATRX, and Ki67. These factors were compared between the well-controlled group and drug-resistant seizure group. Twenty-seven patients experienced seizures; of these, 14 cases were well-controlled, and 13 cases were drug-resistant. Neither clinical nor radiological characteristics were significantly different between these two groups, though p53 immunodetection levels were significantly higher, and the frequency of 1p/19q co-deletion was significantly lower in the group with drug-resistant seizures than in the well-controlled group. In the multivariate analysis, only one item was selected according to stepwise methods, and a significant difference was observed for p53 (OR, 21.600; 95% CI, 2.135–218.579; P = 0.009). Upregulation of p53 may be a molecular mechanism underlying drug resistant epilepsy associated with diffuse astrocytic and oligodendroglial tumors. |
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To elucidate the factors related to drug resistance of brain tumor-associated epilepsy from a pathological perspective. From January 2012 to October 2017, 36 patients diagnosed with diffuse astrocytic or oligodendroglial tumors were included. Assessment for seizure control was performed according to the Engel classification of seizures. Patient clinical, radiological, and pathological data were stratified based on the following 16 variables: age, sex, location of tumor, existence of the preoperative seizure, extent of resection, administration of temozolomide, radiation therapy, recurrence, Karnofsky performance scale, isocitrate dehydrogenase 1, 1p/19q co-deletion, Olig2, platelet-derived growth factor receptor alpha, p53, ATRX, and Ki67. These factors were compared between the well-controlled group and drug-resistant seizure group. Twenty-seven patients experienced seizures; of these, 14 cases were well-controlled, and 13 cases were drug-resistant. Neither clinical nor radiological characteristics were significantly different between these two groups, though p53 immunodetection levels were significantly higher, and the frequency of 1p/19q co-deletion was significantly lower in the group with drug-resistant seizures than in the well-controlled group. In the multivariate analysis, only one item was selected according to stepwise methods, and a significant difference was observed for p53 (OR, 21.600; 95% CI, 2.135–218.579; P = 0.009). Upregulation of p53 may be a molecular mechanism underlying drug resistant epilepsy associated with diffuse astrocytic and oligodendroglial tumors.</description><identifier>ISSN: 0470-8105</identifier><identifier>EISSN: 1349-8029</identifier><identifier>DOI: 10.2176/nmc.oa.2019-0218</identifier><identifier>PMID: 32009124</identifier><language>eng</language><publisher>Tokyo: The Japan Neurosurgical Society</publisher><subject>Brain cancer ; Brain tumors ; Convulsions & seizures ; diffuse astrocytoma ; Drug resistance ; Epilepsy ; glioma ; Isocitrate dehydrogenase ; Multivariate analysis ; Olig2 protein ; oligodendroglioma ; Original ; p53 Protein ; Platelet-derived growth factor ; Quality of life ; Radiation therapy ; Seizures ; Temozolomide ; Tumors</subject><ispartof>Neurologia medico-chirurgica, 2020, Vol.60(3), pp.147-155</ispartof><rights>2020 by The Japan Neurosurgical Society</rights><rights>2020. This work is published under https://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2020 The Japan Neurosurgical Society The Japan Neurosurgical Society The Japan Neurosurgical Society 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c577t-5a65af4b9cc5024468466d37fef9389fdd9e92a97993cf0820bb092712c8d24c3</citedby><cites>FETCH-LOGICAL-c577t-5a65af4b9cc5024468466d37fef9389fdd9e92a97993cf0820bb092712c8d24c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7073702/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7073702/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,882,4010,27904,27905,27906,53772,53774</link.rule.ids></links><search><creatorcontrib>SUZUKI, Hime</creatorcontrib><creatorcontrib>MIKUNI, Nobuhiro</creatorcontrib><creatorcontrib>SUGITA, Shintaro</creatorcontrib><creatorcontrib>AOYAMA, Tomoyuki</creatorcontrib><creatorcontrib>YOKOYAMA, Rintaro</creatorcontrib><creatorcontrib>SUZUKI, Yuto</creatorcontrib><creatorcontrib>ENATSU, Rei</creatorcontrib><creatorcontrib>AKIYAMA, Yukinori</creatorcontrib><creatorcontrib>MIKAMI, Takeshi</creatorcontrib><creatorcontrib>WANIBUCHI, Masahiko</creatorcontrib><creatorcontrib>HASEGAWA, Tadashi</creatorcontrib><title>Molecular Aberrations Associated with Seizure Control in Diffuse Astrocytic and Oligodendroglial Tumors</title><title>Neurologia medico-chirurgica</title><addtitle>Neurol. Med. Chir.(Tokyo)</addtitle><description>Diffuse astrocytic and oligodendroglial tumors are frequently associated with symptomatic epilepsy, and predictive seizure control is important for the improvement of patient quality of life. To elucidate the factors related to drug resistance of brain tumor-associated epilepsy from a pathological perspective. From January 2012 to October 2017, 36 patients diagnosed with diffuse astrocytic or oligodendroglial tumors were included. Assessment for seizure control was performed according to the Engel classification of seizures. Patient clinical, radiological, and pathological data were stratified based on the following 16 variables: age, sex, location of tumor, existence of the preoperative seizure, extent of resection, administration of temozolomide, radiation therapy, recurrence, Karnofsky performance scale, isocitrate dehydrogenase 1, 1p/19q co-deletion, Olig2, platelet-derived growth factor receptor alpha, p53, ATRX, and Ki67. These factors were compared between the well-controlled group and drug-resistant seizure group. Twenty-seven patients experienced seizures; of these, 14 cases were well-controlled, and 13 cases were drug-resistant. Neither clinical nor radiological characteristics were significantly different between these two groups, though p53 immunodetection levels were significantly higher, and the frequency of 1p/19q co-deletion was significantly lower in the group with drug-resistant seizures than in the well-controlled group. In the multivariate analysis, only one item was selected according to stepwise methods, and a significant difference was observed for p53 (OR, 21.600; 95% CI, 2.135–218.579; P = 0.009). Upregulation of p53 may be a molecular mechanism underlying drug resistant epilepsy associated with diffuse astrocytic and oligodendroglial tumors.</description><subject>Brain cancer</subject><subject>Brain tumors</subject><subject>Convulsions & seizures</subject><subject>diffuse astrocytoma</subject><subject>Drug resistance</subject><subject>Epilepsy</subject><subject>glioma</subject><subject>Isocitrate dehydrogenase</subject><subject>Multivariate analysis</subject><subject>Olig2 protein</subject><subject>oligodendroglioma</subject><subject>Original</subject><subject>p53 Protein</subject><subject>Platelet-derived growth factor</subject><subject>Quality of life</subject><subject>Radiation therapy</subject><subject>Seizures</subject><subject>Temozolomide</subject><subject>Tumors</subject><issn>0470-8105</issn><issn>1349-8029</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNpVkcFvFCEYxYmxsZu2d48knmf9BpgBLiab1WqTmh6sZ8IAM0vDQoUZm_rXy3abjV4ggfd738v3EHrfwpq0vP8Y92ad9JpAKxsgrXiDVi1lshFA5Fu0AsahES105-iqFD8AECYYFfwdOqcEQLaErdD0PQVnlqAz3gwuZz37FAvelJKM17Oz-MnPO_zD-T9Ldnib4pxTwD7iz34cl-KqtL6Y59kbrKPFd8FPybpoc5qC1wHfL_uUyyU6G3Uo7ur1vkA_r7_cb781t3dfb7ab28Z0nM9Np_tOj2yQxnQ1L-sF63tL-ehGSYUcrZVOEi25lNSMIAgMA0jCW2KEJczQC_Tp6Pu4DHtnjat5dVCP2e91flZJe_X_T_Q7NaXfigOnHEg1-PBqkNOvxZVZPaQlx5pZESq6uj8JXVXBUWVyKiW78TShBXVoR9V26jR1aEcd2qnI9RF5KLOe3AnQua4uuBegB0UPx7_gSWB2OisX6V-Ka518</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>SUZUKI, Hime</creator><creator>MIKUNI, Nobuhiro</creator><creator>SUGITA, Shintaro</creator><creator>AOYAMA, Tomoyuki</creator><creator>YOKOYAMA, Rintaro</creator><creator>SUZUKI, Yuto</creator><creator>ENATSU, Rei</creator><creator>AKIYAMA, Yukinori</creator><creator>MIKAMI, Takeshi</creator><creator>WANIBUCHI, Masahiko</creator><creator>HASEGAWA, Tadashi</creator><general>The Japan Neurosurgical Society</general><general>Japan Science and Technology Agency</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>5PM</scope></search><sort><creationdate>2020</creationdate><title>Molecular Aberrations Associated with Seizure Control in Diffuse Astrocytic and Oligodendroglial Tumors</title><author>SUZUKI, Hime ; MIKUNI, Nobuhiro ; SUGITA, Shintaro ; AOYAMA, Tomoyuki ; YOKOYAMA, Rintaro ; SUZUKI, Yuto ; ENATSU, Rei ; AKIYAMA, Yukinori ; MIKAMI, Takeshi ; WANIBUCHI, Masahiko ; HASEGAWA, Tadashi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c577t-5a65af4b9cc5024468466d37fef9389fdd9e92a97993cf0820bb092712c8d24c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Brain cancer</topic><topic>Brain tumors</topic><topic>Convulsions & seizures</topic><topic>diffuse astrocytoma</topic><topic>Drug resistance</topic><topic>Epilepsy</topic><topic>glioma</topic><topic>Isocitrate dehydrogenase</topic><topic>Multivariate analysis</topic><topic>Olig2 protein</topic><topic>oligodendroglioma</topic><topic>Original</topic><topic>p53 Protein</topic><topic>Platelet-derived growth factor</topic><topic>Quality of life</topic><topic>Radiation therapy</topic><topic>Seizures</topic><topic>Temozolomide</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SUZUKI, Hime</creatorcontrib><creatorcontrib>MIKUNI, Nobuhiro</creatorcontrib><creatorcontrib>SUGITA, Shintaro</creatorcontrib><creatorcontrib>AOYAMA, Tomoyuki</creatorcontrib><creatorcontrib>YOKOYAMA, Rintaro</creatorcontrib><creatorcontrib>SUZUKI, Yuto</creatorcontrib><creatorcontrib>ENATSU, Rei</creatorcontrib><creatorcontrib>AKIYAMA, Yukinori</creatorcontrib><creatorcontrib>MIKAMI, Takeshi</creatorcontrib><creatorcontrib>WANIBUCHI, Masahiko</creatorcontrib><creatorcontrib>HASEGAWA, Tadashi</creatorcontrib><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neurologia medico-chirurgica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SUZUKI, Hime</au><au>MIKUNI, Nobuhiro</au><au>SUGITA, Shintaro</au><au>AOYAMA, Tomoyuki</au><au>YOKOYAMA, Rintaro</au><au>SUZUKI, Yuto</au><au>ENATSU, Rei</au><au>AKIYAMA, Yukinori</au><au>MIKAMI, Takeshi</au><au>WANIBUCHI, Masahiko</au><au>HASEGAWA, Tadashi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Molecular Aberrations Associated with Seizure Control in Diffuse Astrocytic and Oligodendroglial Tumors</atitle><jtitle>Neurologia medico-chirurgica</jtitle><addtitle>Neurol. Med. Chir.(Tokyo)</addtitle><date>2020</date><risdate>2020</risdate><volume>60</volume><issue>3</issue><spage>147</spage><epage>155</epage><pages>147-155</pages><issn>0470-8105</issn><eissn>1349-8029</eissn><abstract>Diffuse astrocytic and oligodendroglial tumors are frequently associated with symptomatic epilepsy, and predictive seizure control is important for the improvement of patient quality of life. To elucidate the factors related to drug resistance of brain tumor-associated epilepsy from a pathological perspective. From January 2012 to October 2017, 36 patients diagnosed with diffuse astrocytic or oligodendroglial tumors were included. Assessment for seizure control was performed according to the Engel classification of seizures. Patient clinical, radiological, and pathological data were stratified based on the following 16 variables: age, sex, location of tumor, existence of the preoperative seizure, extent of resection, administration of temozolomide, radiation therapy, recurrence, Karnofsky performance scale, isocitrate dehydrogenase 1, 1p/19q co-deletion, Olig2, platelet-derived growth factor receptor alpha, p53, ATRX, and Ki67. These factors were compared between the well-controlled group and drug-resistant seizure group. Twenty-seven patients experienced seizures; of these, 14 cases were well-controlled, and 13 cases were drug-resistant. Neither clinical nor radiological characteristics were significantly different between these two groups, though p53 immunodetection levels were significantly higher, and the frequency of 1p/19q co-deletion was significantly lower in the group with drug-resistant seizures than in the well-controlled group. In the multivariate analysis, only one item was selected according to stepwise methods, and a significant difference was observed for p53 (OR, 21.600; 95% CI, 2.135–218.579; P = 0.009). Upregulation of p53 may be a molecular mechanism underlying drug resistant epilepsy associated with diffuse astrocytic and oligodendroglial tumors.</abstract><cop>Tokyo</cop><pub>The Japan Neurosurgical Society</pub><pmid>32009124</pmid><doi>10.2176/nmc.oa.2019-0218</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Brain cancer Brain tumors Convulsions & seizures diffuse astrocytoma Drug resistance Epilepsy glioma Isocitrate dehydrogenase Multivariate analysis Olig2 protein oligodendroglioma Original p53 Protein Platelet-derived growth factor Quality of life Radiation therapy Seizures Temozolomide Tumors |
title | Molecular Aberrations Associated with Seizure Control in Diffuse Astrocytic and Oligodendroglial Tumors |
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