Pub Date : 2023-05-13eCollection Date: 2023-10-01DOI: 10.1093/nop/npad026
Emma R Earl, Howard Colman, Joe Mendez, Randy L Jensen, Michael Karsy
Background: Social determinants of health (SDOHs)-specifically those related to rurality, health care accessibility, and income-may play as-yet-unidentified roles in prognosis for glioma patients, and their impact on access to clinical trials is important to understand. We examined SDOHs of patients enrolled in glioma clinical trials and evaluate disparities in trial participation and outcomes between rural and urban patients.
Methods: We retrospectively identified patients enrolled in glioma clinical trials at Huntsman Cancer Institute (HCI) from May 2012 to May 2022 to evaluate clinical trial participation. We used multivariable models to evaluate SDOHs and geographic information system mapping to assess representation across Utah's counties. We utilized the most recent 10-year datasets of patients treated for glioma at HCI and from the Utah Cancer Registry to analyze survival and incidence, respectively.
Results: A total of 570 participants (68 trials) resided in Utah, 84.4% from urban counties, 13.5% from rural counties, and 2.1% from frontier (least-populous) counties. Nineteen counties (65.5%) were underrepresented in trials (enrolled participants vs. eligible), 1 (3.5%) was represented in a near-1:1 ratio, and 9 (31.0%) were overrepresented. Counties with greater enrollment had greater population densities, highest per-capita income, and proximity to HCI. Among patients treated at HCI, patients from rural/frontier counties had equivalent survival with urban patients across nearly all glioma types, including glioblastomas, despite underrepresentation in clinical trials.
Conclusions: By highlighting disparities in clinical trial enrollment, our results can support efforts to improve recruitment in underrepresented regions, which can assist providers in delivering equitable care for all patients.
{"title":"An evaluation of biobanking and therapeutic clinical trial representation among adult glioma patients from rural and urban Utah.","authors":"Emma R Earl, Howard Colman, Joe Mendez, Randy L Jensen, Michael Karsy","doi":"10.1093/nop/npad026","DOIUrl":"10.1093/nop/npad026","url":null,"abstract":"<p><strong>Background: </strong>Social determinants of health (SDOHs)-specifically those related to rurality, health care accessibility, and income-may play as-yet-unidentified roles in prognosis for glioma patients, and their impact on access to clinical trials is important to understand. We examined SDOHs of patients enrolled in glioma clinical trials and evaluate disparities in trial participation and outcomes between rural and urban patients.</p><p><strong>Methods: </strong>We retrospectively identified patients enrolled in glioma clinical trials at Huntsman Cancer Institute (HCI) from May 2012 to May 2022 to evaluate clinical trial participation. We used multivariable models to evaluate SDOHs and geographic information system mapping to assess representation across Utah's counties. We utilized the most recent 10-year datasets of patients treated for glioma at HCI and from the Utah Cancer Registry to analyze survival and incidence, respectively.</p><p><strong>Results: </strong>A total of 570 participants (68 trials) resided in Utah, 84.4% from urban counties, 13.5% from rural counties, and 2.1% from frontier (least-populous) counties. Nineteen counties (65.5%) were underrepresented in trials (enrolled participants vs. eligible), 1 (3.5%) was represented in a near-1:1 ratio, and 9 (31.0%) were overrepresented. Counties with greater enrollment had greater population densities, highest per-capita income, and proximity to HCI. Among patients treated at HCI, patients from rural/frontier counties had equivalent survival with urban patients across nearly all glioma types, including glioblastomas, despite underrepresentation in clinical trials.</p><p><strong>Conclusions: </strong>By highlighting disparities in clinical trial enrollment, our results can support efforts to improve recruitment in underrepresented regions, which can assist providers in delivering equitable care for all patients.</p>","PeriodicalId":19234,"journal":{"name":"Neuro-oncology practice","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2023-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10502782/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10308445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Journal Article Forthcoming Meetings Get access Neuro-Oncology Practice, Volume 10, Issue 3, June 2023, Page 315, https://doi.org/10.1093/nop/npad021 Published: 12 May 2023 Article history Corrected and typeset: 12 May 2023 Published: 12 May 2023
Pub Date : 2023-05-11eCollection Date: 2023-12-01DOI: 10.1093/nop/npad027
Evangelia Liouta, Christos Koutsarnakis, Spyridon Komaitis, Aristotelis V Kalyvas, Evangelos Drosos, Juan M García-Gómez, Javier Juan-Albarracín, Vasileios Katsaros, Lampis Stavrinou, George Stranjalis
Background: Aim of the present study is to investigate whether preoperative neurocognitive status is prognostically associated with overall survival (OS) in newly diagnosed glioblastoma (GBM) patients.
Methods: Ninety patients with dominant-hemisphere IDH-wild-type GBM were assessed by Mini Mental Status Exam (MMSE), Trail Making Test (TMT) A and B parts, and Control Word Association Test (COWAT) phonemic and semantic subtests. Demographics, Karnofsky Performance Scale, tumor parameters, type of surgery, and adjuvant therapy data were available for patients.
Results: According to Cox proportional hazards model the neurocognitive variables of TMT B (P < .01), COWAT semantic subset (P < .05), and the MMSE (P < .01) were found significantly associated with survival prediction. From all other factors, only tumor volume and operation type (debulking vs biopsy) showed a statistical association (P < .05) with survival prediction. Kaplan Meier Long rank test showed statistical significance (P < .01) between unimpaired and impaired groups for TMT B, with median survival for the unimpaired group 26 months and 10 months for the impaired group, for COWAT semantic (P < .01) with median survival 23 months and 12 months, respectively and for MMSE (P < .01) with medial survival 19 and 12 months respectively.
Conclusions: Our study demonstrates that neurocognitive status at baseline-prior to treatment-is an independent prognostic factor for OS in wild-type GBM patients, adding another prognostic tool to assist physicians in selecting the best treatment plan.
{"title":"Preoperative neurocognitive function as an independent survival prognostic marker in primary glioblastoma.","authors":"Evangelia Liouta, Christos Koutsarnakis, Spyridon Komaitis, Aristotelis V Kalyvas, Evangelos Drosos, Juan M García-Gómez, Javier Juan-Albarracín, Vasileios Katsaros, Lampis Stavrinou, George Stranjalis","doi":"10.1093/nop/npad027","DOIUrl":"10.1093/nop/npad027","url":null,"abstract":"<p><strong>Background: </strong>Aim of the present study is to investigate whether preoperative neurocognitive status is prognostically associated with overall survival (OS) in newly diagnosed glioblastoma (GBM) patients.</p><p><strong>Methods: </strong>Ninety patients with dominant-hemisphere IDH-wild-type GBM were assessed by Mini Mental Status Exam (MMSE), Trail Making Test (TMT) A and B parts, and Control Word Association Test (COWAT) phonemic and semantic subtests. Demographics, Karnofsky Performance Scale, tumor parameters, type of surgery, and adjuvant therapy data were available for patients.</p><p><strong>Results: </strong>According to Cox proportional hazards model the neurocognitive variables of TMT B (<i>P</i> < .01), COWAT semantic subset (<i>P</i> < .05), and the MMSE (<i>P</i> < .01) were found significantly associated with survival prediction. From all other factors, only tumor volume and operation type (debulking vs biopsy) showed a statistical association (<i>P</i> < .05) with survival prediction. Kaplan Meier Long rank test showed statistical significance (<i>P</i> < .01) between unimpaired and impaired groups for TMT B, with median survival for the unimpaired group 26 months and 10 months for the impaired group, for COWAT semantic (<i>P</i> < .01) with median survival 23 months and 12 months, respectively and for MMSE (<i>P</i> < .01) with medial survival 19 and 12 months respectively.</p><p><strong>Conclusions: </strong>Our study demonstrates that neurocognitive status at baseline-prior to treatment-is an independent prognostic factor for OS in wild-type GBM patients, adding another prognostic tool to assist physicians in selecting the best treatment plan.</p>","PeriodicalId":19234,"journal":{"name":"Neuro-oncology practice","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2023-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10666798/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42279759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-05-03eCollection Date: 2023-08-01DOI: 10.1093/nop/npad018
Tomas Kazda, Katerina Polachova
{"title":"Financial toxicity of radiotherapy for multiple brain metastases: Will it get worse or better?","authors":"Tomas Kazda, Katerina Polachova","doi":"10.1093/nop/npad018","DOIUrl":"10.1093/nop/npad018","url":null,"abstract":"","PeriodicalId":19234,"journal":{"name":"Neuro-oncology practice","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2023-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10346388/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9828964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-05-02eCollection Date: 2023-10-01DOI: 10.1093/nop/npad025
Richard Drexler, Thomas Sauvigny, Ulrich Schüller, Alicia Eckhardt, Cecile L Maire, Robin Khatri, Fabian Hausmann, Sonja Hänzelmann, Tobias B Huber, Stefan Bonn, Helena Bode, Katrin Lamszus, Manfred Westphal, Lasse Dührsen, Franz L Ricklefs
Background: 5-aminolevulinic acid (5-ALA) fluorescence-guided resection increases the percentage of complete CNS tumor resections and improves the progression-free survival of IDH-wildtype glioblastoma patients. A small subset of IDH-wildtype glioblastoma shows no 5-ALA fluorescence. An explanation for these cases is missing. In this study, we used DNA methylation profiling to further characterize non-fluorescent glioblastomas.
Methods: Patients with newly diagnosed and recurrent IDH-wildtype glioblastoma that underwent surgery were analyzed. The intensity of intraoperative 5-ALA fluorescence was categorized as non-visible or visible. DNA was extracted from tumors and genome-wide DNA methylation patterns were analyzed using Illumina EPIC (850k) arrays. Furthermore, 5-ALA intensity was measured by flow cytometry on human gliomasphere lines (BT112 and BT145).
Results: Of 74 included patients, 12 (16.2%) patients had a non-fluorescent glioblastoma, which were compared to 62 glioblastomas with 5-ALA fluorescence. Clinical characteristics were equally distributed between both groups. We did not find significant differences between DNA methylation subclasses and 5-ALA fluorescence (P = .24). The distribution of cells of the tumor microenvironment was not significantly different between the non-fluorescent and fluorescent tumors. Copy number variations in EGFR and simultaneous EGFRvIII expression were strongly associated with 5-ALA fluorescence since all non-fluorescent glioblastomas were EGFR-amplified (P < .01). This finding was also demonstrated in recurrent tumors. Similarly, EGFR-amplified glioblastoma cell lines showed no 5-ALA fluorescence after 24 h of incubation.
Conclusions: Our study demonstrates an association between non-fluorescent IDH-wildtype glioblastomas and EGFR gene amplification which should be taken into consideration for recurrent surgery and future studies investigating EGFR-amplified gliomas.
{"title":"Epigenetic profiling reveals a strong association between lack of 5-ALA fluorescence and <i>EGFR</i> amplification in <i>IDH</i>-wildtype glioblastoma.","authors":"Richard Drexler, Thomas Sauvigny, Ulrich Schüller, Alicia Eckhardt, Cecile L Maire, Robin Khatri, Fabian Hausmann, Sonja Hänzelmann, Tobias B Huber, Stefan Bonn, Helena Bode, Katrin Lamszus, Manfred Westphal, Lasse Dührsen, Franz L Ricklefs","doi":"10.1093/nop/npad025","DOIUrl":"10.1093/nop/npad025","url":null,"abstract":"<p><strong>Background: </strong>5-aminolevulinic acid (5-ALA) fluorescence-guided resection increases the percentage of complete CNS tumor resections and improves the progression-free survival of <i>IDH</i>-wildtype glioblastoma patients. A small subset of <i>IDH</i>-wildtype glioblastoma shows no 5-ALA fluorescence. An explanation for these cases is missing. In this study, we used DNA methylation profiling to further characterize non-fluorescent glioblastomas.</p><p><strong>Methods: </strong>Patients with newly diagnosed and recurrent <i>IDH</i>-wildtype glioblastoma that underwent surgery were analyzed. The intensity of intraoperative 5-ALA fluorescence was categorized as non-visible or visible. DNA was extracted from tumors and genome-wide DNA methylation patterns were analyzed using Illumina EPIC (850k) arrays. Furthermore, 5-ALA intensity was measured by flow cytometry on human gliomasphere lines (BT112 and BT145).</p><p><strong>Results: </strong>Of 74 included patients, 12 (16.2%) patients had a non-fluorescent glioblastoma, which were compared to 62 glioblastomas with 5-ALA fluorescence. Clinical characteristics were equally distributed between both groups. We did not find significant differences between DNA methylation subclasses and 5-ALA fluorescence (<i>P</i> = .24). The distribution of cells of the tumor microenvironment was not significantly different between the non-fluorescent and fluorescent tumors. Copy number variations in <i>EGFR and</i> simultaneous EGFRvIII expression were strongly associated with 5-ALA fluorescence since all non-fluorescent glioblastomas were <i>EGFR</i>-amplified (<i>P</i> < .01). This finding was also demonstrated in recurrent tumors. Similarly, <i>EGFR</i>-amplified glioblastoma cell lines showed no 5-ALA fluorescence after 24 h of incubation.</p><p><strong>Conclusions: </strong>Our study demonstrates an association between non-fluorescent <i>IDH</i>-wildtype glioblastomas and <i>EGFR</i> gene amplification which should be taken into consideration for recurrent surgery and future studies investigating <i>EGFR</i>-amplified gliomas.</p>","PeriodicalId":19234,"journal":{"name":"Neuro-oncology practice","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2023-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10502788/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10360903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-04-24eCollection Date: 2023-08-01DOI: 10.1093/nop/npad022
Shawn Kothari, Anna C Dusenbery, Abigail Doucette, Daniel Y Zhang, Dominique Ballinger, Arati Desai, Jennifer J D Morrissette, Stephen J Bagley, MacLean P Nasrallah
Background: Recurrent gliomas are therapeutically challenging diseases with few treatment options available. One area of potential therapeutic vulnerability is the presence of targetable oncogenic fusion proteins.
Methods: To better understand the clinical benefit of routinely testing for fusion proteins in adult glioma patients, we performed a retrospective review of 647 adult patients with glioma who underwent surgical resection at our center between August 2017 and May 2021 and whose tumors were analyzed with an in-house fusion transcript panel.
Results: Fifty-two patients (8%) were found to harbor a potentially targetable fusion with 11 (21%) of these patients receiving treatment with a fusion-targeted inhibitor. The targetable genes found to be involved in a fusion included FGFR3, MET, EGFR, NTRK1, NTRK2, BRAF, ROS1, and PIK3CA.
Conclusions: This analysis demonstrates that routine clinical testing for gene fusions identifies a diverse repertoire of potential therapeutic targets in adult patients with glioma and can offer rational therapeutic options for patients with recurrent disease.
{"title":"RNA fusion transcript panel identifies diverse repertoire of fusions in adult glioma patients with therapeutic implications.","authors":"Shawn Kothari, Anna C Dusenbery, Abigail Doucette, Daniel Y Zhang, Dominique Ballinger, Arati Desai, Jennifer J D Morrissette, Stephen J Bagley, MacLean P Nasrallah","doi":"10.1093/nop/npad022","DOIUrl":"10.1093/nop/npad022","url":null,"abstract":"<p><strong>Background: </strong>Recurrent gliomas are therapeutically challenging diseases with few treatment options available. One area of potential therapeutic vulnerability is the presence of targetable oncogenic fusion proteins.</p><p><strong>Methods: </strong>To better understand the clinical benefit of routinely testing for fusion proteins in adult glioma patients, we performed a retrospective review of 647 adult patients with glioma who underwent surgical resection at our center between August 2017 and May 2021 and whose tumors were analyzed with an in-house fusion transcript panel.</p><p><strong>Results: </strong>Fifty-two patients (8%) were found to harbor a potentially targetable fusion with 11 (21%) of these patients receiving treatment with a fusion-targeted inhibitor. The targetable genes found to be involved in a fusion included <i>FGFR3, MET, EGFR, NTRK1, NTRK2, BRAF, ROS1,</i> and <i>PIK3CA</i>.</p><p><strong>Conclusions: </strong>This analysis demonstrates that routine clinical testing for gene fusions identifies a diverse repertoire of potential therapeutic targets in adult patients with glioma and can offer rational therapeutic options for patients with recurrent disease.</p>","PeriodicalId":19234,"journal":{"name":"Neuro-oncology practice","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2023-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10346416/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10184109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-04-21eCollection Date: 2023-08-01DOI: 10.1093/nop/npad020
Stefan Oberndorfer
{"title":"Lower middle-income countries: A risk factor for lower survival in glioblastoma? Evidence for health care providers.","authors":"Stefan Oberndorfer","doi":"10.1093/nop/npad020","DOIUrl":"10.1093/nop/npad020","url":null,"abstract":"","PeriodicalId":19234,"journal":{"name":"Neuro-oncology practice","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2023-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10346381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10184112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-04-20eCollection Date: 2023-08-01DOI: 10.1093/nop/npad019
Pim B van der Meer, Linda Dirven, Caroline Hertler, Florien W Boele, Albert Batalla, Tobias Walbert, Alasdair G Rooney, Johan A F Koekkoek
AbstractGlioma patients carry the burden of having both a progressive neurological disease and cancer, and may face a variety of symptoms, including depression and anxiety. These symptoms are highly prevalent in glioma patients (median point prevalence ranging from 16-41% for depression and 24-48% for anxiety when assessed by self-report questionnaires) and have a major impact on health-related quality of life and even overall survival time. A worse overall survival time for glioma patients with depressive symptoms might be due to tumor progression and/or its supportive treatment causing depressive symptoms, an increased risk of suicide or other (unknown) factors. Much is still unclear about the etiology of depressive and anxiety symptoms in glioma. These psychiatric symptoms often find their cause in a combination of neurophysiological and psychological factors, such as the tumor and/or its treatment. Although these patients have a particular idiosyncrasy, standard treatment guidelines for depressive and anxiety disorders apply, generally recommending psychological and pharmacological treatment. Only a few nonpharmacological trials have been conducted evaluating the efficacy of psychological treatments (eg, a reminiscence therapy-based care program) in this population, which significantly reduced depressive and anxiety symptoms. No pharmacological trials have been conducted in glioma patients specifically. More well-designed trials evaluating the efficacy of nonpharmacological treatments for depressive and anxiety disorders in glioma are urgently needed to successfully treat psychiatric symptoms in brain tumor patients and to improve (health-related) quality of life.
{"title":"Depression and anxiety in glioma patients.","authors":"Pim B van der Meer, Linda Dirven, Caroline Hertler, Florien W Boele, Albert Batalla, Tobias Walbert, Alasdair G Rooney, Johan A F Koekkoek","doi":"10.1093/nop/npad019","DOIUrl":"10.1093/nop/npad019","url":null,"abstract":"<p><p>AbstractGlioma patients carry the burden of having both a progressive neurological disease and cancer, and may face a variety of symptoms, including depression and anxiety. These symptoms are highly prevalent in glioma patients (median point prevalence ranging from 16-41% for depression and 24-48% for anxiety when assessed by self-report questionnaires) and have a major impact on health-related quality of life and even overall survival time. A worse overall survival time for glioma patients with depressive symptoms might be due to tumor progression and/or its supportive treatment causing depressive symptoms, an increased risk of suicide or other (unknown) factors. Much is still unclear about the etiology of depressive and anxiety symptoms in glioma. These psychiatric symptoms often find their cause in a combination of neurophysiological and psychological factors, such as the tumor and/or its treatment. Although these patients have a particular idiosyncrasy, standard treatment guidelines for depressive and anxiety disorders apply, generally recommending psychological and pharmacological treatment. Only a few nonpharmacological trials have been conducted evaluating the efficacy of psychological treatments (eg, a reminiscence therapy-based care program) in this population, which significantly reduced depressive and anxiety symptoms. No pharmacological trials have been conducted in glioma patients specifically. More well-designed trials evaluating the efficacy of nonpharmacological treatments for depressive and anxiety disorders in glioma are urgently needed to successfully treat psychiatric symptoms in brain tumor patients and to improve (health-related) quality of life.</p>","PeriodicalId":19234,"journal":{"name":"Neuro-oncology practice","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2023-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/8c/c7/npad019.PMC10346395.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10098814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Evangelia Liouta, Aristotelis V Kalyvas, Spyridon Komaitis, Evangelos Drosos, Christos Koutsarnakis, Juan M García-Gómez, Javier Juan-Albarracín, Vasileios Katsaros, Theodosis Kalamatianos, Theodoros Argyrakos, George Stranjalis
Background: High-grade glioma (HGG) patients present with variable impairment in neurocognitive function (NCF). Based on that, isocitrate dehydrogenase 1 (IDH1) wild-type HGGs are more aggressive than IDH1 mutant-type ones, we hypothesized that patients with IDH1 wild-type HGG would exhibit more severe NCF deficits than their IDH1 mutant counterparts.
Methods: NCF was assessed by Mini Mental Status Exam (MMSE), Trail Making Test (TMT), Digit Span (DS), and Controlled Word Association Test (COWAT) tests in 147 HGG patients preoperatively.
Results: Analyses between IDH1 groups revealed a significant difference on MMSE concentration component (p ≤ .01), DS (p ≤ .01), TMTB (p ≤ .01), and COWAT (p ≤ .01) scores, with the IDH1 wild group performing worse than the IDH1 mutant one. Age and tumor volume were inversely correlated with MMSE concentration component (r = -4.78, p < .01), and with MMSE concentration (r = -.401, p < .01), TMTB (r = -.328, p < .01), and COWAT phonemic scores (r = -.599, p < .01), respectively, but only for the IDH1 wild-type group. Analyses between age-matched subsamples of IDH1 groups revealed no age effect on NCF. Tumor grade showed nonsignificance on NCF (p > .05) between the 2 IDH1 mutation subgroups of grade IV tumor patients. On the contrary, grade III group showed a significant difference in TMTB (p < .01) and DS backwards (p < .01) between IDH1 subgroups, with the mutant one outperforming the IDH1 wild one.
Conclusions: Our findings indicate that IDH1 wild-type HGG patients present greater NCF impairment, in executive functions particularly, compared to IDH1 mutant ones, suggesting that tumor growth kinetics may play a more profound role than other tumor and demographic parameters in clinical NCF of HGG patients.
背景:高级别胶质瘤(HGG)患者表现为神经认知功能(NCF)的可变损害。基于此,异柠檬酸脱氢酶1 (IDH1)野生型HGG比IDH1突变型HGG更具侵袭性,我们假设IDH1野生型HGG患者比IDH1突变型HGG患者表现出更严重的NCF缺陷。方法:对147例HGG患者术前采用Mini Mental Status examination (MMSE)、Trail Making Test (TMT)、Digit Span (DS)、Controlled Word Association Test (COWAT)进行NCF评估。结果:IDH1组间MMSE浓度组成(p≤0.01)、DS (p≤0.01)、TMTB (p≤0.01)、COWAT (p≤0.01)评分差异均有统计学意义,且IDH1野生组表现差于IDH1突变组。年龄、肿瘤体积与MMSE浓度组分呈负相关(r = -4.78, p < 0.01),与MMSE浓度组分呈负相关(r = -)。401, p < 0.01), TMTB (r = -。328, p < 0.01),而COWAT音位评分(r = -。599, p < 0.01),但仅适用于IDH1野生型组。对年龄匹配的IDH1组亚样本的分析显示,年龄对NCF没有影响。肿瘤分级对IV级肿瘤患者2个IDH1突变亚组NCF的影响无统计学意义(p > 0.05)。III级组在TMTB (p < 0.01)和DS倒位(p < 0.01)上在IDH1亚组间有显著差异,突变型优于野生型。结论:我们的研究结果表明,与IDH1突变型HGG患者相比,IDH1野生型HGG患者存在更大的NCF损伤,特别是在执行功能方面,这表明肿瘤生长动力学可能比其他肿瘤和人口统计学参数在HGG患者的临床NCF中发挥更深远的作用。
{"title":"Association between preoperative neurocognitive status and IDH1 mutation status in high-grade gliomas.","authors":"Evangelia Liouta, Aristotelis V Kalyvas, Spyridon Komaitis, Evangelos Drosos, Christos Koutsarnakis, Juan M García-Gómez, Javier Juan-Albarracín, Vasileios Katsaros, Theodosis Kalamatianos, Theodoros Argyrakos, George Stranjalis","doi":"10.1093/nop/npac077","DOIUrl":"https://doi.org/10.1093/nop/npac077","url":null,"abstract":"<p><strong>Background: </strong>High-grade glioma (HGG) patients present with variable impairment in neurocognitive function (NCF). Based on that, isocitrate dehydrogenase 1 (IDH1) wild-type HGGs are more aggressive than IDH1 mutant-type ones, we hypothesized that patients with IDH1 wild-type HGG would exhibit more severe NCF deficits than their IDH1 mutant counterparts.</p><p><strong>Methods: </strong>NCF was assessed by Mini Mental Status Exam (MMSE), Trail Making Test (TMT), Digit Span (DS), and Controlled Word Association Test (COWAT) tests in 147 HGG patients preoperatively.</p><p><strong>Results: </strong>Analyses between IDH1 groups revealed a significant difference on MMSE concentration component (<i>p</i> ≤ .01), DS (<i>p</i> ≤ .01), TMTB (<i>p</i> ≤ .01), and COWAT (<i>p</i> ≤ .01) scores, with the IDH1 wild group performing worse than the IDH1 mutant one. Age and tumor volume were inversely correlated with MMSE concentration component (<i>r</i> = -4.78, <i>p</i> < .01), and with MMSE concentration (<i>r</i> = -.401, <i>p</i> < .01), TMTB (<i>r</i> = -.328, <i>p</i> < .01), and COWAT phonemic scores (<i>r</i> = -.599, <i>p</i> < .01), respectively, but only for the IDH1 wild-type group. Analyses between age-matched subsamples of IDH1 groups revealed no age effect on NCF. Tumor grade showed nonsignificance on NCF (<i>p</i> > .05) between the 2 IDH1 mutation subgroups of grade IV tumor patients. On the contrary, grade III group showed a significant difference in TMTB (<i>p</i> < .01) and DS backwards (<i>p</i> < .01) between IDH1 subgroups, with the mutant one outperforming the IDH1 wild one.</p><p><strong>Conclusions: </strong>Our findings indicate that IDH1 wild-type HGG patients present greater NCF impairment, in executive functions particularly, compared to IDH1 mutant ones, suggesting that tumor growth kinetics may play a more profound role than other tumor and demographic parameters in clinical NCF of HGG patients.</p>","PeriodicalId":19234,"journal":{"name":"Neuro-oncology practice","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10037936/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9246419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}