Neuro-oncology Advances最新文献

{"title":"Comparison of Volumetric and 2D-based Response Methods in the PNOC-001 Pediatric Low-Grade Glioma Clinical Trial","authors":"M. von Reppert, D. Ramakrishnan, Sarah C Brüningk, Fatima Memon, Sandra Abi Fadel, Nazanin Maleki, R.C. Bahar, Arman E Avesta, L. Jekel, Matthew Sala, J. Lost, N. Tillmanns, Manpreet Kaur, S. Aneja, A. Kazerooni, A. Nabavizadeh, Ming De Lin, Karl-Titus Hoffmann, K. Bousabarah, Kristin R Swanson, Daphne A Haas-Kogan, Sabine Mueller, Mariam S Aboian","doi":"10.1093/noajnl/vdad172","DOIUrl":"https://doi.org/10.1093/noajnl/vdad172","url":null,"abstract":"Although response in pediatric low-grade glioma (pLGG) includes volumetric assessment, more simplified 2D-based methods are often used in clinical trials. The study purpose was to compare volumetric to 2D methods. An expert neuroradiologist performed solid and whole tumor (including cyst and edema) volumetric measurements on MR images using a PACS-based manual segmentation tool in 43 pLGG participants (213 total follow-up images) from the PNOC-001 trial. Classification based on changes in volumetric and 2D measurements of solid tumor were compared to neuroradiologist visual response assessment using the Brain Tumor Reporting and Data System (BT-RADS) criteria for a subset of 65 images using receiver operating characteristic (ROC) analysis. Longitudinal modeling of solid tumor volume was used to predict BT-RADS classification in 54 of the 65 images. There was a significant difference in ROC area under the curve (AUC) between 3D solid tumor volume and 2D area (0.96 vs. 0.78, p = 0.005) and between 3D solid and 3D whole volume (0.96 vs. 0.84, p = 0.006) when classifying BT-RADS progressive disease (PD). Thresholds of 15-25% increase in 3D solid tumor volume had an 80% sensitivity in classifying BT-RADS PD included in their 95% confidence intervals. The longitudinal model of solid volume response had a sensitivity of 82% and positive predictive value of 67% for detecting BT-RADS PD. Volumetric analysis of solid tumor was significantly better than 2D measurements in classifying tumor progression as determined by BT-RADS criteria and will enable more comprehensive clinical management.","PeriodicalId":19138,"journal":{"name":"Neuro-oncology Advances","volume":"51 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139154521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Does Exogenous Hormonal Therapy Affect the Risk of Glioma among Females: A Systematic Review and Meta-analysis","authors":"Ghady Alfuridy, Rana Alghamdi, Abdulaziz Alkhoshi, Ahood A Mahjari, Abdullah Alhussein, E. Alshehri, Ahmed Lary, Abdulrahman Sabagh, Soha A. Alomar","doi":"10.1093/noajnl/vdad167","DOIUrl":"https://doi.org/10.1093/noajnl/vdad167","url":null,"abstract":"The effect of exogenous hormone replacement therapy (HRT) and oral contraceptive pills ( OCPs) on glioma risk in females is unclear despite numerous studies; hence, we conducted a meta-analysis to evaluate this relationship. Studies investigating the impact of exogenous female hormones on glioma risk were retrieved by searching four databases from inception until September 2022. Articles of any design, such as case–control and cohort studies, proving the relative risk (RR), odd ratio (OR), or hazard ratio were included. Summary OR values were calculated using a random effects model. Both HRT and OCP use of any duration decreased the risk of developing glioma [HRT OR = 0.78, 95%CI 0.66–0.91, p = 0.00; OCP: OR = 0.80, 95%CI 0.67–0.96, p = 0.02]. When stratified by duration of use, HRT use >1 year significantly reduced glioma risk (<1 year: OR = 0.82, 95%CI 0.63–1.07, p = 0.15; 1–5 years: OR = 0.79, 95%CI 0.67–0.92, p = 0.00; 5–10 years: OR = 0.80, 95%CI 0.66–0.97, p = 0.02; >10 years: OR = 0.69, 95%CI 0.54–0.88, p = 0.00). In contrast, only OCP use for >10 years significantly reduced glioma risk (<1 year: OR = 0.72, 95%CI 0.49–1.05, p = 0.09; 1–5 years: OR = 0.88, 95%CI 0.72–1.02, p = 0.09; 5–10 years: OR = 0.85, 95%CI 0.65–1.1, p = 0.21; >10 years: OR = 0.58, 95%CI 0.45–0.74, p = 0.00). Our pooled results strongly suggest that sustained HRT and OCP use is associated with reduced risk of glioma development.","PeriodicalId":19138,"journal":{"name":"Neuro-oncology Advances","volume":"201 2‐3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139161065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the Multifaceted Role of NRF2 in Brain Physiology and Cancer: A Comprehensive Review","authors":"Maya M Moubarak, Antonio C Pagano Zottola, Claire M Larrieu, Sylvain Cuvellier, T. Daubon, O. C. Martin","doi":"10.1093/noajnl/vdad160","DOIUrl":"https://doi.org/10.1093/noajnl/vdad160","url":null,"abstract":"Chronic oxidative stress plays a critical role in the development of brain malignancies due to the high rate of brain oxygen utilization and concomitant production of reactive oxygen species (ROS). The nuclear factor-erythroid-2-related factor 2 (NRF2), a master regulator of antioxidant signaling, is a key factor in regulating brain physiology and the development of age-related neurodegenerative diseases. Also, NRF2 is known to exert a protective antioxidant effect against the onset of oxidative stress-induced diseases, including cancer, along with its pro-oncogenic activities through regulating various signaling pathways and downstream target genes. In glioblastoma (GB), grade IV glioma, tumor resistance, and recurrence are caused by the glioblastoma stem cell (GSC) population constituting a small bulk of the tumor core. The persistence and self-renewal capacity of these cell populations is enhanced by NRF2 expression in GB tissues. This review outlines NRF2's dual involvement in cancer and highlights its regulatory role in human brain physiology and diseases, in addition to the development of primary brain tumors and therapeutic potential, with a focus on GB.","PeriodicalId":19138,"journal":{"name":"Neuro-oncology Advances","volume":"22 5","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139162730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TGF-β and BMP Signaling are Associated with the Transformation of Glioblastoma to Gliosarcoma and then Osteosarcoma","authors":"Aiguo Li, John C Hancock, Martha Quezado, Susie Ahn, Nicole J Briceno, O. Celiku, Surabhi Ranjan, O. Aboud, Nicole Colwell, Sun A Kim, E. Nduom, Skyler Kuhn, Deric M. Park, Elizabeth Vera, Ken Aldape, Terri S. Armstrong, Mark R Gilbert","doi":"10.1093/noajnl/vdad164","DOIUrl":"https://doi.org/10.1093/noajnl/vdad164","url":null,"abstract":"\u0000 \u0000 \u0000 Gliosarcoma, an isocitrate dehydrogenase wildtype (IDH-WT) variant of glioblastoma, is defined by clonal biphasic differentiation into gliomatous and sarcomatous components. While the transformation from a glioblastoma to gliosarcoma is uncommon, the subsequent transformation to osteosarcoma is rare, but may provide additional insights into the biology of these typically distinct cancers. We observed a patient initially diagnosed with glioblastoma, that differentiated into gliosarcoma at recurrence, and further evolved to an osteosarcoma at second relapse. Our objective was to characterize the molecular mechanisms of tumor progression associated with this phenotypic transformation.\u0000 \u0000 \u0000 \u0000 Tumor samples were collected at all three stages of disease and RNA sequencing was performed to capture their transcriptomic profiles. Sequential clonal evolution was confirmed by maintenance of an identical PTEN mutation throughout the tumor differentiation using the TSO500 gene panel. Publicly available datasets and the Nanostring nCounter technology were used to validate the results.\u0000 \u0000 \u0000 \u0000 The glioblastoma tumor from this patient possessed mixed features of all three TCGA-defined transcriptomic subtypes of an IDH-WT glioblastoma and a proportion of osteosarcoma signatures were upregulated in the original tumor. Analysis showed that enhanced TGF-β and BMP signaling were associated with tumor transformation. Regulatory network analysis revealed that TGF-β family signaling committed the lineage tumor to osteogenesis by stimulating expression of runt-related transcription factor 2 (RUNX2), a master regulator of bone formation.\u0000 \u0000 \u0000 \u0000 This unusual clinical case provided an opportunity to explore the modulators of longitudinal sarcomatous transformation, potentially uncovering markers indicating predisposition to this change and identification of novel therapeutic targets.\u0000","PeriodicalId":19138,"journal":{"name":"Neuro-oncology Advances","volume":" 46","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138961270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quantification perineural satellitosis in pretreatment glioblastoma with structural MRI and a diffusion tensor imaging template","authors":"Rik van den Elshout, Benthe Ariëns, Joost Blaauboer, Frederick J A Meijer, Anja G van der Kolk, Morteza Esmaeili, Tom W J Scheenen, D. Henssen","doi":"10.1093/noajnl/vdad168","DOIUrl":"https://doi.org/10.1093/noajnl/vdad168","url":null,"abstract":"\u0000 \u0000 \u0000 Survival outcomes for glioblastoma (GBM) patients remain unfavorable, and tumor recurrence is often observed. Understanding the radiological growth patterns of GBM could aid in improving outcome. This study aimed to examine the relationship between contrast-enhancing tumor growth direction and white matter, using an image registration and deformation strategy.\u0000 \u0000 \u0000 \u0000 In GBM patients two pretreatment scans (diagnostic and neuronavigation) were gathered retrospectively, co-registered to a template and DTI atlas. The GBM lesions were segmented and co-registered to the same space. Growth vectors were derived and divided into vector populations parallel (Φ = 0-20 degrees) and perpendicular (Φ = 70-90 degrees) to white matter. To test for statistical significance between parallel and perpendicular groups, a paired samples Students T-test was performed. O6-methylguanine-DNA methyltransferase (MGMT) methylation status and its correlation to growth rate was also tested using a one-way ANOVA test.\u0000 \u0000 \u0000 \u0000 For 78 GBM patients (mean age 61 years ± 13 SD, 32 men), the included GBM lesions showed a predominant preference of perineural satellitosis (p<0.001), with a mean percentile growth of 30.8% (95CI 29.6% – 32.0%) parallel (0° < |Φ| <20°) to white matter. Perpendicular tumor growth with respect to white matter microstructure (70° < |Φ| <90°) showed to be 22.7% (95CI 21.3% – 24.1%) of total tumor growth direction.\u0000 \u0000 \u0000 \u0000 The presented strategy showed that tumor growth direction in pretreatment GBM patients correlated with white matter architecture. Future studies with patient-specific DTI data are required to verify the accuracy of this method prospectively to identify its usefulness as a clinical metric in pre- and posttreatment setting.\u0000","PeriodicalId":19138,"journal":{"name":"Neuro-oncology Advances","volume":" 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138961879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MGMT function determines the differential response of ATR inhibitors with DNA-damaging agents in glioma stem cells for GBM therapy","authors":"Vincent W S Leong, Sabbir Khan, P. Sharma, Shaofang Wu, Riya R Thomas, Xiaolong Li, Sanjay K. Singh, Frederick F Lang, W. A. Yung, D. Koul","doi":"10.1093/noajnl/vdad165","DOIUrl":"https://doi.org/10.1093/noajnl/vdad165","url":null,"abstract":"\u0000 \u0000 \u0000 The most prevalent cancer treatments cause cell death through DNA damage. However, DNA damage response (DDR) repair pathways, initiated by tumor cells, can withstand the effects of anticancer drugs, providing justification for combining DDR inhibitors with DNA-damaging anticancer treatments.\u0000 \u0000 \u0000 \u0000 Cell viability assays were performed with CellTiter-Glo assay. DNA damage was evaluated using Western blotting analysis. RNA-seq and single-cell level expression was used to identify the DDR signatures. In vivo studies were conducted in mice to determine the effect of ATris with TMZ sensitization.\u0000 \u0000 \u0000 \u0000 We found a subpopulation of glioma sphere-forming cells (GSCs) with substantial synergism with temozolomide (TMZ) using a panel of 3 clinical-grade ataxia telangiectasia- and Rad3-related kinase inhibitors (ATRis), (elimusertib, berzosertib, and ceralasertib). Interestingly, most synergistic cell lines had O6-methylguanine-DNA methyltransferase (MGMT) promoter methylation, indicating that ATRi mainly benefit tumors with no MGMT repair. Further, TMZ activated the ATR-checkpoint kinase 1 (Chk1) axis in an MGMT-dependent way. TMZ caused ATR-dependent Chk1 phosphorylation and DNA double-strand breaks as shown by increased γH2AX. Increased DNA damage and decreased Chk1 phosphorylation was observed upon the addition of ATRis to TMZ in MGMT-methylated (MGMT-) GSCs.TMZ also improved sensitivity to ATRis in vivo, as shown by increased mouse survival with the TMZ and ATRi combination treatment.\u0000 \u0000 \u0000 \u0000 This research provides a rationale for selectively targeting MGMT-methylated cells using ATRis and TMZ combination. Overall, we believe that MGMT methylation status in GBM could serve as a robust biomarker for patient selection for ATRi combined with TMZ.\u0000","PeriodicalId":19138,"journal":{"name":"Neuro-oncology Advances","volume":"102 16","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138959401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Volumetric Analysis: Rethinking Brain Metastases Response Assessment","authors":"B. Ocaña-Tienda, J. Pérez-Beteta, J. A. Romero-Rosales, B. Asenjo, A. Ortiz de Mendivil, Luis Alberto Pérez Romasanta, Jose David Albillo Labarra, Fátima Nagib, María Vidal Denis, B. Luque, Estanislao Arana, Víctor M. Pérez-García","doi":"10.1093/noajnl/vdad161","DOIUrl":"https://doi.org/10.1093/noajnl/vdad161","url":null,"abstract":"\u0000 \u0000 \u0000 The Response Assessment in Neuro-Oncology for Brain Metastases (RANO-BM) criteria are the gold standard for assessing brain metastases (BMs) treatment response. However, they are limited by their reliance on one dimension, despite the routine use of high-resolution T1-weighted MRI scans for BMs, which allows for 3D measurements. Our study aimed to investigate whether volumetric measurements could improve the response assessment in patients with BMs.\u0000 \u0000 \u0000 \u0000 We retrospectively evaluated a dataset comprising 783 BMs and analyzed the response of 185 of them from 132 patients who underwent stereotactic radiotherapy between 2007 and 2021 at five hospitals. We used T1-weighted MRIs to compute the volume of the lesions. For the volumetric criteria, progressive disease was defined as at least a 30% increase in volume, and partial response was characterized by a 20% volume reduction.\u0000 \u0000 \u0000 \u0000 Our study showed that the proposed volumetric criteria outperformed the RANO-BM criteria in several aspects: 1) Evaluating every lesion, while RANO-BM failed to evaluate 9.2% of them. 2) Classifying response effectively in 140 lesions, compared to only 72 lesions classified by RANO-BM. 3) Identifying BM recurrences a median of 3.3 months earlier than RANO-BM criteria.\u0000 \u0000 \u0000 \u0000 Our study demonstrates the superiority of volumetric criteria in improving the response assessment of BMs compared to the RANO-BM criteria. Our proposed criteria allow for evaluation of every lesion, regardless of its size or shape, better classification, and enable earlier identification of progressive disease. Volumetric criteria provide a standardized, reliable, and objective tool for assessing treatment response.\u0000","PeriodicalId":19138,"journal":{"name":"Neuro-oncology Advances","volume":"5 10","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138584771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Network targeting combination therapy (NTCT) of synthetic lethal (SL) vulnerabilities in 9p21 deficient glioblastoma (GBM): a case report","authors":"Michael P Castro, Kristin Dittmar","doi":"10.1093/noajnl/vdad162","DOIUrl":"https://doi.org/10.1093/noajnl/vdad162","url":null,"abstract":"\u0000 Patients with relapsed or progressive glioblastoma only rarely respond to salvage therapies. Nevertheless, comprehensive genomic profiling can provide insight that can identify promising approaches. Signaling pathway analyses have revealed synthetic lethal partnerships which create the possibility of targeting vulnerabilities arising from loss of tumor suppressor genes. For synthetic lethal vulnerabilities that are not present in normal tissues, lethal cytotoxicity against cancer cells can be achieved without the necessity of causing normal tissue toxicity. This case reports describes a patient with progressive glioblastoma with homozygous deletion of chromosome 9p21. Vulnerabilities created by CDKN2A and MTAP loss were exploited with pemetrexed, bevacizumab, and candesartan (PBC) to achieve a clinically meaningful remission by targeting multiple synthetic lethal nodes. Synthetic lethality can reveal the basis for exceptional responsiveness, thus extending the utility of molecular profiling and fulfilling the promise of precision medicine.","PeriodicalId":19138,"journal":{"name":"Neuro-oncology Advances","volume":"12 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138982006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A LINE-1 Mediated Deletion Resulting in Germline Retinoblastoma Predisposition","authors":"Erica L Macke, Anthony R Miller, Eileen Stonerock, Randal Olshefski, Kristin N Zajo, Tracy A Bedrosian, Elaine R Mardis, Yassmine M N Akkari, C. Cottrell, K. Schieffer","doi":"10.1093/noajnl/vdad163","DOIUrl":"https://doi.org/10.1093/noajnl/vdad163","url":null,"abstract":"\u0000 Retinoblastoma is an ocular cancer associated with genomic variation in the RB1 gene. In individuals with bilateral retinoblastoma, a germline variant in RB1 is identified in virtually all cases. We describe herein an individual with bilateral retinoblastoma for whom multiple clinical lab assays performed by outside commercial laboratories failed to identify a germline RB1 variant. Paired tumor/normal exome sequencing, long-read whole genome sequencing, and long-read isoform sequencing performed on a translational research basis ultimately identified a germline likely de novo LINE-1 mediated deletion resulting in a premature stop of translation of RB1 as the underlying genetic cause of retinoblastoma in this individual. Based on these research findings, the LINE-1 mediated deletion was confirmed via Sanger sequencing in our clinical laboratory and results reported into the patient medical record to allow for appropriate genetic counseling.","PeriodicalId":19138,"journal":{"name":"Neuro-oncology Advances","volume":"7 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138584881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Keeping a Track on Leptomeningeal Disease in Non-Small Cell Lung Cancer: A Single Institution Experience with CNSideTM","authors":"S. Puri, R. Malani, Anna W Chalmers, K. Kerrigan, Shiven B. Patel, Kelly Monynahan, L. Cannon, Barbara Blouw, Wallace Akerley","doi":"10.1093/noajnl/vdad150","DOIUrl":"https://doi.org/10.1093/noajnl/vdad150","url":null,"abstract":"\u0000 \u0000 \u0000 Leptomeningeal Disease (LMD) is a devastating complication for patients with advanced cancer. Diagnosis and monitoring the response to therapy remains challenging due to limited sensitivity and specificity of standard-of-care (SOC) diagnostic modalities, including cerebrospinal fluid (CSF) cytology, MRI, and clinical evaluation. These hindrances contribute to the poor survival of LMD patients. CNSide is a CLIA-validated test that detects and characterizes CSF-derived tumor cells and cell-free (cf) DNA. We performed a retrospective analysis on the utility of CNSide to analyze CSF obtained from advanced non-small cell lung cancer (aNSCLC) patients with suspected LMD treated at the Huntsman Cancer Institute in Salt Lake City, Utah.\u0000 \u0000 \u0000 \u0000 CNSide was used to evaluate CSF from fifteen patients with aNSCLC. CSF tumor cell quantification was performed throughout treatment for five patients. CSF tumor cells and cfDNA were characterized for actionable mutations.\u0000 \u0000 \u0000 \u0000 In LMD-positive patients, CNSide detected CSF tumor cells in 88% (22/25) samples vs. 40% (10/25) for cytology (matched samples). CSF tumor cell numbers tracked response to therapy in five patients where CNSide was used to quantify tumor cells throughout treatment. In 75% (9/12) of the patients genetic alterations were detected in CSF, with majority representing gene mutations and amplifications with therapeutic potential. The median survival for LMD patients was 16.1 m (5.2- NR).\u0000 \u0000 \u0000 \u0000 We show that CNSide can supplement the management of LMD in conjunction with SOC methods for the diagnosis, monitoring response to therapy, and identifying actionable mutations unique to the CSF in patients with LMD.\u0000","PeriodicalId":19138,"journal":{"name":"Neuro-oncology Advances","volume":"2 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138585857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}