Matthew Alexander Abikenari

All Publications

• Normative network-based programming for deep brain stimulation-Concept and case report INTERDISCIPLINARY NEUROSURGERY-ADVANCED TECHNIQUES AND CASE MANAGEMENT Sadeghzadeh, S., Reid, B., Nageeb, G., Abikenari, M. A., Lev-Tov, L., Park, J. J., Barbosa, D. A. N., Bhanot, P., McNab, J., Halpern, C. H., Buch, V. P. 2026; 45

  View details for DOI 10.1016/j.inat.2026.102298

  View details for Web of Science ID 001800035600001

• Vestibular schwannoma: genetic and epigenetic mechanisms, hearing loss, and emerging therapies. Journal of neuro-oncology Otaner, F., Himic, V., Vargas, L. O., Abikenari, M., Pandey, N., Sivanathan, S., Kalmanson, O., Govindan, A., Jung, D., Estevez-Ordonez, D., Wang, A., Jeyaretna, S., Shah, A. H., Komotar, R. J., Gampel, B., Dinh, C., Ivan, M. E. 2026; 178 (1)

  Abstract

  Although most vestibular schwannomas (VS) occur sporadically, both sporadic and hereditary tumors share common molecular features beyond the loss of NF2. New evidence highlights the role of interconnected signaling pathways and epigenetic regulation in Schwann cell tumorigenesis, pointing toward potential molecularly targeted therapeutic strategies.This review synthesizes preclinical, molecular, and clinical evidence to examine genetic and epigenetic mechanisms underlying VS, therapeutic strategies, and contributors to hearing loss. A structured search of ClinicalTrials.gov identified 21 Phase 1-3 interventional therapeutic trials.VS pathogenesis is driven by NF2 loss and merlin deficiency, leading to dysregulation of Hippo/YAP-TAZ, PI3K/AKT/mTOR, VEGF, MAPK, and adhesion pathways. Epigenetic alterations, including DNA methylation, chromatin remodeling, non-coding RNAs, and SOX10 dysfunction, further shape tumor behavior. Clinical trial analysis revealed a predominance of early-phase, non-comparative studies, limited progression to later-phase trials, and incomplete results reporting, indicating gaps in high-quality evidence. Bevacizumab remains the most consistent systemic therapy for select NF2-related cases, while other agents such as icotinib, lapatinib, everolimus, selumetinib, and brigatinib have shown modest activity, primarily disease stabilization. Emerging approaches, including TEAD inhibition, PI3K/mTOR blockade, MEK inhibition, and combined signaling-epigenetic strategies, show preclinical promise. Hearing loss is multifactorial, involving tumor-secreted factors, inflammation, vascular changes, and inner ear damage alongside nerve compression.VS biology reflects integrated genetic and epigenomic dysregulation. Advancing care will require multi-omic classification, biomarker-driven trials, and combination therapies targeting both signaling and epigenetic vulnerabilities. Future management is expected to shift toward personalized, mechanism-based strategies aimed at durable tumor control while preserving hearing and quality of life.

  View details for DOI 10.1007/s11060-026-05621-4

  View details for PubMedID 42143176

  View details for PubMedCentralID 12521331

• Gliomas as network diseases: Neuron-tumor interactions, connectome disruption, and clinical implications. Clinical neurology and neurosurgery Vargas, L. O., Latzman, S., Tickoo, L., Abikenari, M., Syed, S. A., Mittelman, L., Cassimatis, N., Teng, C. L., Sistiaga, I. L., D'Amico, R. S. 2026; 267: 109475

  Abstract

  Gliomas are increasingly understood as disorders of distributed brain networks rather than focal lesions confined within radiographic margins. Emerging evidence suggests that glioma cells interact with neural circuits, alter structural and functional connectivity, and contribute to cognitive, neuropsychiatric, and functional decline through network-level mechanisms.This structured narrative review synthesizes preclinical, molecular, neuroimaging, and clinical evidence on how gliomas disrupt the brain connectome. Evidence is organized into sections on neuron-glioma interactions, white matter-guided invasion, functional network disruption, grade- and subtype-specific vulnerability, prognostic biomarkers, recurrence detection, network-guided surgery, and exploratory neuromodulatory strategies.Glioma-related connectome disruption is mediated by activity-dependent neuron-glioma synaptic coupling, paracrine signaling, tumor microtubule networks, gap junction communication, tumor microenvironment remodeling, and white matter tract-guided invasion. These mechanisms enable gliomas to integrate into and remodel neural circuits, producing structural disconnection and functional network instability beyond the visible tumor core. Large-scale cognitive and affective networks, including the default mode, salience, and central executive networks, are frequently altered and may contribute to early neuropsychiatric symptoms, cognitive impairment, seizures, and functional decline. Disruption patterns vary by tumor biology: low-grade gliomas often show compensatory plasticity, whereas high-grade gliomas and glioblastomas exhibit extensive bilateral network disruption and reduced interhemispheric connectivity. Connectome-derived metrics have been associated with tumor grade, molecular subtype, recurrence, cognitive outcomes, and survival. In selected glioblastoma cohorts, preserved intratumoral functional connectivity may correlate with improved outcomes, suggesting a marker of local tumor aggressiveness and preserved host tissue architecture. Translational applications include connectome-informed surgical planning, noninvasive prognostication, recurrence monitoring, and network-based rehabilitation or neuromodulation, although these approaches remain investigational.Glioma biology reflects dynamic interactions between tumor cells and distributed neural networks. A connectome-informed framework may complement conventional imaging and molecular classification by identifying global brain vulnerability, functional risk, and therapeutic targets. Clinical implementation will require standardized imaging pipelines, prospective multicenter validation, and integration with patient-centered outcomes. Only then can connectome-guided strategies be routinely incorporated into glioma care.

  View details for DOI 10.1016/j.clineuro.2026.109475

  View details for PubMedID 42119240

• Extent of resection, cognition, and health-related quality of life after adult glioma surgery: a systematic review. Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia Vargas, L. O., Mittelman, L., Syed, S. A., Croft, Z., Chen, J., Abikenari, M., Schultz, A., Ferreira, M. Y., Duehr, J., Cassimatis, N., D'Amico, R. S. 2026; 150: 112064

  Abstract

  Although maximizing the extent of resection (EOR) has been associated with improved survival in adults with diffuse gliomas, the impact of surgery on postoperative cognition and health-related quality of life (HRQoL) is less clearly defined. We aimed to synthesize evidence on the relationship between the extent of resection, postoperative cognition, and HRQoL in adults with diffuse gliomas, and to identify prognostic predictors.We conducted a systematic review of PubMed, MEDLINE, Embase, and Scopus from inception through June 1, 2025, including adult studies evaluating surgical management (biopsy, subtotal, gross-total, or supratotal resection) of diffuse gliomas. Studies reporting both neurocognitive and HRQoL outcomes were included.Nine studies (n = 958 patients) met inclusion criteria. Greater extent of resection was associated with more favorable postoperative cognitive trajectories when new permanent neurologic deficits were avoided. Early postoperative declines most often affected attention, working memory, and processing speed, while language and global screens remained stable. HRQoL declined in the early postoperative period, especially in physical and role-functioning domains. Objective cognition and HRQoL often diverged. Prognostic data were limited; greater extent of resection, and higher baseline MMSE, but not global HRQoL, predicted longer overall survival.This systematic review identified that safe maximal resection may align with favorable or stable cognitive and HRQoL trajectories in the absence of new neurologic deficits. Routine domain-level neurocognitive testing may be useful in supporting surgical decision-making. Although greater resection aligns with better cognitive and HRQoL outcomes, these associations may partly reflect selection bias. Baseline function influences extent of resection. Larger studies are needed to evaluate prognostic indicators and to improve function-preserving strategies.

  View details for DOI 10.1016/j.jocn.2026.112064

  View details for PubMedID 42096730

• Biomarkers for predicting immunotherapy response and resistance in glioblastoma. Frontiers in immunology Kim, S., Abikenari, M., Bergsneider, B., Kim, L. H., Lim, M. 2026; 17: 1823338

  Abstract

  Glioblastoma is the most common and aggressive primary brain tumor in adults that fails to meet survival endpoint criteria in current immunotherapy Phase III clinical trials. As a small subset of immunotherapy-responsive patients has been identified, biomarkers that can nominate patients for immunotherapy and inform treatment combinations have been increasingly urgent. Mechanistically-driven single biomarkers (e.g. PD-1/PD-L1 enrichment, tumor mutational burden, and MGMT methylation) are early opportunities for immunotherapy response prediction but have had inconsistent results across studies. In contrast, new context-dependent biomarker signals such as interferon signaling, immune cell population studies, and radiographic biomarkers show promise in vaccine-based therapies and in immune checkpoint blockade. Ongoing clinical trials are increasingly implementing early exploratory endpoints for biomarker discovery from several body compartments (e.g. CSF, blood, tissue). Present advancements in machine learning and liquid biopsy have provided nuanced biomarker signatures that can be composed of several biomarker categories. Progress in standardizing biomarkers in glioblastoma immunotherapy relies on the early implementation and uniformity of biomarker-driven endpoints in clinical trials.

  View details for DOI 10.3389/fimmu.2026.1823338

  View details for PubMedID 42164498

  View details for PubMedCentralID PMC13183666

• SPP1-driven immunometabolic reprogramming of tumor-associated neutrophils in glioblastoma Abikenari, M., Choi, J., Medikonda, R., Kim, L., Verma, R., Liu, J., Sjoholm, A., Nageeb, G., Bergsneider, B., Wu, C., Cho, K., Tran, A., Bakalov, D., Banu, M., Lim, M. AMER ASSOC CANCER RESEARCH. 2026

  View details for DOI 10.1158/1538-7445.AM2026-3879

  View details for Web of Science ID 001734050100001

• Biphasic, time-dependent neutrophil biology in glioblastoma revealed by <i>in vivo</i> survival and flow cytometry with single-cell transcriptomic corroboration Abikenari, M., Choi, J., Liu, J., Sjoholm, A., Nageeb, G., Poe, J., Hwa-Lin Bergsneider, B., Tran, A., Bakalov, D., Medikonda, R., Kim, L., Verma, R., Wu, C., Cho, K., Banu, M., Lim, M. AMER ASSOC CANCER RESEARCH. 2026

  View details for DOI 10.1158/1538-7445.AM2026-170

  View details for Web of Science ID 001734193700022

• Precision Immunotherapeutics for Glioblastoma: Current Approaches and Emerging Strategies in 2026. Cells Poe, J., Kim, C., Coleman, C., Nguyen, H., Velazhahan, V., Bergsneider, B., Sanker, V., Kim, S., Chen, Y., Abikenari, M., Choi, J., Lim, M. 2026; 15 (6)

  Abstract

  Glioblastoma (GBM) persists as one of the greatest challenges in the treatment of human cancer, despite extensive efforts to leverage the therapeutic potential of immunotherapy. While checkpoint blockade and other forms of immunotherapy have revolutionized the treatment of various cancers, their therapeutic efficacy in GBM has been hindered by the profound immunosuppressive environment, spatial heterogeneity, and dynamic immune metabolic challenges associated with the tumor microenvironment. In this review, we will synthesize recent advances and insights to develop a next-generation framework for GBM immunotherapy based on systems biology approaches to understanding the complex interplay between GBM and the immune system, as opposed to single-axis approaches to immune activation and modulation. We will discuss how the functional competence of the interferon system, myeloid antigen presentation status, T-cell clone status, spatial organization of the immune microenvironment, and resource competition between GBM and the immune system dictate therapeutic responsiveness. Furthermore, the current paper elucidates how recent advances in spatial transcriptomics, single-cell analysis, and high-parameter imaging enable us to understand how immune phenotype status varies across GBM regions and treatment status, and how this information can be used to develop predictive and pharmacodynamic biomarkers of therapeutic efficacy and failure. We will then discuss how these advances form the basis for rational combination approaches to GBM immunotherapy, which involve the integration of checkpoint blockade with metabolic reprogramming, myeloid modulation, and interferon system reactivation, and how artificial intelligence-based analytics and adaptive clinical trial design can guide the development of biomarker-based therapeutic selection approaches.

  View details for DOI 10.3390/cells15060561

  View details for PubMedID 41892350

  View details for PubMedCentralID PMC13025625

• Endogenous immune recruitment in glioblastoma CAR T therapy: cytokine, myeloid, and chemokine circuitry. Journal of neuro-oncology Liu, J., Abikenari, M., Annagiri, S., Ha, J. H., Nageeb, G., Sjoholm, M. A., Velazhahan, V., Medikonda, R., Choi, J., Li, G., Lim, M. 2026; 177 (1)

  Abstract

  Glioblastoma (GBM) has remained relatively unresponsive to immunotherapy, with scattered durable responses reported in early CAR T-cell studies, but without clear benefit at the population level. The major challenge for GBM has been its heterogeneous nature with a significantly immunosuppressive microenvironment that is predominantly composed of myeloid cells, inhibiting T-cell infiltration, function, and providing a rapid pathway for adaptive resistance. The focus of this review is to reposition GBM CAR T-cell therapy as a systems-level issue, turning localized CAR T-cell cytotoxicity into sustained control of the disease by engaging endogenous antitumor immunity via cytokine myeloid chemokine networks.We integrated both mechanism- and translation-oriented evidence for how inflammatory mediators derived from CAR T cells (Type I IFNs, IFN-γ, TNF) may license microglia/tumor-associated macrophages for antigen presentation and chemokine secretion, thus recruiting host effector cells and promoting antigen epitope spreading. To place this work within the context of current engineering trends, the current paper undertook a structured meta-synthesis on registry trials for interventional CAR T therapy for GBM using ClinicalTrials.gov. Using a structured advanced search strategy, we searched 91 registry records, found 44 trials for interventional CAR T therapy, and evaluated 23 active trials commenced after January 2020. Trials were classified based on target antigen choice, multi-antigen OR-gated approaches, conditional AND-gated synNotch logic, as well as safety and controllability measures (inducible off-switches).The effectiveness of CAR T cells for GBM is not likely to be actualized by targeting alone and needs to incorporate both killing and productive self-reinforcing endogenous immunity via myeloid licensing and chemokine amplification. Current trials are increasingly integrating this paradigm with a focus on more comprehensive antigens, gated CARs, immune-conjugate payloads, and safety designs amenable to the CNS without major toxicity such as ICANS. Future translation will require a focus on implementing endogenous immune activation as a quantified endpoint (including cytokine and chemokine analysis within CSF) and a simultaneous focus on immune set points that maintain cross-priming and memory without unmasking neuroinflammatory toxicity.

  View details for DOI 10.1007/s11060-026-05497-4

  View details for PubMedID 41820710

  View details for PubMedCentralID 11456825

• Nexus of IDO1/Kynurenine Pathway to T-Cell Exhaustion: Hypoxia-Induced Tryptophan Metabolism in Glioblastoma. Metabolites Abikenari, M., Nageeb, G., Ha, J. H., Sjoholm, M. A., Liu, J., Bergsneider, B., Valenzuela, J., Poe, J., Bog Cho, K., Verma, R., Wu, C., Sanker, V., Medikonda, R., Kim, L. H., Choi, J., Banu, M. A., Lim, M. 2026; 16 (3)

  Abstract

  Glioblastoma (GBM) is a universally fatal cancer for which the standard of care has remained largely unchanged for the last 20 years. Recent work has demonstrated that most therapeutic trials for GBM fail due to complex mechanisms of immunosuppression mediated by both the innate and adaptive immune systems. Various metabolic alterations in the tumor microenvironment help maintain this local and systemic immunosuppression, of which the axis of hypoxia-driven tryptophan degradation has garnered substantial attention over the last decade. This paper synthesizes a much-needed elucidation of the immunometabolic reshaping of glioma, myeloid, endothelial, and lymphoid cell lineages induced by hypoxia. The current paper critically evaluates the role of IDO1/TDO2-mediated breakdown of tryptophan and the consequent accumulation of kynurenine, a metabolite that triggers GCN2- and AHR-mediated CD8+ T-cell exhaustion and supports regulatory T-cell differentiation and expansion. Furthermore, we propose a synthesis of mechanistic evidence that establishes a role for the Trp-GCN2-ATF4-VEGFA axis in hypoxia-induced immunosuppression, supporting that pro-tumoral metabolic dysregulation is directly linked to angiogenesis. In GBM, hypoxia and tryptophan-kynurenine pathway dysregulation operate as an integrated metabolic circuit that drives widespread immunosuppression. These mechanisms can be captured by a metabolic signature shared across nearly every cell type in the GBM microenvironment. Drawing on recent spatial transcriptomic, metabolomic, and pharmacologic studies, we outline how this metabolic axis shapes disease biology and how it can be targeted to restore effective antitumor immunity.

  View details for DOI 10.3390/metabo16030185

  View details for PubMedID 41893336

  View details for PubMedCentralID PMC13028454

• When Central Tolerance Fails: Thymic Malignancies at the Intersection of Cancer Immunity and Autoimmunity. Cancers Abikenari, M., Choi, J., Enayati, I., Tucker, A., Bhatnagar, K., Chen, Y., Himic, V., Liu, J., Nageeb, G., Poe, J., Ong, S. J., Sanker, V., Diehl, M., Szeifert, V., Terasaki, A., Prolo, L. M., Engleman, E., Okwan-Duodu, D. 2026; 18 (5)

  Abstract

  Thymic malignancies are rare cancers arising from thymic epithelial cells and are characterized by a highly diverse clinical phenotype, substantial histologic and morphologic heterogeneity, and frequent associations with autoimmune syndromes. Although the clinical, immunological, and cytoarchitectural changes associated with thymomas have been increasingly elucidated in the contemporary literature, very few studies have interrogated the direct role of tumor staging and histological grading in shaping autoimmunity burden and infection risk. In this narrative review, we synthesize contemporary clinical, immunological, and morphologic evidence linking thymic architecture and selection defects to the spectrum of paraneoplastic autoimmunity (MG, pure red cell aplasia, Good's syndrome) and to infectious vulnerability. We further appraise emerging therapeutic strategies, including immune checkpoint inhibition and adoptive cellular approaches, through a patient-stratified lens, emphasizing efficacy signals, immune-related adverse events, and practical considerations for selection and monitoring. We conclude by highlighting priorities for future investigation, including refining autoantibody signatures; mapping thymic microenvironments that drive tolerance failure, and prospectively evaluating stratified immunotherapeutic regimens that balance benefit with immune-mediated risk.

  View details for DOI 10.3390/cancers18050747

  View details for PubMedID 41827683

• Value of Inpatient Neuromodulation: A National Analysis of Paddle Spinal Cord Stimulation Outcomes. Neurosurgery Jain, B., Abikenari, M. A., Sadeghzadeh, S., Shah, A., Yoo, K. H., Azad, T. D., Hani, U., Ratliff, J. K., Ramayya, A. G., Veeravagu, A. 2026

  Abstract

  Spinal cord stimulation (SCS) effectively manages chronic pain and degenerative spine conditions. Paddle SCS often necessitates inpatient care because of surgical complexity, yet the impact of procedural setting on outcomes, costs, and disparities remains unclear. This study evaluates total costs, 90-day readmission and complication rates, and socioeconomic disparities in paddle SCS delivery.Using Merative MarketScan data (2007-2023), we retrospectively identified adults undergoing initial paddle lead SCS implantation. Outcomes were total costs, 90-day readmission, and complication rates. Multivariable regression adjusted for age, sex, insurance, geographic region, surgery year, and Elixhauser comorbidity index. Propensity score matching minimized confounding, and longitudinal analyses assessed temporal outcome trends.Of 13 704 patients, 89.4% underwent outpatient procedures. Inpatients had higher comorbidities (Elixhauser comorbidity index: 1.47 vs 0.55, P < .001). After propensity score matching, complication (4.76% vs 3.51%, P = .093) and readmission rates (16.54% vs 16.88%, P = .804) were similar between groups, but inpatient procedures incurred significantly higher costs (difference = $5341.15, P = .001). Over 17 years, readmissions declined from 18% to 5% (-0.76% annually, P < .001), complications decreased from 4% to 0% (-0.33% annually, P < .001), yet costs rose annually by $912 (P < .001). Cost disparities were influenced by age (-$347/year, inpatient), insurance type ($10 940 higher for outpatient high-deductible plans), and region (North Central vs Northeast: -$13 505, inpatient). Readmissions varied by sex (female odds ratio [OR] = 1.206, outpatient), age (OR = 0.982/year, inpatient), and region (North Central OR = 0.506 vs Northeast). Southern inpatient patients had higher complication risks (OR = 3.878).Outpatient paddle SCS demonstrates equivalent short-term safety at substantially lower cost for appropriately selected patients. Inpatient implantation remains appropriate for select higher-risk patients at the surgical team's discretion, and payer policies should consider preserving coverage across both settings when clinically indicated to ensure access and equity.

  View details for DOI 10.1227/neu.0000000000003959

  View details for PubMedID 41718492

• The Bone Microenvironment and Therapeutic Resistance in Spinal Metastases: Mechanisms and Clinical Implications. Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia Mittelman, L., Vargas, L. O., Abikenari, M., Latzman, S., Chen, J., Rangavajhula, K., Syed, S., Santhumayor, B. A., Duehr, J., Cassimatis, N., Caridi, J., Lo, S. L., Sciubba, D. M., D'Amico, R. S. 2026; 147: 111928

  Abstract

  Spinal metastases represent a biologically distinct manifestation of systemic cancer, frequently progressing despite durable visceral response. The vertebral niche is defined by hypoxia, immune suppression, osteoclast-osteoblast coupling, and stromal signaling. These features create a therapeutic sanctuary that fosters tumor dormancy, clonal evolution, and resistance to systemic therapy.We aim to synthesize current knowledge of the bone niche in spinal metastases, explain how microenvironmental factors and tumor-intrinsic changes converge to drive therapeutic resistance, and provide translational implications for prognosis and treatment design.A narrative review of English-language studies (1990-2024) from PubMed and Scopus was conducted, examining pathophysiology, bone-tumor crosstalk, dormancy, immune evasion, and resistance genetics. Foundational pre-1990 works were included when biologically essential. When available, bone-specific outcomes (skeletal progression, skeletal-related events, spine-PFS) were prioritized.Spinal metastases are driven by unique interactions between tumor cells and the bone microenvironment, including RANK/RANKL signaling, hypoxia-induced HIF activation, immune sequestration, and dormancy niches. Specific molecular alterations include EGFR and ALK mutations in NSCLC, BRCA and PI3K/AKT pathway dysregulation in prostate and breast cancers, and VHL/HIF pathway alterations in RCC. Resistance patterns such as EGFR T790M and BRCA reversion mutations emerge disproportionately in bone, reflecting site-specific selective pressure. Conventional systemic therapies achieve lower efficacy in the spine, underscoring the need for site-specific biomarkers, advanced imaging, and tailored therapeutic strategies.The vertebral niche constitutes a treatment-resistant microenvironment where dormant tumor cells persist, immune surveillance is impaired, and resistant clones evolve. Integrating bone-microenvironment biology with molecular profiling, liquid biopsy, and advanced imaging is essential for refining prognostic models, guiding intervention timing, and designing spine-specific clinical trials. By reframing spinal metastases as a biologically and therapeutically distinct disease entity, this review establishes a framework for developing bone-directed treatment strategies and advancing precision oncology in metastatic spine care.

  View details for DOI 10.1016/j.jocn.2026.111928

  View details for PubMedID 41690056

• Risk-stratified management of ankylosing spondylitis-related spinal fractures-a meta-synthesis of contemporary surgical and nonsurgical strategies: a narrative review. Journal of spine surgery (Hong Kong) Abikenari, M. A., Yoo, K. H., Liu, J., Ha, J., Nageeb, G., Jain, B., Park, L., Hani, U., Veeravagu, A. 2025; 11 (4): 1095-1110

  Abstract

  Ankylosing spondylitis (AS) spinal fractures pose unique diagnostic and therapeutic challenges due to the altered biomechanics, rigid ankylosed spine, and risk for extensive neurologic injury. The optimal practice is not established with rising clinical occurrences. This article aims to review the current literature regarding diagnosis, classification, and operative and non-operative treatment paradigms of spinal fractures due to AS in adults and present a cohesive perspective to facilitate evidence-based clinical practice.A narrative systematic review was conducted on the basis of the PubMed database, including English-language papers from January 2000 to May 2025. Keywords included "AS", "spinal fracture", "vertebral trauma", "surgical management", and "neurological outcomes". Studies identified were evaluated based on clinical relevance, level of evidence, and representation of evolving concepts in diagnosis and management.The review discusses the specific biomechanical frailties of the ankylosed spine, recent classification methods like AO Spine and Denis classifications, and recent imaging modalities for diagnosis. It highlights operative decision-making approaches, posterior-only, anterior, and combination, in fracture morphology, neurologic status, and patient comorbidities. It discusses perioperative concerns such as positioning issues, blood loss, and complications like hardware failure and infection. Four summary tables provide insight into imaging preference, surgical interventions, outcomes, and complication profiles.Prompt diagnosis and personalized treatment of AS-related spinal fractures are essential to reducing morbidity and mortality. Emerging literature supports the use of posterior-only methods in selected cases, but highly context-specific surgical choices must remain. The review stresses the importance of prospective studies as a guide to standard treatment protocols and improved outcomes for this difficult patient group.

  View details for DOI 10.21037/jss-25-119

  View details for PubMedID 41509825

  View details for PubMedCentralID PMC12775638

• Adaptive immunotherapeutic paradigms in diffuse midline glioma: integrating epigenetic reprogramming, neuron-glioma interactions, and tumor microenvironment modulation. Journal of neuro-oncology Liu, J., Ha, J. H., Abikenari, M., Sjoholm, M. A., Annagiri, S., Ravi, K., Bergsneider, B. H., Verma, R., Theodros, D., Medikonda, R., Li, G., Prolo, L. M., Monje, M., Lim, M. 2025; 176 (2): 144

  Abstract

  Diffuse midline gliomas, including diffuse intrinsic pontine gliomas, represent one of the most aggressive pediatric malignancies in the central nervous system with a uniformly poor prognosis. They can be consistently identified by mutations in histone H3 K27M, which are associated with aggressive tumor biology, marked resistance to therapies, and abysmal survival. The current review critically assesses the existing application of immunotherapeutic modalities in DMGs, emphasizing biological hurdles in efficacy, translation methodologies, and prospects in attaining sustained responses.We examined preclinical and early clinical studies in DMGs for immune therapies such as peptide vaccines against H3K27M antigens, chimeric antigen receptor T-cell therapies, immune checkpoint modulation, and radioimmunotherapy. Current developments in the interface of cancer neuroscience and tumor interaction with neurons were incorporated in a manner relevant to immune suppression in the microenvironment of DMG. Although these tumors have traditionally shown poor immune reactivity because of low tumor mutational burden, immune-privileged sites, and a strongly suppressive tumor microenvironment, a variety of different immune therapeutic approaches have shown promising early efficacy. Of particular interest are neoantigen-targeted vaccines and CAR T-cell therapy using surface antigens. Preliminary findings suggest an important role for neuron-glioma synaptic and paracrine signaling in mediating tumor progression and immune evasion.Immunotherapy for DMGs is moving from a conceptual state to a translational reality. A better understanding of the realm of tumor immune-neural crosstalk, combination therapies, and immune biology in pediatric patients will be critical in addressing resistance and providing durable control for these aggressive malignancies.

  View details for DOI 10.1007/s11060-025-05347-9

  View details for PubMedID 41460355

  View details for PubMedCentralID 9533228

• Molecular and biophysical remodeling of the blood-brain barrier in glioblastoma: mechanistic drivers of tumor-neurovascular crosstalk FRONTIERS IN PHYSICS Abikenari, M., Sjoholm, M., Liu, J., Nageeb, G., Ha, J. H., Wu, J., Ren, A., Sayadi, J., Lim, J., Cho, K., Verma, R., Medikonda, R., Banu, M., Lim, M. 2025; 13

  View details for DOI 10.3389/fphy.2025.1723329

  View details for Web of Science ID 001651720600001

• Modulating the glioma microenvironment with laser interstitial thermal therapy: mechanisms and therapeutic implications. Journal of neuro-oncology Vargas, L. O., Himic, V., Otaner, F., Abikenari, M., Chandar, J., Govindarajan, V., Kreatsoulas, D., Jahangiri, A., Komotar, R. J., Ivan, M. E., Shah, A. H. 2025; 176 (1): 99

  Abstract

  Glioblastoma (GBM) remains one of the most deadly brain tumors through its invasiveness, rapid growth, its immunosuppressive microenvironment, and limited treatment options. Laser interstitial thermal therapy (LITT) is an MR-guided, minimally invasive ablation technique increasingly used in GBM management. This narrative review examines how LITT modulates the glioma microenvironment and explores its therapeutic implications. We cover both preclinical and clinical studies and synthesize the effects of LITT on immune activation, blood-brain barrier (BBB) permeability, and thermal dynamics in gliomas. LITT generates three spatially distinct thermal zones, promoting damage-associated molecular pattern (DAMP) release, immune cell activation, and transient BBB disruption. These changes may help convert immunologically "cold" gliomas into "hot" tumors and enhance the delivery of chemotherapy, immunotherapy, and viral or gene-based therapies. Technical limitations, such as the heat sink effect near vascular structures, are increasingly addressed through innovations like dual-fiber systems and advanced thermal modeling. LITT is emerging as much more than a cytoreductive tool for unresectable glioma; it may provide a platform for immune modulation and therapeutic enhancement in glioma care. Potential benefits of LITT's interaction with the microenvironment and the BBB include: (1) recruitment and mobilization of the immune system to better target cancerous cells; (2) improved penetration of existing therapies; (3) which enables a lower effective dose for previously barred-drugs, reducing peripheral adverse effects; (4) improved potential for peripheral liquid biopsy. Optimizing treatment timing, patient selection, and combination protocols will be essential to fully harness LITT's biological effects and improve clinical outcomes.

  View details for DOI 10.1007/s11060-025-05305-5

  View details for PubMedID 41307758

  View details for PubMedCentralID PMC12660436

• ConvNeXt-Driven Detection of Alzheimer's Disease: A Benchmark Study on Expert-Annotated AlzaSet MRI Dataset Across Anatomical Planes. Diagnostics (Basel, Switzerland) Basereh, M., Abikenari, M. A., Sadeghzadeh, S., Dunn, T., Freichel, R., Siddarth, P., Ghahremani, D., Lavretsky, H., Buch, V. P. 2025; 15 (23)

  Abstract

  Background: Alzheimer's disease (AD) is a leading worldwide cause of cognitive impairment, necessitating accurate, inexpensive diagnostic tools to enable early recognition. Methods: In this study, we present a robust deep learning approach for AD classification based on structural MRI scans, ConvNeXt, an emergent convolutional architecture inspired by vision transformers. We introduce AlzaSet, a clinically curated T1-weighted MRI dataset of 79 subjects (63 with Alzheimer's disease [AD], 16 cognitively normal controls [NC]) acquired on a 1.5 T Siemens Aera in axial, coronal, and sagittal planes, respectively (12,947 slices in total). Images are neuroradiologist-labeled. Results are reported per plane, with awareness of the class imbalance at the subject level. We further present AlzaSet, a novel, expertly labeled clinical dataset with axial, coronal, and sagittal perspectives from AD and cognitively normal control subjects. Three ConvNeXt sizes (Tiny, Small, Base) were compared and benchmarked against existing state-of-the-art CNN models (VGG16, VGG19, InceptionV3, DenseNet121). Results: ConvNeXt-Base consistently outperformed the other models on coronal slices with an accuracy of 98.37% and an AUC of 0.992. Coronal views were determined to be most diagnostically informative, with emphasis on visualization of the medial temporal lobe. Moreover, comparison with recent ensemble-based techniques showed superior performance with comparable computational efficiency. Conclusions: These results indicate that ConvNeXt-capable models applied to clinically curated datasets have strong potential to provide scalable, real-time AD screening in diverse settings, including both high-resource and resource-constrained settings.

  View details for DOI 10.3390/diagnostics15232997

  View details for PubMedID 41374378

• sEEG-guided responsive neurostimulation to treat neocortical epilepsy: A multicenter retrospective study of the efficacy and safety of depth electrode-mediated neuromodulation. Epilepsia open Sadeghzadeh, S., Purger, D. A., Bhanot, P., Johnson, N., Barbosa, D. A., Huang, Y., Park, J. J., Schonfeld, E., Abikenari, M. A., Jain, B., Aronson, J. P., Drees, C., Fisher, T. L., Gerrard, J., Gray, T. E., Ghatan, S., Hines, K., Jobst, B. C., Karakis, I., Ojemann, S. G., Quraishi, I. H., Raslan, A. M., Sather, M. D., Skidmore, C. T., Willie, J. T., Wu, C., Yoo, J. Y., Graber, K. D., Halpern, C. H., Buch, V. P., Parker, J. J. 2025

  Abstract

  OBJECTIVES: Pivotal trials have established the effectiveness of the Responsive Neurostimulation System (RNS System) in treating focal epilepsy. In clinical trials, depth leads were primarily used to treat mesial temporal seizure onsets while cortical strip leads were used to treat neocortical seizure onsets. Here, we systematically analyze the safety and efficacy of stereoelectroencephalography (sEEG)-guided depth leads to provide responsive stimulation to neocortical gray matter.METHODS: Patients were stratified as strong responders (>median cohort seizure reduction %), weak responders (>0% and ≤median cohort seizure reduction %), and anti-responders (≤0%) based on percent seizure reduction at 1 year post-implant (1-Y). Pre-operative T1-weighted magnetic resonance imaging and post-operative computed tomography images were merged, and the Euclidean distance between the sEEG epileptic focus (sEEG-EF) and the nearest RNS System depth lead contacts was calculated.RESULTS: A total of 87 depth leads were implanted in 55 patients across neocortical brain regions. The median reduction in clinical seizures improved from 66.7% at 1-Y to 77.5% at long-term follow-up (LTFU: 2.35±0.95years), with 10 patients (18.2%) achieving complete seizure freedom. Seven patients (12.7%) experienced six serious adverse events. At 1-Y, shorter Euclidean distance between the sEEG-EF and RNS System depth leads predicted improved seizure outcome in strong responders (beta=-0.84, p=0.008) but not in weak responders (beta=0.21, p=0.9) or anti-responders (beta=-20.34, p=0.11). At LTFU, there was no significant relationship between Euclidean distance and seizure reduction in strong responders (beta=0.77, p=0.18), weak responders (beta=2.05, p=0.54), or anti-responders (beta=0.24, p=0.99). Exploratory analyses at 1-Y showed nominal associations between older age (rho=0.32), longer epilepsy duration (rho=0.27), and non-mesial temporal sEEG-EFs and greater seizure reduction; however, none survived Bonferroni correction (adjusted alpha=0.0027; all post-correction p>0.0027), and no associations were observed at LTFU.SIGNIFICANCE: In this series, neocortical depth leads for RNS therapy had favorable safety and efficacy and proximity to the sEEG-EF drove initial outcomes for strong responders to RNS therapy.PLAIN LANGUAGE SUMMARY: In this multi-center study, patients with difficult-to-treat seizures received brain-responsive stimulation using a device called responsive neurostimulation (RNS), which delivers small electrical pulses to reduce seizures. We focused on patients treated with electrodes placed in the brain's outer regions (the neocortex) and guided by a mapping procedure called sEEG. On average, patients had their seizures cut by two-thirds after one year and by more than three-quarters with longer follow-up, with about one in five becoming seizure-free. The treatment was safe, and closer electrode placement to the seizure source helped explain early-but not long-term-improvements.

  View details for DOI 10.1002/epi4.70180

  View details for PubMedID 41251192

• Tumor-Associated Neutrophils: A Double-Edged Sword in Glioblastoma Progression Abikenari, M., Choi, J., Medikonda, R., Kim, L., Verma, R., Tran, A., Annagiri, S., Lim, M. OXFORD UNIV PRESS INC. 2025: v454

  View details for DOI 10.1093/neuonc/noaf201.1798

  View details for Web of Science ID 001613255100034

• 'Time is brain': Enhancing stroke knowledge and emergency response readiness in seniors HEALTH EDUCATION JOURNAL Sadeghzadeh, S., Adu-Brimpong, J., Abikenari, M. A., Bhatia, A., Harary, P. M., Bhanot, P., Muller, R. K., Escalante, R., Schonfeld, E., Jain, B., Nageeb, G., Wu, A., Hsin, G. S., Vora, N., Dodd, R. L. 2025

  View details for DOI 10.1177/00178969251371488

  View details for Web of Science ID 001586652700001

• The immunological landscape of traumatic brain injury: insights from pathophysiology to experimental models. Frontiers in neurology Abikenari, M., Ha, J. H., Liu, J., Ren, A., Cho, K. B., Lim, J., Kim, L. H., Medikonda, R., Choi, J., Lim, M. 2025; 16: 1668480

  Abstract

  Traumatic brain injury (TBI) is a complex, heterogeneous neuropathological disease that continues to be among the prominent causes of mortality and disability around the world. Translational success in TBI has been significant, yet therapies are limited as the intersection of the initial mechanical traumas and secondary neuroinflammatory cascades, which predispose to long-term neurological deficits, is poorly understood. The pathogenesis of TBI is not limited to the primary mechanical injury. The secondary damage, including ischemia, excitotoxicity, oxidative stress, and immune dysfunction, leads to neuronal apoptosis, the breakdown of the blood-brain barrier (BBB), and chronic neuroinflammation. The preclinical controlled cortical impact (CCI) and fluid percussion injury (FPI) TBI models have generated valuable biomechanical data related to TBI-induced immune responses, including microglial priming, astrocyte dysregulation, and peripheral leukocyte recruitment. However, experimental models today are unable to completely replicate the intricate immune cascades in human TBI, particularly delayed and context-specific innate and adaptive immune response activation. Cytokine signaling (IL-1β, TNF-α, and IL-6), neuroinflammatory amplification through the IL-23/IL-17 pathway, and autoantibody-mediated neurodegeneration are emerging as significant secondary injury mechanisms. Additionally, TBI-induced immunosuppression, which presents as generalized T lymphocyte depletion and aberrant macrophage polarization, enhances the risk of infection and delayed neurological recovery. Emerging immunotherapeutics such as cytokine blockade, complement blockade, and targeted modulation of T lymphocytes have the potential to optimize the post-TBI immune microenvironment for reducing secondary damage. Inclusion of next-generation experimental models combined with secondary injuries, such as hypoxia, polytrauma, and systemic inflammation, is needed to shift towards innovative, biomarker-driven, patient-stratified trials. Thus, integration of immunological phenotyping with translationally relevant models of TBI represents an important cornerstone in the development of targeted therapeutic treatments designed to improve neuroprotection, repair, and long-term functional outcome.

  View details for DOI 10.3389/fneur.2025.1668480

  View details for PubMedID 41050281

  View details for PubMedCentralID PMC12488441

• Spatially Encoded Oncogenesis and Transcriptional Plasticity in Meningioma: Drivers of Therapeutic Resistance and Opportunities for Targeted Intervention. Cancers Abikenari, M. A., Regev, A., Bergsneider, B. H., Himic, V., Annagiri, S., Kim, L. H., Medikonda, R., Choi, J., Jeyaretna, S., Fountain, D. M., Lim, M. 2025; 17 (16)

  Abstract

  Whilst typically benign, a subset of meningiomas displays aggressive and recurrent behavior. There is a paucity of reliable treatment options for this subset of patients and a relative lack of consensus on how to best manage these patients. This clinical challenge reflects underlying molecular complexity, driven by NF2, TRAF7, and CDKN2A/B mutations alongside pervasive epigenetic dysregulation. High-throughput molecular profiling studies have proposed biologically distinct meningioma subgroups with varying clinical trajectories and therapeutic vulnerabilities. Distinct cell lineages of meningeal precursors are now appreciated to be essential in the establishment of the meninges. The numerous cellular lineages involved in meningeal development, the heterogeneity of meningioma location and (epi)genomic behavior, and the variability in its clinical and radiological manifestations raise the question of what critical insights can be gained by understanding meningeal development during embryogenesis to understand meningioma tumorigenicity. The current paper examines this paradigm by highlighting spatially linked mechanisms of anaplasia and treatment resistance, including the role of neural crest-derived convexity meninges in promoting dedifferentiation via YAP/TAZ signaling and mesoderm-derived skull base regions in maintaining TRAF7-mediated vulnerabilities. We further elucidate the emerging synthetic lethal paradigms, CRISPR-enabled target discovery, and PROTAC-mediated degradation strategies that may transform the therapeutic landscape of clinically challenging meningiomas driven by complex oncogenic circuitry. By bridging embryogenesis, spatial genomics, and molecular targeting, we propose a developmentally informed, lineage-stratified model for advancing precision therapeutics in high-grade and recurrent meningiomas.

  View details for DOI 10.3390/cancers17162694

  View details for PubMedID 40867323

• Emerging trends in cell-based therapies: contemporary advances and ethical considerations in translational neurosurgical oncology. Journal of neuro-oncology Abikenari, M., Liu, J., Ha, J. H., Annagiri, S., Himic, V., Medikonda, R., Kim, L., Choi, J., Lim, M. 2025

  Abstract

  Emerging cell-based therapies represent a promising advancement in neurosurgical oncology, offering novel therapeutic possibilities for challenging diagnoses such as high-grade gliomas. Traditional treatment modalities, including surgical resection, chemotherapy, and radiotherapy, offer limited efficacy due to the highly infiltrative nature and genomic heterogeneity of malignant brain tumors. The recent integration of molecular profiling and genotypic characterization into diagnostic and therapeutic frameworks underscores a significant evolution toward personalized medicine. Stem-cell-based approaches, notably neural and mesenchymal stem cells, demonstrate remarkable tropism for pathological tissues, providing innovative strategies for targeted therapeutic delivery and intrinsic anti-tumoral effects. Concurrently, immunotherapeutic advancements, particularly immune checkpoint inhibitors (ICIs), chimeric antigen receptor T-cell (CAR T-cell) therapies, and tumor vaccination techniques, have significantly altered therapeutic paradigms by leveraging patient-specific immune responses with minimal systemic toxicity. To contextualize such therapeutic innovations, we systematically reviewed and analyzed 28 ongoing glioblastoma clinical trials initiated since 2022 investigating cell-based strategies. This dataset elucidates key patterns in trial design, cellular targets, and combinatorial immunotherapeutic regimens. Despite the immense clinical promise, integrating cell-based and immunological therapeutics necessitates careful ethical deliberation and complex clinical management strategies, particularly when combined with conventional therapies. This review critically evaluates contemporary advancements, highlights emerging clinical trial outcomes, explores the ethical dimensions of novel therapeutics, and underscores the imperative for continued translational research to refine patient-specific therapeutic paradigms in neurosurgical oncology.

  View details for DOI 10.1007/s11060-025-05170-2

  View details for PubMedID 40696259

  View details for PubMedCentralID 6889232

• Multilevel spinal fractures in ankylosing spondylitis: illustrative case. Journal of neurosurgery. Case lessons Abikenari, M. A., Park, L. S., Yoo, K. H., Hani, U., Jain, B., Veeravagu, A. 2025; 9 (26)

  Abstract

  Ankylosing spondylitis (AS) is a chronic inflammatory disease marked by spinal rigidity, which predisposes patients to unstable fractures even after minor trauma. While isolated spinal fractures in AS are well described, multilevel fractures across the cervical, thoracic, and lumbar spine following a single traumatic event are exceedingly rare and pose substantial diagnostic and surgical challenges.The authors present the case of a 41-year-old male with advanced AS and a history of alcohol use and diabetes who sustained six unstable spinal fractures spanning the cervical, thoracic, and lumbar regions after a motor vehicle accident. The surgical intervention involved staged posterior spinal fusion (C3-T7, L2-S2 with pelvic extension), open reduction and internal fixation (C6-7, T2-3, L4), and laminectomy (T2-3). Neuronavigation and intraoperative fluoroscopy guided precise instrumentation. The patient had no postoperative neurological deficits and was discharged with a comprehensive postoperative care plan, including physical therapy and follow-up imaging.This case underscores the importance of high clinical suspicion and early imaging in AS patients with trauma, given their high risk for occult spinal fractures. Posterior-only surgical approaches can provide effective stabilization in complex multilevel injuries, especially in patients with comorbidities that preclude anterior exposure. https://thejns.org/doi/10.3171/CASE25236.

  View details for DOI 10.3171/CASE25236

  View details for PubMedID 40587889

• Top advances of the year: The status of chimeric antigen receptor T cells in neuro-oncology. Cancer Medikonda, R., Abikenari, M. A., Schonfeld, E., Lim, M. 2025; 131 (12): e35935

  View details for DOI 10.1002/cncr.35935

  View details for PubMedID 40483564

• The Metabolic Orchestration of Immune Evasion in Glioblastoma: From Molecular Perspectives to Therapeutic Vulnerabilities. Cancers Medikonda, R., Abikenari, M., Schonfeld, E., Lim, M. 2025; 17 (11)

  Abstract

  Glioblastoma (GBM) is a highly aggressive primary brain cancer with dismal prognoses despite current standards of care. Immunotherapy is being explored for GBM, given its promising results in other solid malignancies; however, the results from early clinical studies in GBM are disappointing. It has been discovered that GBM has numerous mechanisms of immune resistance, including the physical blood-brain barrier, high intratumoral and intertumoral heterogeneity, and numerous cellular and molecular components in the tumor microenvironment (TME) that promote immunosuppression. Furthermore, GBM utilizes numerous metabolic pathways to establish a survival advantage in the TME. Recently, it has begun to become evident that these complex metabolic pathways that promote GBM growth and invasion also contribute to tumor immune resistance. Aerobic glycolysis provides tumor cells with ample ATP while depleting key glucose and increasing acidity in the TME. Increased glutamine, tryptophan, and arginine metabolism deprives T cells of these necessary amino acids for proper anti-tumor function. Sphingolipid metabolism promotes an immunosuppressive phenotype in the TME and affects immune cell trafficking. This review will discuss, in detail, the key metabolic pathways relevant to GBM pathophysiology which also modulate host immunosuppression.

  View details for DOI 10.3390/cancers17111881

  View details for PubMedID 40507361

• Peripheral Alzheimer's Disease Biomarkers Are Related to Change in Subjective Memory in Older Women with Cardiovascular Risk Factors in a Trial of Yoga vs. Memory Training CANADIAN JOURNAL OF PSYCHIATRY-REVUE CANADIENNE DE PSYCHIATRIE Oughli, H., Siddarth, P., Lum, M., Tang, L., Ito, B., Abikenari, M., Cappelleti, M., Khalsa, D. S., Nguyen, S., Lavretsky, H. 2025

  View details for DOI 10.1177/07067437251343291

  View details for Web of Science ID 001499493600001

• The hormonal nexus in PIK3CA-mutated meningiomas: implications for targeted therapy and clinical trial design. Journal of neuro-oncology Abikenari, M., Regev, A., Himic, V., Choi, J., Jeyaretna, S., Fountain, D. M., Lim, M. 2025

  Abstract

  The presence of hormonal receptors in meningiomas has been known for decades. More recently, evidence has shown increased prevalence of meningiomas in patients taking certain types of hormonal treatments, such as oral contraceptives, progestins or hormone replacement therapy. Epidemiological evidence suggests that patients undergoing hormonal therapy harbor higher mutational rates of the oncogene PIK3CA. Due to the relative paucity of literature describing the intersection of hormone therapy and mutated PIK3CA pathways in meningioma, we have conducted a narrative review on this topic. Similarly, the clinical trial landscape for hormonal therapies for meningioma currently focuses on somatostatin receptor-targeted therapies and peptide receptor radionucleotide therapy, and the PIK3CA-hormonal signaling axis has not been explicitly targeted. Given the role of PIK3CA mutations in promoting cancer progression in other hormone-sensitive tumors, such as breast and prostate cancer, exploring this axis could inform drug repurposing including hormonal therapy specifically for these tumors.

  View details for DOI 10.1007/s11060-025-05082-1

  View details for PubMedID 40392516

  View details for PubMedCentralID 8491279

• Characterizing and Inhibiting the FGF7/FGFR2-THBS1 Axis in Melanoma Brain Metastasis Tran, A., Bergsneider, B., Choi, J., Kim, L. H., Schonfeld, E., Abikenari, M., Verma, R., Cho, K., Lim, M. LIPPINCOTT WILLIAMS & WILKINS. 2025: 69-70

  View details for DOI 10.1227/neu.0000000000003360_285

  View details for Web of Science ID 001446056100050

• Local Delivery of Type 1 Interferon-Stimulating Agent Within Tumor Microenvironment Promotes Dendritic Cell Antigen Presentation and T Cell Activation in Glioblastoma Wu, J., Cho, K., Ren, A., Lee, S., Choi, J., Nitta, R., Wu, C., Schonfeld, E., Abikenari, M., Li, G., Lim, M. LIPPINCOTT WILLIAMS & WILKINS. 2025: 219

  View details for DOI 10.1227/neu.0000000000003360_1324

  View details for Web of Science ID 001446056700012

• Single Position Lateral Anterior Lumbar Interbody Fusion at L5/S1. Neurosurgery Stienen, M. N., Yoo, K., Schonfeld, E., Shah, V., Abikenari, M., Pangal, D., Chandra, V., Veeravagu, A. 2025; 96 (3S): S17-S25

  Abstract

  Anterior lumbar interbody fusion (ALIF) is an established surgical approach for spinal fusion, offering distinct advantages in restoring lumbar lordosis, indirectly decompressing neural elements, and facilitating high fusion rates because of the increase in the fusion surface area. Traditionally, ALIF is performed with the patient in a supine position, necessitating repositioning for additional posterior interventions, which increases operative time, anesthetic time, and complexity. The recent development of single position lateral ALIF (SPL-ALIF) enables anterior and posterior access without repositioning, enables gravity facilitated retroperitoneal access, and optimizes surgical efficiency, particularly in cases necessitating multilevel anterior column fusion. The current review comprehensively examines SPL-ALIF at the L5-S1 level, presenting technical considerations and comparative benefits over traditional techniques. The approach has demonstrated significant reductions in operative time, blood loss, and postoperative ileus, with equivalent radiographic outcomes compared with supine ALIF. Furthermore, SPL-ALIF has been evidenced to have a similar safety profile to supine ALIF with equivalent vascular, abdominal, and neurological complications, as well as comparable revision rates between the two procedures. However, SPL-ALIF is not without limitations. The technique may be less effective in cases requiring direct decompression or in patients with complex vascular anatomy or extensive retroperitoneal scarring. These challenges necessitate careful patient selection to optimize outcomes and minimize intraoperative risks. Future studies are warranted to validate the clinical benefits of SPL-ALIF, particularly concerning fusion rates, patient-reported outcomes, and complication profiles, thereby solidifying its role in the evolving landscape of minimally invasive spine surgery.

  View details for DOI 10.1227/neu.0000000000003332

  View details for PubMedID 39950780

• Restoring Tamoxifen Sensitivity in Breast Cancer: The Role of lncRNA MALAT1 and NanoCurcumin as Modulators of Drug Resistance BIOMED RESEARCH INTERNATIONAL Nasiri Kenari, F., Saberian, M., Abikenari, M., Najafi, S., Sadeghizadeh, M. 2025; 2025 (1): 5824748

  Abstract

  Background: Tamoxifen resistance remains a major clinical challenge in estrogen receptor-positive (ER+) breast cancer, contributing to recurrence and poor prognosis. Long noncoding RNAs (lncRNAs), including MALAT1, UCA1, CYTOR, GAS5, and HOTAIR, have emerged as key regulators of endocrine resistance. Curcumin, a polyphenol with anticancer properties, modulates lncRNA expression, and its bioavailable formulation, NanoCurcumin, enhances therapeutic efficacy. This study evaluates the effects of NanoCurcumin in combination with tamoxifen on lncRNA expression and resistance mechanisms in ER+ breast cancer. Methods: Plasma levels of the selected lncRNAs were assessed via qRT-PCR in luminal breast cancer patients receiving tamoxifen alone or in combination with NanoCurcumin oral soft gels for 6 months. Bioinformatics analysis of MALAT1 expression was performed using the GEO database. In vitro, MALAT1 expression was evaluated in breast cancer (MCF7) and normal breast (MCF10) cell lines via qRT-PCR. Tamoxifen-resistant MCF7 cells were generated through prolonged treatment, and the effects of NanoCurcumin on MALAT1 expression were analyzed over 4 months. Results: In clinical samples, NanoCurcumin significantly reduced MALAT1 expression (p = 0.02) and trended toward decreased UCA1, CYTOR, and HOTAIR while increasing GAS5 expression. Bioinformatics analysis confirmed MALAT1 upregulation in tamoxifen-resistant cell lines. In vitro, MALAT1 was significantly elevated in MCF7 cells compared to MCF10 and increased over time with tamoxifen treatment alone. NanoCurcumin reversed this trend, sustaining low MALAT1 levels and mitigating resistance. Conclusion: Our findings suggest that NanoCurcumin mitigates tamoxifen resistance by downregulating MALAT1, offering a novel epigenetic strategy to enhance endocrine therapy efficacy. Further studies should explore lncRNA-targeted interventions to improve treatment outcomes in ER+ breast cancer.

  View details for DOI 10.1155/bmri/5824748

  View details for Web of Science ID 001561702400001

  View details for PubMedID 41031251

  View details for PubMedCentralID PMC12407302

• INFIGRATINIB INHIBITION OF THE THBS1 PATHWAY IN MELANOMA BRAIN METASTASIS Tran, A., Choi, J., Bergsneider, B., Kim, L., Schonfeld, E., Abikenari, M., Verma, R., Cho, K., Lim, M. OXFORD UNIV PRESS INC. 2024

  View details for DOI 10.1093/neuonc/noae165.1210

  View details for Web of Science ID 001362565900048

• Inflammatory Markers of Geriatric Depression Response to Tai Chi or Health Education Adjunct Interventions. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry Siddarth, P., Abikenari, M., Grzenda, A., Cappelletti, M., Oughli, H., Liu, C., Millillo, M. M., Lavretsky, H. 2023; 31 (1): 22-32

  Abstract

  Underlying inflammation is associated with an increased risk of depression in older adults. In this study, we examined the role of inflammatory biomarkers in antidepressant response in depressed older adults undergoing adjunct Tai Chi Chih (TCC) or Health education interventions.Older adults aged 60 years and above with a diagnosis of major depression were randomized to 12 weeks of TCC versus Health and Wellness Education (HEW) as an adjunct therapy to their stable antidepressant treatment regimen. A panel of 19 cytokine/chemokines was measured at baseline and 12 weeks. Five factors were derived using factor analysis. General linear models were estimated to examine the change in factor scores and the association of these changes on depression remission rates, controlling for age, sex, and body mass index.Of the 170 randomized participants (TCC: n = 85 and HEW: n = 85), 55 TCC and 58 HEW completed the 3-month assessment. The groups did not differ at baseline in any measure. At follow-up, neither the changes in cytokine/chemokines scores nor the depression remission rate differed significantly between TCC and HEW. However, remitters and non-remitters differed significantly in changes in a factor composed of growth-regulated oncogene protein-alpha (GRO-alpha), epidermal growth factor (EGF), and soluble CD40 ligand (sCD40L). GRO-alpha and EGF levels (in both groups) were significantly increased in remitters compared to non-remitters.Changes in certain cytokines/chemokines may accompany improvement in depressive symptoms in older adults. Future studies will need to explore the role of these molecules in remission of late-life depression.

  View details for DOI 10.1016/j.jagp.2022.08.004

  View details for PubMedID 36175271

• Minimizing the COVID-19 spread in hospitals through optimization of ventilation systems. Physics of fluids (Woodbury, N.Y. : 1994) Arjmandi, H., Amini, R., Kashfi, M., Abikenari, M. A., Davani, A. 2022; 34 (3): 037103

  Abstract

  The rapid spread of SARS-CoV-2 virus has overwhelmed hospitals with patients in need of intensive care, which is often limited in capacity and is generally reserved for patients with critical conditions. This has led to higher chances of infection being spread to non-COVID-19 patients and healthcare workers and an overall increased probability of cross contamination. The effects of design parameters on the performance of ventilation systems to control the spread of airborne particles in intensive care units are studied numerically. Four different cases are considered, and the spread of particles is studied. Two new criteria for the ventilation system-viz., dimensionless timescale and extraction timescale-are introduced and their performances are compared. Furthermore, an optimization process is performed to understand the effects of design variables (inlet width, velocity, and temperature) on the thermal comfort conditions (predicted mean vote, percentage of people dissatisfied, and air change effectiveness) according to suggested standard values and the relations for calculating these parameters based on the design variables are proposed. Desirability functions that are comprised of all three thermal condition parameters are used to determine the range of variables that result in thermally comfortable conditions and a maximum desirability of 0.865 is obtained. The results show that a poorly designed ventilation system acts like a perfectly stirred reactor-which enormously increases the possibilities of contamination-and that when air is injected from the ceiling and extracted from behind the patient beds, the infection spread is least probable since the particles exit the room orders of magnitude faster.

  View details for DOI 10.1063/5.0081291

  View details for PubMedID 35342279

  View details for PubMedCentralID PMC8939549

• The values work of restorative ventures: The role of founders’ embodied embeddedness with at-risk social groups Journal of Business Venturing Insights Awad, M., Sanchez, M., Abikenari, M. A. 2022; 18 (e00337)

  View details for DOI 10.1016/j.jbvi.2022.e00337