Neuro-oncology

Engineered retargeting to overcome systemic delivery challenges in oncolytic adenoviral therapy

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Type of study: Original research (experimental study, engineering approach) First author: Leparc et al. Affiliations:

  • Department of Neurosurgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA
  • Laboratory of Nervous System Disorders and Therapy, GIGA Institute, University of Liège, Liège, Belgium

Journal: Molecular Therapy – Oncolytics Purpose: To engineer adenoviruses with modified tropism for systemic delivery—aiming to reduce off-target accumulation and enhance tumor retention via retargeting strategies.

Conclusions: Engineered vectors exhibited improved immune evasion, diminished sequestration by non-tumor tissues, and improved intratumoral delivery, indicating the feasibility of retargeting modifications for systemic adenoviral therapy.

Critical Review

Methodology: The study lacks transparency in the engineering protocol. Crucial elements such as ligand selection, targeting affinity, and vector modifications are insufficiently described. No rigorous dose-responsiveness or replication kinetics are provided.

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Clinical outcome and deep learning imaging characteristics of patients treated by radio-chemotherapy for a “molecular” glioblastoma

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In a retrospective observational cohort study, Zerbib et al., from the Department of Radiation Oncology, Institut Universitaire du Cancer de Toulouse Oncopole (IUCT-Oncopole), Claudius Regaud; INSERM UMR 1037, Cancer Research Center of Toulouse (CRCT); IRT Saint-Exupéry; Department of Engineering and Medical Physics, IUCT-Oncopole; Biostatistics & Health Data Science Unit, IUCT-Oncopole; Department of Neuroradiology, Hôpital Pierre-Paul Riquet, CHU Purpan; Department of Medical Oncology & Clinical Research Unit, IUCT-Oncopole; Pathology and Cytology Department, CHU Toulouse, IUCT-Oncopole; CerCo, Université de Toulouse, CNRS, UPS, CHU Purpan; Department of Neurosurgery, Hôpital Pierre-Paul Riquet, CHU Purpan; and University Toulouse III – Paul Sabatier, published in The Oncologist, sought to evaluate and compare the clinical outcomes of patients with molecular glioblastoma (molGB) and histological glioblastoma (histGB) treated with standard radio-chemotherapy. They also assessed whether artificial intelligence (AI) models could accurately distinguish molGB without contrast enhancement (CE) from low-grade gliomas (LGG) using MRI FLAIR imaging features.

Conclusion: Patients with molGB and histGB showed similar overall survival under standard treatment.

  • However, molGB without contrast enhancement (CE) demonstrated a significantly better median overall survival (31.2 vs 18 months).
  • AI models based on FLAIR MRI features were able to differentiate non-enhancing molGB from LGG, achieving a best-performing ROC AUC of 0.85.

→ These findings support the clinical relevance of non-enhancing molGB as a distinct subgroup with better prognosis and highlight the potential diagnostic utility of AI tools in radiologically ambiguous cases.

This study presents itself as cutting-edge — mixing radiotherapy outcomes with artificial intelligence — but beneath the polished language and deep learning jargon lies a set of predictable flaws:

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Inadvertent intrathecal application of vindesine and its neurological outcome: case report and systematic review of the literature

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In a case report + systematic review Babaee et al. from:

  1. Department of Neurosurgery, University Hospital OWL, Campus Bethel, Bielefeld, NRW, Germany
  2. Institute for Neuroradiology, University Hospital OWL, Campus Bethel, Bielefeld, NRW, Germany

* Journal: Brain & Spine * Purpose: Assess outcomes and optimal management—particularly CSF irrigation—following inadvertent intrathecal administration of vinca alkaloids (vindesine or vincristine). * Conclusions: Intrathecal vinca alkaloids are nearly universally fatal without aggressive intervention; CSF irrigation improves survival odds (40% vs 0%) but survivors suffer severe neurological deficits 1).

This paper offers a sobering update, but several critical flaws undermine its impact:

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Hypoxia-elective prodrug restrains tumor cells through triggering mitophagy and inducing apoptosis

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In a preclinical research, Wang et al. — from the Children’s Hospital Affiliated to Zhengzhou University, Henan Children’s Hospital; Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University; The Affiliated Hospital of Qingdao University; The First Affiliated Hospital of Jinzhou Medical University; and the Department of Drug Clinical Trials, Zibo Central Hospital — published in the European Journal of Medicinal Chemistry a targeted cancer therapy that leverages tumor hypoxia to maximize antitumor effects while reducing systemic side effects.

They concluded that CHD‑1 functions as a selective prodrug that becomes activated under hypoxia typical of solid tumors. It effectively inhibits tumor cell growth, triggers mitophagy, and induces apoptosis in these hypoxic cancer cells. In vivo, CHD‑1 significantly suppressed HeLa xenograft growth in mice. It also demonstrated a safer toxicity profile compared to the parent compound, based on acute toxicity assessments.

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🧠 Takeaway for Neurosurgeons

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