OSCR

Magnetically actuated nanoantennas for wireless glioblastoma therapy.

Overview

  1. MIT Media Lab, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
Institutions: MIT Media Lab (United States); Massachusetts Institute of Technology (United States)
Journal: Science advances, volume 12, issue 37, article eaeb1237
Dates: received 31 July 2025; accepted 3 August 2026; published online 9 September 2026; in print September 2026
Type: Research article · Language: English
License: CC BY-NC
Identifiers: DOI 10.1126/sciadv.aeb1237 · PMID 42715333 · PMCID PMC13557086 · OpenAlex W7212019808
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: human (organism), mouse (organism), other condition (population), clinical / translational (subfield)
Methods: Machine learning, Evoked potentials, Physiology & signal measures, Statistics
MeSH: Brain Neoplasms*, Glioblastoma*, Wireless Technology*, Animals, Cell Line, Tumor, Humans, Mice, Temozolomide, Xenograft Model Antitumor Assays (* major topic)
Topic: Micro and Nano Robotics (Condensed Matter Physics, Physics and Astronomy), according to OpenAlex
Funding: The ChadTough Defeat DIPG Foundation; The Sontag Foundation Distinguished Scientist Award
Citations: not cited yet (Europe PMC); 108 references in the paper

Abstract

Glioblastoma (GBM) remains a formidable clinical challenge, characterized by invasive growth, therapeutic resistance, and dismal patient survival. We report the development of HITMAN (highly localized electric field–induced tumor therapy using magnetically actuated nanoantennas), a wireless bioelectric therapy that selectively eradicates GBM cells with cellular precision. Magnetically actuated nanoantennas convert low-frequency (≤200 kHz), deep-brain–penetrant magnetic fields into localized electric fields, thereby triggering protein unfolding, membrane disruption, and ER stress. In vitro, HITMAN demonstrated superior efficacy compared to temozolomide (TMZ), significantly decreasing viability in drug-resistant, patient-derived GBM cells by 52.2%, versus 10% with TMZ while sparing neurons and astrocytes. Mechanistically, HITMAN activated the unfolded protein response and autophagy pathways, suppressed cell cycle and adhesion genes, reduced Ki-67 expression, disrupted cytoskeletal architecture, and elevated p53 levels, underscoring a multifaceted antitumor mechanism. In orthotopic mouse models, HITMAN significantly inhibited tumor growth, extended median survival by more than 50%, and exhibited no systemic toxicity. Thus, HITMAN offers a minimally invasive, spatially precise, and clinically translatable therapy for GBM.

Reproduced under the paper's license (CC BY-NC), from the paper cited above.

Code

The paper links to its data, not to its authors' code: see the Data section.

The paper's code and data availability statement is in the Data section.

Tracing map

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Data

Datasets cited

Data, code, and materials availability

All data needed to evaluate the conclusions in the paper are present in the paper and/or the Supplementary Materials. RNA-seq data have been deposited in GEO under accession number GSE324656 (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE324656) (www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE324656). The Mayo Clinic PDX models used in this study can be provided by Mayo Foundation for Medical Education and Research pending scientific review and a completed material transfer agreement with Mayo Foundation for Medical Education and Research. Requests for the PDX models should be submitted to Dr. J. N. Sarkaria at . No new code was generated in this study.

Reproduced under the paper's license (CC BY-NC), from the paper cited above.

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 1, 27 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 10 authors, 9 MeSH terms, 2 funders, 90 references.

Cite

This paper

Saha, M., Khan, I. N., Joy, B., Chen, S.-Y., Yang, H.-T., Patel, P., Jang, K., Zhang, P., Azeemi, F., & Sarkar, D. (2026). Magnetically actuated nanoantennas for wireless glioblastoma therapy. Science advances, 12(37), eaeb1237. https://doi.org/10.1126/sciadv.aeb1237

BibTeX

@article{saha2026magnetically,
author = {Saha, Monochura and Khan, Ishaq N and Joy, Baju and Chen, Shun-Ying and Yang, Hao-Tung and Patel, Preet and Jang, Kyuho and Zhang, Pengrui and Azeemi, Faheem and Sarkar, Deblina},
title = {{Magnetically actuated nanoantennas for wireless glioblastoma therapy}},
journal = {Science advances},
year = {2026},
month = sep,
volume = {12},
number = {37},
pages = {eaeb1237},
publisher = {American Association for the Advancement of Science},
issn = {2375-2548},
doi = {10.1126/sciadv.aeb1237},
url = {https://doi.org/10.1126/sciadv.aeb1237},
pmid = {42715333},
pmcid = {PMC13557086}
}

RIS

TY - JOUR
AU - Saha, Monochura
AU - Khan, Ishaq N
AU - Joy, Baju
AU - Chen, Shun-Ying
AU - Yang, Hao-Tung
AU - Patel, Preet
AU - Jang, Kyuho
AU - Zhang, Pengrui
AU - Azeemi, Faheem
AU - Sarkar, Deblina
TI - Magnetically actuated nanoantennas for wireless glioblastoma therapy
T2 - Science advances
J2 - Sci Adv
PY - 2026
DA - 2026/09/09
VL - 12
IS - 37
SP - eaeb1237
SN - 2375-2548
PB - American Association for the Advancement of Science
DO - 10.1126/sciadv.aeb1237
UR - https://doi.org/10.1126/sciadv.aeb1237
LA - en
ER -

CSL-JSON

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