Evidence map›Paper›PMID 42620288›Full record

ArticleResearch square2026

Tumor Treating Fields (TTFields) sensitize anti-PD1-resistant lung tumors to PD1 blockade and remodel myeloid and lymphoid states.

Yun Hu, Fatemeh Maspourour, Qi Wang, Ailing Huang, Hampartsoum Barsoumian, Zahid Rafiq, Ashley Hoffman, Denton Robinson, Jing Wang, James W Welsh

Abstract readPreprint
In one paragraph

Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Yun HuThe University of Texas MD Anderson Cancer Center.
Fatemeh MaspourourThe University of Texas MD Anderson Cancer Center.
Qi WangThe University of Texas MD Anderson Cancer Center.
Ailing HuangThe University of Texas MD Anderson Cancer Center.
Hampartsoum BarsoumianThe University of Texas MD Anderson Cancer Center.
Zahid RafiqThe University of Texas MD Anderson Cancer Center.
Ashley HoffmanThe University of Texas MD Anderson Cancer Center.
Denton RobinsonThe University of Texas MD Anderson Cancer Center.
Jing WangThe University of Texas MD Anderson Cancer Center.
James W WelshThe University of Texas MD Anderson Cancer Center.

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DIANE BODURKA · 1985 to 2026
$290.8M
NovaSeq6000S10OD024977 · OD · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUFF, VICKI · 2018 to 2018
$995k
NCI NIH HHS P30 CA016672NIH HHS S10 OD024977
6 · The paper itself

Abstract

Background: Primary resistance to programmed cell death protein 1 (PD1) blockade is sustained by defective antigen presentation, immunosuppressive myeloid programs, regulatory T-cell (Treg) dominance, and dysfunctional lymphocyte states. Tumor Treating Fields (TTFields) are non-ionizing alternating electric fields with established antiproliferative activity; however, whether they can overcome resistance to immune checkpoint blockade remains unclear. Methods: The antitumor and immunomodulatory effects of TTFields were investigated in anti-PD1-resistant 344SQR murine lung adenocarcinoma cells and syngeneic tumors. Cells were exposed to TTFields for 24, 48, or 72 h and evaluated for proliferation, clonogenic survival, and transcriptional pathway changes. Tumor-bearing mice received control treatment, anti-PD1, matched heating control, TTFields, or their combinations. Tumor growth, survival, and pulmonary metastatic burden were assessed, and tumor-infiltrating immune populations were characterized by single-cell RNA sequencing and T-cell receptor clonotype analysis. Results: TTFields suppressed tumor-cell proliferation and clonogenic survival in a time-dependent manner, with maximal inhibition at 48 h and partial recovery at 72 h. This biphasic response coincided with early suppression followed by reactivation of cell-cycle, metabolic, and interferon-related transcriptional programs. Anti-PD1 monotherapy showed minimal activity in vivo, whereas TTFields combined with anti-PD1 delayed tumor growth, reduced pulmonary metastases, and prolonged survival. Single-cell analysis showed that TTFields decreased Treg abundance, increased the CD8 Conclusions: TTFields sensitized anti-PD1-refractory lung tumors to PD1 blockade and induced coordinated remodeling of tumor-cell fitness and the tumor immune microenvironment. These findings identify TTFields as a potential tumor-conditioning strategy for overcoming resistance to immune checkpoint blockade.

Indexed as

lung adenocarcinomamacrophage reprogrammingPD1 blockade resistancetumor immune microenvironmentTumor Treating Fields

Identifiers

PMID42620288
PMCPMC13484854

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.