Evidence map›Paper›PMID 41529696›Full record

ArticleCell metabolism2026

Mitochondrial transfer from immune to tumor cells enables lymph node metastasis.

Azusa Terasaki, Keshav Bhatnagar, Alexis T Weiner, Yuhao Tan, Viktoria Szeifert, Han-Li Huang, Lukas Wiggers, Viviana Rodrigues, Cara C Rada, Vishnu Shankar and 12 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
–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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

24 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  6. Mitochondrial dynamics and T cells immunity in cancer.Biochemistry and biophysics reports · 2026
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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

22 authors.

Azusa TerasakiDepartment of Pathology, Stanford University, Stanford, CA 94305, USA.
Keshav BhatnagarDepartment of Pathology, Stanford University, Stanford, CA 94305, USA.
Alexis T WeinerDepartment of Pathology, Stanford University, Stanford, CA 94305, USA.
Yuhao TanChildren's Hospital of Pennsylvania, Philadelphia, PA, USA.
Viktoria SzeifertDepartment of Pathology, Stanford University, Stanford, CA 94305, USA.
Han-Li HuangDepartment of Pathology, Stanford University, Stanford, CA 94305, USA.
Lukas WiggersDepartment of Pathology, Stanford University, Stanford, CA 94305, USA.
Viviana RodriguesDepartment of Pathology, Stanford University, Stanford, CA 94305, USA.
Cara C RadaDepartment of Medicine, Stanford University, Stanford, CA 94305, USA.
Vishnu ShankarImmunology Graduate Program, Stanford University, Stanford, CA 94305, USA.
Suguru SaitoDepartment of Pathology, Cedars Sinai Medical Center, Los Angeles, CA 90066, USA.
Peter Ofori AnkomahMassachusetts General Hospital, Boston, MA, USA.
Theodore RothDepartment of Pathology, Stanford University, Stanford, CA 94305, USA; Arc Institute, Palo Alto, CA, USA; Stanford Cancer Institute, Stanford, CA 94305, USA.
Bill ChiuDepartment of Surgery, Stanford University, Stanford, CA 94305, USA.
Robert WestDepartment of Pathology, Stanford University, Stanford, CA 94305, USA.
Lingyin LiArc Institute, Palo Alto, CA, USA; Department of Biochemistry, Program in Chemistry, Engineering, and Medicine for Human Health (ChEM-H), Stanford University, Stanford, CA 94305, USA.
Nathan Reticker-FlynnStanford Cancer Institute, Stanford, CA 94305, USA; Department of Otolaryngology, Stanford University, Stanford, CA 94305, USA.
Jeffrey D AxelrodDepartment of Pathology, Stanford University, Stanford, CA 94305, USA.
Jonathan R BrestoffDepartment of Pathology and Immunology, Washington University School of Medicine, Saint Louis, MO 63110, USA.
Bo LiChildren's Hospital of Pennsylvania, Philadelphia, PA, USA.
Edgar EnglemanDepartment of Pathology, Stanford University, Stanford, CA 94305, USA; Stanford Cancer Institute, Stanford, CA 94305, USA.
Derick Okwan-DuoduDepartment of Pathology, Stanford University, Stanford, CA 94305, USA; Stanford Cancer Institute, Stanford, CA 94305, USA. Electronic address: dokwan@stanford.edu.

Funding

Project 3: Impact of tumor genetics on PDAC immunobiology and responses to macrophage-targeted immunotherapyP01CA244114 · NCI · STANFORD UNIVERSITY · PI PARK, WALTER GWANG-UP · 2021 to 2025
$10.0M
Systems Biology of Tumor-Immune-Stromal Interactions in Metastatic ProgressionU54CA274511 · NCI · STANFORD UNIVERSITY · PI JOSEPH B SHRAGER · 2023 to 2026
$9.5M
Targeting Lymph Node Dependent Immune Tolerance in CancerR01CA251174 · NCI · STANFORD UNIVERSITY · PI EDGAR G. ENGLEMAN · 2021 to 2026
$3.2M
High dimensional atlas of circulating neutrophils as reporters of solid organ functional statusR01ES034235 · NIEHS · STANFORD UNIVERSITY · PI OKWAN-DUODU, DERICK · 2021 to 2025
$2.1M
Harnessing mitochondria transfer pathways to ameliorate Leigh Syndrome-like diseaseR01NS134932 · NINDS · WASHINGTON UNIVERSITY · PI Jonathan R Brestoff · 2024 to 2026
$1.8M
Dissecting intrinsic variability in engineered T Cell immunotherapiesK08CA286740 · NCI · STANFORD UNIVERSITY · PI Theodore Lee Roth · 2024 to 2026
$747k
NCI NIH HHS K08 CA286740NCI NIH HHS P01 CA244114NCI NIH HHS R01 CA251174NCI NIH HHS U54 CA274511NIEHS NIH HHS R01 ES034235NINDS NIH HHS R01 NS134932
6 · The paper itself

Abstract

Although the immune system is a significant barrier to tumor growth and spread, established tumors evade immune attack and frequently colonize immune populated areas such as the lymph node. The mechanisms by which cancer cells subvert the tumor-immune microenvironment to favor spread to the lymph node remain incompletely understood. Here, we show that, as a common attribute, tumor cells hijack mitochondria from a wide array of immune cells. Mitochondria loss by immune cells decreases antigen-presentation and co-stimulatory machinery, as well as reducing the activation and cytotoxic capacity of natural killer (NK) and CD8 T cells. In cancer cells, the exogenous mitochondria fuse with endogenous mitochondria networks, leak mtDNA into the cytosol, and stimulate cGAS/STING, activating type I interferon-mediated immune evasion programs. Blocking mitochondrial transfer machinery-including cGAS, STING, or type I interferon-reduced cancer metastasis to the lymph node. These findings suggest that cancer cells leverage mitochondria hijacking to weaken anti-tumor immunosurveillance and use the acquired mitochondria to fuel the immunological requirements of lymph node colonization.

Indexed as

Lymphatic MetastasisMitochondriaAnimalsCD8-Positive T-LymphocytesCell Line, TumorcGAS-STING Signaling PathwayCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNA, MitochondrialFemaleHumansInterferon Type IKiller Cells, NaturalLymph NodesMembrane ProteinsMiceMice, Inbred C57BLCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNA, MitochondrialInterferon Type IMembrane ProteinsNucleotidyltransferasesSTING ProteincGAS/STINGimmune evasionlymph node cancer metastasisMERCImitochondrial transfer

Identifiers

PMID41529696
PMCPMC13386577

What Socratic holds

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Registered trials

None linked

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 Socratic graph.