Evidence map›Paper›PMID 26858439›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Self-targeting of TNF-releasing cancer cells in preclinical models of primary and metastatic tumors.

Eleonora Dondossola, Andrey S Dobroff, Serena Marchiò, Marina Cardó-Vila, Hitomi Hosoya, Steven K Libutti, Angelo Corti, Richard L Sidman, Wadih Arap, Renata Pasqualini

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.0field-weighted citation impact, top 9% of its field
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

23 citing papers in PubMed, 45 citations in OpenAlex.

  1. Repurposing Tumor Cells: A Paradigm Shift in Cell-Based Therapies for Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
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  9. Overcharged lipid metabolism in mechanisms of antitumor byInternational journal of oncology · 2023
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  18. Toxicology reports · 2018
    Article
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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

10 authors at 8 institutions in 3 countries.

Eleonora DondossolaDavid H. Koch Center for Applied Research of Genitourinary Cancers, MD Anderson Cancer Center, University of Texas, Houston, TX 77030;
Andrey S DobroffUniversity of New Mexico Comprehensive Cancer Center, Albuquerque, NM 87131; Division of Molecular Medicine, Department of Internal Medicine, University of New Mexico School of Medicine, Albuquerque, NM 87131;
Serena MarchiòUniversity of New Mexico Comprehensive Cancer Center, Albuquerque, NM 87131; Division of Molecular Medicine, Department of Internal Medicine, University of New Mexico School of Medicine, Albuquerque, NM 87131; Department of Oncology, University of Torino, Candiolo 10060, Italy;
Marina Cardó-VilaUniversity of New Mexico Comprehensive Cancer Center, Albuquerque, NM 87131; Division of Molecular Medicine, Department of Internal Medicine, University of New Mexico School of Medicine, Albuquerque, NM 87131;
Hitomi HosoyaDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8656, Japan; The University of Tokyo Hospital, Tokyo 113-8656, Japan;
Steven K LibuttiDepartment of Surgery and Department of Genetics, Albert Einstein College of Medicine of Yeshiva University, Bronx, NY 10461;
Angelo CortiDivision of Molecular Oncology, San Raffaele Scientific Institute and VIta Salute San Raffaele University, Milan 20132, Italy;
Richard L SidmanHarvard Medical School and Department of Neurology, Beth Israel-Deaconess Medical Center, Boston, MA 02215; richard_sidman@hms.harvard.edu warap@salud.unm.edu rpasqual@salud.unm.edu.
Wadih ArapUniversity of New Mexico Comprehensive Cancer Center, Albuquerque, NM 87131; Division of Hematology/Oncology, Department of Internal Medicine, University of New Mexico School of Medicine, Albuquerque, NM 87131 richard_sidman@hms.harvard.edu warap@salud.unm.edu rpasqual@salud.unm.edu.
Renata PasqualiniUniversity of New Mexico Comprehensive Cancer Center, Albuquerque, NM 87131; Division of Molecular Medicine, Department of Internal Medicine, University of New Mexico School of Medicine, Albuquerque, NM 87131; richard_sidman@hms.harvard.edu warap@salud.unm.edu rpasqual@salud.unm.edu.
New Mexico Cancer Center · USUNM Comprehensive Cancer CenterAlbert Einstein College of Medicine · USBeth Israel Deaconess Medical Center · USThe University of Texas MD Anderson Cancer Center · USUniversity of New Mexico · USUniversity of Tokyo Hospital · JPVita-Salute San Raffaele University · IT

Funding

Special Animal CoreP30DK041296 · NIDDK · YESHIVA UNIVERSITY · PI ROY-CHOWDHURY, JAYANTA · 1989 to 2018
$22.9M
NIDDK NIH HHS P30 DK041296
6 · The paper itself

Abstract

Circulating cancer cells can putatively colonize distant organs to form metastases or to reinfiltrate primary tumors themselves through a process termed "tumor self-seeding." Here we exploit this biological attribute to deliver tumor necrosis factor alpha (TNF), a potent antitumor cytokine, directly to primary and metastatic tumors in a mechanism that we have defined as "tumor self-targeting." For this purpose, we genetically engineered mouse mammary adenocarcinoma (TSA), melanoma (B16-F10), and Lewis lung carcinoma cells to produce and release murine TNF. In a series of intervention trials, systemic administration of TNF-expressing tumor cells was associated with reduced growth of both primary tumors and metastatic colonies in immunocompetent mice. We show that these malignant cells home to tumors, locally release TNF, damage neovascular endothelium, and induce massive cancer cell apoptosis. We also demonstrate that such tumor-cell-mediated delivery avoids or minimizes common side effects often associated with TNF-based therapy, such as acute inflammation and weight loss. Our study provides proof of concept that genetically modified circulating tumor cells may serve as targeted vectors to deliver anticancer agents. In a clinical context, this unique paradigm represents a personalized approach to be translated into applications potentially using patient-derived circulating tumor cells as self-targeted vectors for drug delivery.

Indexed as

AnimalsApoptosisCarcinoma, Lewis LungCell- and Tissue-Based TherapyCell EngineeringCell Line, TumorDrug Delivery SystemsEndothelium, VascularFemaleHumansMammary Neoplasms, ExperimentalMelanoma, ExperimentalMiceMice, Inbred BALB CMice, Inbred C57BLNeoplasms, ExperimentalRecombinant ProteinsTumor Necrosis Factor-alphaapoptosisendothelial cellsengineered tumor cellstumor necrosis factorvascular damaging agent

Identifiers

PMID26858439
PMCPMC4776485
OpenAlexW2260223907

What OpenQuestion holds

Textmetadata
Read underepoch 390

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 OpenQuestion graph.