Evidence map›Paper›PMID 26826488›Full record

ArticleJournal of theoretical biology2016

A cancer treatment based on synergy between anti-angiogenic and immune cell therapies.

Luis Soto-Ortiz, Stacey D Finley

Registry-linked trialAbstract read
In one paragraph

Article in Journal of theoretical biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03762018 (A Multicentre Randomised Phase III Trial Comparing Atezolizumab Plus Bevacizumab and Standard Chemotherapy Versus Bevacizumab and Standard Chemotherapy as First-line Treatment for Advanced Malignant Pleural Mesothelioma), which is not on this map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

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.

NCT03762018 phase3completednot on this mapstarted 2019, after this paper: background citation

A Multicentre Randomised Phase III Trial Comparing Atezolizumab Plus Bevacizumab and Standard Chemotherapy Versus Bevacizumab and Standard Chemotherapy as First-line Treatment for Advanced Malignant Pleural Mesothelioma

TypeinterventionalSponsorETOP IBCSG Partners FoundationRan2019 to 2024Enrolled400ConditionsPleural Mesothelioma Malignant AdvancedArmsCarboplatin, Pemetrexed, Bevacizumab, Atezolizumab
3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Article
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  4. Review
  5. Article
  6. Article
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  8. Review
  9. Review
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

2 authors.

Luis Soto-OrtizDepartment of Mathematics, East Los Angeles College, 1301 Avenida Cesar Chavez, Monterey Park, CA 91754, USA. Electronic address: lsoto@alumni.caltech.edu.
Stacey D FinleyDepartment of Biomedical Engineering, University of Southern California, Los Angeles, CA 90089, USA.

Funding

USC/NORRIS COMPREHENSIVE CANCER CENTER (CORE) SUPPORTP30CA014089 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI MYLES G COCKBURN · 1985 to 2026
$181.4M
NCI NIH HHS P30 CA014089
6 · The paper itself

Abstract

A mathematical model integrating tumor angiogenesis and tumor-targeted cytotoxicity by immune cells was developed to identify the therapeutic window of two distinct modes to treat cancer: (1) an anti-angiogenesis treatment based on the monoclonal antibody bevacizumab that targets tumor vasculature, and (2) immunotherapy involving the injection of unlicensed dendritic cells to boost the anti-tumor adaptive response. The angiogenic cytokine Vascular Endothelial Growth Factor (VEGF) contributes to the immunosuppressive tumor microenvironment, which is responsible for the short-lived therapeutic effect of cancer-targeted immunotherapy. The effect of immunosuppression on the width of the therapeutic window of each treatment was quantified. Experimental evidence has shown that neutralizing immunosuppressive cytokines results in an enhanced immune response against infections and chronic diseases. The model was used to determine treatment protocols involving the combination of anti-VEGF and unlicensed dendritic cell injections that enhance tumor regression. The model simulations predicted that the most effective method to treat tumors involves administering a series of biweekly anti-VEGF injections to disrupt angiogenic processes and limit tumor growth. The simulations also verified the hypothesis that reducing the concentration of the immunosuppressive factor VEGF prior to an injection of unlicensed dendritic cells enhances the cytotoxicity of CD8+ T cells and results in complete tumor elimination. Feasible treatment protocols for tumors that are diagnosed late and have grown to a relatively large size were identified.

Indexed as

ImmunotherapyAngiogenesis InhibitorsAntigens, NeoplasmCell CountCell ProliferationComputer SimulationDendritic CellsHumansImmune EvasionImmunosuppression TherapyModels, BiologicalNeoplasmsT-Lymphocytes, CytotoxicTransforming Growth Factor betaVascular Endothelial Growth Factor AAngiogenesis InhibitorsAntigens, NeoplasmTransforming Growth Factor betaVascular Endothelial Growth Factor AImmunosuppressionImmunotherapyMathematical modelingMonoclonal antibodyTumor angiogenesisVEGF

Identifiers

PMID26826488
PMCPMC7467856

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Registered trials

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.