Evidence map›Paper›PMID 31218069›Full record

ArticleRoyal Society open science2019

Hanwen Wang, Oleg Milberg, Imke H Bartelink, Paolo Vicini, Bing Wang, Rajesh Narwal, Lorin Roskos, Cesar A Santa-Maria, Aleksander S Popel

Open access · goldAbstract read
In one paragraph

Article in Royal Society open science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  5. Review
  6. An industry perspective on current QSP trends in drug development.Journal of pharmacokinetics and pharmacodynamics · 2024
    Article
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  8. Article
  9. Article
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  13. Treatment of evolving cancers will require dynamic decision support.Annals of oncology : official journal of the European Society for Medical Oncology · 2023
    Review
  14. 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

9 authors at 2 institutions in 2 countries.

Hanwen WangDepartment of Biomedical Engineering, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA.ORCID 0000-0001-5480-431X
Oleg MilbergDepartment of Biomedical Engineering, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA.
Imke H BartelinkDepartment of Medicine, University of California, San Francisco, CA, USA.
Paolo ViciniClinical Pharmacology, Pharmacometrics and DMPK, MedImmune, Cambridge, UK.
Bing WangAmador Bioscience Inc, Pleasanton, CA 94588, USA.
Rajesh NarwalClinical Pharmacology and DMPK (CPD), MedImmune, Gaithersburg, MD, USA.
Lorin RoskosClinical Pharmacology and DMPK (CPD), MedImmune, Gaithersburg, MD, USA.
Cesar A Santa-MariaDepartment of Oncology and Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Aleksander S PopelDepartment of Biomedical Engineering, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA.
Johns Hopkins University · USUniversity of California, San Francisco · US

Funding

Predictive experiment-based multiscale models of the tumor immune microenvironment and immunotherapy in breast cancerR01CA138264 · NCI · JOHNS HOPKINS UNIVERSITY · PI POPEL, ALEKSANDER S. · 2009 to 2023
$8.1M
NCI NIH HHS R01 CA138264
6 · The paper itself

Abstract

The low response rate of immune checkpoint blockade in breast cancer has highlighted the need for predictive biomarkers to identify responders. While a number of clinical trials are ongoing, testing all possible combinations is not feasible. In this study, a quantitative systems pharmacology model is built to integrate immune-cancer cell interactions in patients with breast cancer, including central, peripheral, tumour-draining lymph node (TDLN) and tumour compartments. The model can describe the immune suppression and evasion in both TDLN and the tumour microenvironment due to checkpoint expression, and mimic the tumour response to checkpoint blockade therapy. We investigate the relationship between the tumour response to checkpoint blockade therapy and composite tumour burden, PD-L1 expression and antigen intensity, including their individual and combined effects on the immune system, using model-based simulations. The proposed model demonstrates the potential to make predictions of tumour response of individual patients given sufficient clinical measurements, and provides a platform that can be further adapted to other types of immunotherapy and their combination with molecular-targeted therapies. The patient predictions demonstrate how this systems pharmacology model can be used to individualize immunotherapy treatments. When appropriately validated, these approaches may contribute to optimization of breast cancer treatment.

Indexed as

computational biologycomputational modelimmune checkpoint inhibitorimmuno-oncologysystems biology

Identifiers

PMID31218069
PMCPMC6549962
OpenAlexW2945644530

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.