Evidence map›Paper›PMID 28585066›Full record

ArticleBulletin of mathematical biology2017

Modeling the Dichotomy of the Immune Response to Cancer: Cytotoxic Effects and Tumor-Promoting Inflammation.

Kathleen P Wilkie, Philip Hahnfeldt

Open access · greenAbstract read
In one paragraph

Article in Bulletin of mathematical biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact, top 100% 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

18 citing papers in PubMed, 2 citations in OpenAlex.

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  16. Article
  17. Mathematical modeling of tumor-immune cell interactions.Journal of theoretical biology · 2019
    Review
  18. How Should Cancer Models Be Constructed?Cancer control : journal of the Moffitt Cancer Center
    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 at 2 institutions in 2 countries.

Kathleen P WilkieCenter of Cancer Systems Biology, Boston, MA, USA. kpwilkie@ryerson.ca.
Philip HahnfeldtCenter of Cancer Systems Biology, Boston, MA, USA. Hahnfeldt@cancer-systems-biology.org.
Center for Systems Biology · USToronto Metropolitan University · CA

Funding

Project 5 UC BerkleyU54CA149233 · NCI · STEWARD ST. ELIZABETH'S MEDICAL CENTER · PI HLATKY, LYNN · 2010 to 2014
$7.3M
NCI NIH HHS U54 CA149233
6 · The paper itself

Abstract

Although the immune response is often regarded as acting to suppress tumor growth, it is now clear that it can be both stimulatory and inhibitory. The interplay between these competing influences has complex implications for tumor development, cancer dormancy, and immunotherapies. In fact, early immunotherapy failures were partly due to a lack in understanding of the nonlinear growth dynamics these competing immune actions may cause. To study this biological phenomenon theoretically, we construct a minimally parameterized framework that incorporates all aspects of the immune response. We combine the effects of all immune cell types, general principles of self-limited logistic growth, and the physical process of inflammation into one quantitative setting. Simulations suggest that while there are pro-tumor or antitumor immunogenic responses characterized by larger or smaller final tumor volumes, respectively, each response involves an initial period where tumor growth is stimulated beyond that of growth without an immune response. The mathematical description is non-identifiable which allows an ensemble of parameter sets to capture inherent biological variability in tumor growth that can significantly alter tumor-immune dynamics and thus treatment success rates. The ability of this model to predict non-intuitive yet clinically observed patterns of immunomodulated tumor growth suggests that it may provide a means to help classify patient response dynamics to aid identification of appropriate treatments exploiting immune response to improve tumor suppression, including the potential attainment of an immune-induced dormant state.

Indexed as

ImmunotherapyInflammationNeoplasmsAntineoplastic AgentsHumansModels, TheoreticalAntineoplastic AgentsCancer modelingImmunoeditingOrdinary differential equationsTheoretical cancer immunologyTumor–immune dynamics

Identifiers

PMID28585066
PMCPMC5611811
OpenAlexW1813961470

What OpenQuestion 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 OpenQuestion graph.