Evidence map›Paper›PMID 30279659›Full record

ArticleFrontiers in pharmacology2018

Bystander Effects of Hypoxia-Activated Prodrugs: Agent-Based Modeling Using Three Dimensional Cell Cultures.

Cho R Hong, Gib Bogle, Jingli Wang, Kashyap Patel, Frederik B Pruijn, William R Wilson, Kevin O Hicks

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

22 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Pimonidazole-alkyne conjugate for sensitive detection of hypoxia by Cu-catalyzed click reaction.Analytical sciences : the international journal of the Japan Society for Analytical Chemistry · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Nitroaromatic Hypoxia-Activated Prodrugs for Cancer Therapy.Pharmaceuticals (Basel, Switzerland) · 2022
    Review
  13. Article
  14. Therapeutic targeting of the hypoxic tumour microenvironment.Nature reviews. Clinical oncology · 2021
    Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Engineering theFrontiers in pharmacology · 2021
    Article
  20. Article
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

7 authors at 3 institutions in 1 country.

Cho R HongAuckland Cancer Society Research Centre, University of Auckland, Auckland, New Zealand.
Gib BogleAuckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.
Jingli WangAuckland Cancer Society Research Centre, University of Auckland, Auckland, New Zealand.
Kashyap PatelAuckland Cancer Society Research Centre, University of Auckland, Auckland, New Zealand.
Frederik B PruijnAuckland Cancer Society Research Centre, University of Auckland, Auckland, New Zealand.
William R WilsonAuckland Cancer Society Research Centre, University of Auckland, Auckland, New Zealand.
Kevin O HicksAuckland Cancer Society Research Centre, University of Auckland, Auckland, New Zealand.
University of Auckland · NZCancer Society of New Zealand · NZMaurice Wilkins Centre · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intra-tumor heterogeneity represents a major barrier to anti-cancer therapies. One strategy to minimize this limitation relies on bystander effects via diffusion of cytotoxins from targeted cells. Hypoxia-activated prodrugs (HAPs) have the potential to exploit hypoxia in this way, but robust methods for measuring bystander effects are lacking. The objective of this study is to develop experimental models (monolayer, multilayer, and multicellular spheroid co-cultures) comprising 'activator' cells with high expression of prodrug-activating reductases and reductase-deficient 'target' cells, and to couple these with agent-based models (ABMs) that describe diffusion and reaction of prodrugs and their active metabolites, and killing probability for each cell. HCT116 cells were engineered as activators by overexpressing P450 oxidoreductase (POR) and as targets by knockout of POR, with fluorescent protein and antibiotic resistance markers to enable their quantitation in co-cultures. We investigated two HAPs with very different pharmacology: SN30000 is metabolized to DNA-breaking free radicals under hypoxia, while the dinitrobenzamide PR104A generates DNA-crosslinking nitrogen mustard metabolites. In anoxic spheroid co-cultures, increasing the proportion of activator cells decreased killing of both activators and targets by SN30000. An ABM parameterized by measuring SN30000 cytotoxicity in monolayers and diffusion-reaction in multilayers accurately predicted SN30000 activity in spheroids, demonstrating the lack of bystander effects and that rapid metabolic consumption of SN30000 inhibited prodrug penetration. In contrast, killing of targets by PR104A in anoxic spheroids was markedly increased by activators, demonstrating that a bystander effect more than compensates any penetration limitation. However, the ABM based on the well-studied hydroxylamine and amine metabolites of PR104A did not fit the cell survival data, indicating a need to reassess its cellular pharmacology. Characterization of extracellular metabolites of PR104A in anoxic cultures identified more stable, lipophilic, activated dichloro mustards with greater tissue diffusion distances. Including these metabolites explicitly in the ABM provided a good description of activator and target cell killing by PR104A in spheroids. This study represents the most direct demonstration of a hypoxic bystander effect for PR104A to date, and demonstrates the power of combining mathematical modeling of pharmacokinetics/pharmacodynamics with multicellular culture models to dissect bystander effects of targeted drug carriers.

Indexed as

agent-based modelingbystander effectshypoxia-activated prodrugsmulticellular spheroidsnitrogen mustardsPKPD modelsPR104ASN30000

Identifiers

PMID30279659
PMCPMC6153434
OpenAlexW2890554801

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.