Evidence map›Paper›PMID 29423593›Full record

ReviewTargeted oncology2018

Tumor Hypoxia As an Enhancer of Inflammation-Mediated Metastasis: Emerging Therapeutic Strategies.

Josh W DiGiacomo, Daniele M Gilkes

Abstract readReview
PubMed Publisher
In one paragraph

Review in Targeted oncology, 2018. 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
1.4field-weighted citation impact, top 21% 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, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Hypoxia A Typical Target in Human Lung Cancer Therapy.Current protein & peptide science · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Hypoxia-induced HIF1α dependent COX2 promotes ovarian cancer progress.Journal of bioenergetics and biomembranes · 2021
    Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Parallel Accumulation of Tumor Hyaluronan, Collagen, and Other Drivers of Tumor Progression.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Article
  18. 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 1 institution in 1 country.

Josh W DiGiacomoDepartment of Chemical & Biomolecular Engineering, Johns Hopkins University, Baltimore, MD, 21218, USA.
Daniele M GilkesDepartment of Chemical & Biomolecular Engineering, Johns Hopkins University, Baltimore, MD, 21218, USA. dgilkes1@jhu.edu.
Johns Hopkins University · US

Funding

The Role of Physical Cues in Collective Cell InvasionU54CA210173 · NCI · JOHNS HOPKINS UNIVERSITY · PI WIRTZ, DENIS · 2016 to 2020
$9.9M
The role of the hypoxic ECM on integrin-induced breast cancer metastasisR00CA181352 · NCI · JOHNS HOPKINS UNIVERSITY · PI GILKES, DANIELE MARIE · 2015 to 2017
$747k
Center for Strategic Scientific Initiatives, National Cancer Institute U54-CA210173NCI NIH HHS R00-CA181352
6 · The paper itself

Abstract

Metastasis is the leading cause of cancer-related deaths. Recent research has implicated tumor inflammation as a promoter of metastasis. Myeloid, lymphoid, and mesenchymal cells in the tumor microenvironment promote inflammatory signaling amongst each other and together with cancer cells to modulate sustained inflammation, which may enhance cancer invasiveness. Tumor hypoxia, a state of reduced available oxygen present in the majority of solid tumors, acts as a prognostic factor for a worse outcome and is known to have a role in tumor inflammation through the regulation of inflammatory mediator signals in both cancer and neighboring cells in the microenvironment. Multiple methods to target tumor hypoxia have been developed and tested in clinical trials, and still more are emerging as the impacts of hypoxia become better understood. These strategies include mechanistic inhibition of the hypoxia inducible factor signaling pathway and hypoxia activated pro-drugs, leading to both anti-tumor and anti-inflammatory effects. This prompts a need for further research on the prevention of hypoxia-mediated inflammation in cancer. Hypoxia-targeting strategies seem to have the most potential for therapeutic benefit when combined with traditional chemotherapy agents. This paper will serve to summarize the role of the inflammatory response in metastasis, to discuss how hypoxia can enable or enhance inflammatory signaling, and to review established and emerging strategies to target the hypoxia-inflammation-metastasis axis.

Indexed as

HumansInflammationInflammation MediatorsNeoplasm MetastasisTumor HypoxiaInflammation Mediators

Identifiers

PMID29423593
OpenAlexW2793141200

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.