Evidence map›Paper›PMID 32708855›Full record

ReviewInternational journal of molecular sciences2020

Cellular Mechanisms of Circulating Tumor Cells During Breast Cancer Metastasis.

Han-A Park, Spenser R Brown, Yonghyun Kim

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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.

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

36 citing papers in PubMed.

  1. Article
  2. Article
  3. Role of circulating tumor cell clusters in breast cancer.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2026
    Review
  4. Article
  5. Lamin A/C as a biomarker for breast cancer.Molecular biology reports · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Onco-Breastomics: An Eco-Evo-Devo Holistic Approach.International journal of molecular sciences · 2024
    Review
  16. Article
  17. Article
  18. Review
  19. 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

3 authors.

Han-A ParkDepartment of Human Nutrition and Hospitality Management, College of Human Environmental Sciences, The University of Alabama, P.O. Box 870311, Tuscaloosa, AL 35487, USA.ORCID 0000-0001-5563-5255
Spenser R BrownDepartment of Chemical and Biological Engineering, College of Engineering, The University of Alabama, Tuscaloosa, AL 35487, USA.
Yonghyun KimDepartment of Chemical and Biological Engineering, College of Engineering, The University of Alabama, Tuscaloosa, AL 35487, USA.ORCID 0000-0001-6344-1258

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Circulating tumor cells (CTCs) are cancer cells that detach from the primary site and travel in the blood stream. A higher number of CTCs increases the risk of breast cancer metastasis, and it is inversely associated with the survival rates of patients with breast cancer. Although the numbers of CTCs are generally low and the majority of CTCs die in circulation, the survival of a few CTCs can seed the development of a tumor at a secondary location. An increasing number of studies demonstrate that CTCs undergo modification in response to the dynamic biophysical environment in the blood due in part to fluid shear stress. Fluid shear stress generates reactive oxygen species (ROS), triggers redox-sensitive cell signaling, and alters the function of intracellular organelles. In particular, the mitochondrion is an important target organelle in determining the metastatic phenotype of CTCs. In healthy cells, mitochondria produce adenosine triphosphate (ATP) via oxidative phosphorylation in the electron transport chain, and during oxidative phosphorylation, they produce physiological levels of ROS. Mitochondria also govern death mechanisms such as apoptosis and mitochondrial permeability transition pore opening to, in order eliminate unwanted or damaged cells. However, in cancer cells, mitochondria are dysregulated, causing aberrant energy metabolism, redox homeostasis, and cell death pathways that may favor cancer invasiveness. In this review, we discuss the influence of fluid shear stress on CTCs with an emphasis on breast cancer pathology, then discuss alterations of cellular mechanisms that may increase the metastatic potentials of CTCs.

Indexed as

Adenosine TriphosphateAnimalsBreast NeoplasmsFemaleHumansMitochondriaNeoplasm MetastasisNeoplastic Cells, CirculatingOxidative StressReactive Oxygen SpeciesStress, MechanicalAdenosine TriphosphateReactive Oxygen Speciesbreast cancercirculating tumor cellsfluid shear stressmitochondriaoxidative stress

Identifiers

PMID32708855
PMCPMC7404335

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.