Evidence map›Paper›PMID 34670140›Full record

ReviewSeminars in cancer biology2022

The life cycle of polyploid giant cancer cells and dormancy in cancer: Opportunities for novel therapeutic interventions.

Jinsong Liu, Na Niu, Xiaoran Li, Xudong Zhang, Anil K Sood

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. RHAMM drives formation of polyploid cancer cells and confers resistance to ER-targeted therapy in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  18. Review
  19. Review
  20. Cells in the Polyaneuploid Cancer Cell State are Pro-Metastatic.bioRxiv : the preprint server for biology · 2024
    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

5 authors at 1 institution in 1 country.

Jinsong LiuDepartments of Anatomic Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA; Departments of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA. Electronic address: jliu@mdanderson.org.
Na NiuDepartments of Anatomic Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
Xiaoran LiDepartments of Anatomic Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
Xudong ZhangDepartments of Anatomic Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
Anil K SoodDepartments of Gynecologic Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
The University of Texas MD Anderson Cancer Center · US

Funding

U.T. M. D. Anderson Cancer Center SPORE in Ovarian CancerP50CA217685 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BAST, ROBERT C, SOOD, ANIL K · 2017 to 2021
$7.9M
NCI NIH HHS P50 CA217685
6 · The paper itself

Abstract

Recent data suggest that most genotoxic agents in cancer therapy can lead to shock of genome and increase in cell size, which leads whole genome duplication or multiplication, formation of polyploid giant cancer cells, activation of an early embryonic program, and dedifferentiation of somatic cells. This process is achieved via the giant cell life cycle, a recently proposed mechanism for malignant transformation of somatic cells. Increase in both cell size and ploidy allows cells to completely or partially restructures the genome and develop into a blastocyst-like structure, similar to that observed in blastomere-stage embryogenesis. Although blastocyst-like structures with reprogrammed genome can generate resistant or metastatic daughter cells or benign cells of different lineages, they also acquired ability to undergo embryonic diapause, a reversible state of suspended embryonic development in which cells enter dormancy for survival in response to environmental stress. Therapeutic agents can activate this evolutionarily conserved developmental program, and when cells awaken from embryonic diapause, this leads to recurrence or metastasis. Understanding of the key mechanisms that regulate the different stages of the giant cell life cycle offers new opportunities for therapeutic intervention.

Indexed as

NeoplasmsAnimalsBlastomeresFemaleGiant CellsHumansLife Cycle StagesPolyploidyPregnancyDormancyEmbryonic diapauseGiant cell life cycle (giant cell cycle)Polyploid giant cancer cellsTherapeutic resistance

Identifiers

PMID34670140
PMCPMC9007823
OpenAlexW3206829843

What OpenQuestion holds

Textmetadata
LicenceTDM
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.