Evidence map›Paper›PMID 28125050›Full record

ReviewGenes2017

Links between DNA Replication, Stem Cells and Cancer.

Alex Vassilev, Melvin L DePamphilis

Open access · goldAbstract readReview
In one paragraph

Review in Genes, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Ubiquitin-Specific Protease 29 Regulates Cdc25A-Mediated Tumorigenesis.International journal of molecular sciences · 2021
    Article
  18. Review
  19. Article
  20. DNA repair fidelity in stem cell maintenance, health, and disease.Biochimica et biophysica acta. Molecular basis of disease · 2020
    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.

Alex VassilevEunice Kennedy Shriver National Institute of Child Health and Human Development, Bldg. 6A, Room 3A15, 6 Center Drive, Bethesda, MD 20892-2790, USA. vassilev@mail.nih.gov.
Melvin L DePamphilisEunice Kennedy Shriver National Institute of Child Health and Human Development, Bldg. 6A, Room 3A15, 6 Center Drive, Bethesda, MD 20892-2790, USA. depamphm@mail.nih.gov.
Eunice Kennedy Shriver National Institute of Child Health and Human Development · US

Funding

Initiation Of DNA Replication In Mammalian ChromosomesZIAHD000506 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI DEPAMPHILIS, MELVIN · 2009 to 2023
$15.4M
Gene Expression At The Beginning Of Mammalian DevelopmentZIAHD000507 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI DEPAMPHILIS, MELVIN · 2009 to 2018
$8.6M
6 · The paper itself

Abstract

Cancers can be categorized into two groups: those whose frequency increases with age, and those resulting from errors during mammalian development. The first group is linked to DNA replication through the accumulation of genetic mutations that occur during proliferation of developmentally acquired stem cells that give rise to and maintain tissues and organs. These mutations, which result from DNA replication errors as well as environmental insults, fall into two categories; cancer driver mutations that initiate carcinogenesis and genome destabilizing mutations that promote aneuploidy through excess genome duplication and chromatid missegregation. Increased genome instability results in accelerated clonal evolution leading to the appearance of more aggressive clones with increased drug resistance. The second group of cancers, termed germ cell neoplasia, results from the mislocation of pluripotent stem cells during early development. During normal development, pluripotent stem cells that originate in early embryos give rise to all of the cell lineages in the embryo and adult, but when they mislocate to ectopic sites, they produce tumors. Remarkably, pluripotent stem cells, like many cancer cells, depend on the Geminin protein to prevent excess DNA replication from triggering DNA damage-dependent apoptosis. This link between the control of DNA replication during early development and germ cell neoplasia reveals Geminin as a potential chemotherapeutic target in the eradication of cancer progenitor cells.

Indexed as

cancer stem cellsDNA re-replicationembryonal carcinoma cellsembryonic stem cellsendoreplicationGeminingerm cell neoplasiamitotic slippageteratocarcinomateratoma

Identifiers

PMID28125050
PMCPMC5333035
OpenAlexW2582478837

What Socratic 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 Socratic graph.