Evidence map›Paper›PMID 22138778›Full record

ReviewCancer metastasis reviews2012

Potential roles for prions and protein-only inheritance in cancer.

H Antony, A P Wiegmans, M Q Wei, Y O Chernoff, K K Khanna, A L Munn

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Human RAD51 Protein Forms Amyloid-like AggregatesInternational journal of molecular sciences · 2022
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Pathway-Based Kernel Boosting for the Analysis of Genome-Wide Association Studies.Computational and mathematical methods in medicine · 2017
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

6 authors at 3 institutions in 2 countries.

H AntonyGriffith Health Institute, Griffith University, Southport, Queensland, Australia. helmageorge@gmail.com
A P Wiegmans
M Q Wei
Y O Chernoff
K K Khanna
A L Munn
Griffith University · AUQIMR Berghofer Medical Research Institute · AUGeorgia Institute of Technology · US

Funding

GENETIC STUDY OF THE YEAST PRION INTERACTING PROTEINSR01GM058763 · NIGMS · GEORGIA INSTITUTE OF TECHNOLOGY · PI CHERNOFF, YURY O · 1999 to 2010
$2.6M
NIGMS NIH HHS R01 GM058763NIGMS NIH HHS R01GM58763
6 · The paper itself

Abstract

Inherited mutations are known to cause familial cancers. However, the cause of sporadic cancers, which likely represent the majority of cancers, is yet to be elucidated. Sporadic cancers contain somatic mutations (including oncogenic mutations); however, the origin of these mutations is unclear. An intriguing possibility is that a stable alteration occurs in somatic cells prior to oncogenic mutations and promotes the subsequent accumulation of oncogenic mutations. This review explores the possible role of prions and protein-only inheritance in cancer. Genetic studies using lower eukaryotes, primarily yeast, have identified a large number of proteins as prions that confer dominant phenotypes with cytoplasmic (non-Mendelian) inheritance. Many of these have mammalian functional homologs. The human prion protein (PrP) is known to cause neurodegenerative diseases and has now been found to be upregulated in multiple cancers. PrP expression in cancer cells contributes to cancer progression and resistance to various cancer therapies. Epigenetic changes in the gene expression and hyperactivation of MAP kinase signaling, processes that in lower eukaryotes are affected by prions, play important roles in oncogenesis in humans. Prion phenomena in yeast appear to be influenced by stresses, and there is considerable evidence of the association of some amyloids with biologically positive functions. This suggests that if protein-only somatic inheritance exists in mammalian cells, it might contribute to cancer phenotypes. Here, we highlight evidence in the literature for an involvement of prion or prion-like mechanisms in cancer and how they may in the future be viewed as diagnostic markers and potential therapeutic targets.

Indexed as

HeredityHumansModels, BiologicalMolecular Targeted TherapyNeoplasm MetastasisNeoplasmsPrionsPrions

Identifiers

PMID22138778
PMCPMC3315606
OpenAlexW2065703956

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.