Evidence map›Paper›PMID 25381823›Full record

ReviewOncogene2015

A balancing act: orchestrating amino-truncated and full-length p73 variants as decisive factors in cancer progression.

D Engelmann, C Meier, V Alla, B M Pützer

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-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

31 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. TAp73 represses NF-κB-mediated recruitment of tumor-associated macrophages in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Article
  15. Mechanisms of Functional Pleiotropy of p73 in Cancer and Beyond.Frontiers in cell and developmental biology · 2021
    Review
  16. p73 as a Tissue Architect.Frontiers in cell and developmental biology · 2021
    Review
  17. The p53/p73 - p21Oncogene · 2021
    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

4 authors at 1 institution in 1 country.

D EngelmannInstitute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, Rostock, Germany.
C MeierInstitute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, Rostock, Germany.
V AllaInstitute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, Rostock, Germany.
B M PützerInstitute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, Rostock, Germany.
University of Rostock · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p73 is the older sibling of p53 and mimics most of its tumor-suppressor functions. Through alternative promoter usage and splicing, the TP73 gene generates more than two dozen isoforms of which N-terminal truncated DNp73 variants have a decisive role in cancer pathogenesis as they outweigh the positive effects of full-length TAp73 and p53 in acting as a barrier to tumor development. Beyond the prevailing view that DNp73 predominantly counteract cell cycle arrest and apoptosis, latest progress indicates that these isoforms acquire novel functions in epithelial-to-mesenchymal transition, metastasis and therapy resistance. New insight into the mechanisms underlying this behavior reinforced the expectation that DNp73 variants contribute to aggressive cellular traits through both loss of wild-type tumor-suppressor activity and gain-of-function, suggesting an equally important role in cancer progression as mutant p53. In this review, we describe the novel properties of DNp73 in the invasion metastasis cascade and outline the comprehensive p73 regulatome with an emphasis on molecular processes putting TAp73 out of action in advanced tumors. These intriguing insights provoke a new understanding of the acquisition of aggressive traits by cancer cells and may help to set novel therapies for a broad range of metastatic tumors.

Indexed as

AnimalsDisease ProgressionDNA-Binding ProteinsHumansNeoplasm InvasivenessNeoplasmsNuclear ProteinsTumor Protein p73Tumor Suppressor ProteinsDNA-Binding ProteinsNuclear ProteinsTP73 protein, humanTumor Protein p73Tumor Suppressor Proteins

Identifiers

PMID25381823
OpenAlexW2004479656

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.