Evidence map›Paper›PMID 27235476›Full record

ReviewCold Spring Harbor perspectives in medicine2016

Oncogenic Mutant p53 Gain of Function Nourishes the Vicious Cycle of Tumor Development and Cancer Stem-Cell Formation.

Yoav Shetzer, Alina Molchadsky, Varda Rotter

Abstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
–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

35 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023
    Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Journal of extracellular biology · 2023
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Gain-of-Function Mutations in p53 in Cancer Invasiveness and Metastasis.International journal of molecular sciences · 2020
    Review
  17. Article
  18. Article
  19. Review
  20. 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

3 authors.

Yoav ShetzerDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel.
Alina MolchadskyDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel.
Varda RotterDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

More than half of human tumors harbor an inactivated p53 tumor-suppressor gene. It is well accepted that mutant p53 shows an oncogenic gain-of-function (GOF) activity that facilitates the transformed phenotype of cancer cells. In addition, a growing body of evidence supports the notion that cancer stem cells comprise a seminal constituent in the initiation and progression of cancer development. Here, we elaborate on the mutant p53 oncogenic GOF leading toward the acquisition of a transformed phenotype, as well as placing mutant p53 as a major component in the establishment of cancer stem cell entity. Therefore, therapy targeted toward cancer stem cells harboring mutant p53 is expected to pave the way to eradicate tumor growth and recurrence.

Indexed as

Gain of Function MutationAnimalsAntineoplastic AgentsHumansMiceMolecular Targeted TherapyNeoplasmsNeoplastic Stem CellsPhenotypeTumor Suppressor Protein p53Antineoplastic AgentsTumor Suppressor Protein p53

Identifiers

PMID27235476
PMCPMC5046690

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.