Evidence map›Paper›PMID 26637438›Full record

ReviewCold Spring Harbor perspectives in medicine2015

p53 as an Effector or Inhibitor of Therapy Response.

Julien Ablain, Brigitte Poirot, Cécile Esnault, Jacqueline Lehmann-Che, Hugues de Thé

Open access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Mutant p53 in cell-cell interactions.Genes & development · 2021
    Review
  6. Article
  7. Article
  8. Review
  9. Zebrafish as a Model Organism for the Development of Drugs for Skin Cancer.International journal of molecular sciences · 2017
    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

5 authors at 3 institutions in 1 country.

Julien AblainUniversité Paris Diderot, Sorbonne Paris Cité, Institut Universitaire d'Hématologie, Hôpital St. Louis, 75475 Paris, France INSERM UMR 944, Equipe Labellisée par la Ligue Nationale contre le Cancer, Hôpital St. Louis, 75475 Paris, France CNRS UMR 7212, Hôpital St. Louis, 75475 Paris, France.
Brigitte PoirotUniversité Paris Diderot, Sorbonne Paris Cité, Institut Universitaire d'Hématologie, Hôpital St. Louis, 75475 Paris, France INSERM UMR 944, Equipe Labellisée par la Ligue Nationale contre le Cancer, Hôpital St. Louis, 75475 Paris, France CNRS UMR 7212, Hôpital St. Louis, 75475 Paris, France Assistance Publique des Hôpitaux de Paris, Oncologie Moléculaire, Hôpital St. Louis, 75475 Paris, France.
Cécile EsnaultUniversité Paris Diderot, Sorbonne Paris Cité, Institut Universitaire d'Hématologie, Hôpital St. Louis, 75475 Paris, France INSERM UMR 944, Equipe Labellisée par la Ligue Nationale contre le Cancer, Hôpital St. Louis, 75475 Paris, France CNRS UMR 7212, Hôpital St. Louis, 75475 Paris, France.
Jacqueline Lehmann-CheUniversité Paris Diderot, Sorbonne Paris Cité, Institut Universitaire d'Hématologie, Hôpital St. Louis, 75475 Paris, France INSERM UMR 944, Equipe Labellisée par la Ligue Nationale contre le Cancer, Hôpital St. Louis, 75475 Paris, France CNRS UMR 7212, Hôpital St. Louis, 75475 Paris, France Assistance Publique des Hôpitaux de Paris, Oncologie Moléculaire, Hôpital St. Louis, 75475 Paris, France.
Hugues de ThéUniversité Paris Diderot, Sorbonne Paris Cité, Institut Universitaire d'Hématologie, Hôpital St. Louis, 75475 Paris, France INSERM UMR 944, Equipe Labellisée par la Ligue Nationale contre le Cancer, Hôpital St. Louis, 75475 Paris, France CNRS UMR 7212, Hôpital St. Louis, 75475 Paris, France Assistance Publique des Hôpitaux de Paris, Oncologie Moléculaire, Hôpital St. Louis, 75475 Paris, France Collège de France, 75005 Paris, France.
Sorbonne Paris Cité · FRUniversité Paris Cité · FRCollège de France · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although integrity of the p53 signaling pathway in a given tumor was expected to be a critical determinant of response to therapies, most clinical studies failed to link p53 status and treatment outcome. Here, we present two opposite situations: one in which p53 is an essential effector of cure by targeted leukemia therapies and another one in advanced breast cancers in which p53 inactivation is required for the clinical efficacy of dose-dense chemotherapy. If p53 promotes or blocks therapy response, therapies must be tailored on its status in individual tumors.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsArsenicalsArsenic TrioxideBreast NeoplasmsFemaleHumansLeukemia, Promyelocytic, AcuteMolecular Targeted TherapyOncogene Proteins, FusionOxidesTreatment OutcomeTretinoinTumor Suppressor Protein p53ArsenicalsArsenic TrioxideOncogene Proteins, FusionOxidespromyelocytic leukemia-retinoic acid receptor alpha fusion oncoproteinTP53 protein, humanTretinoinTumor Suppressor Protein p53

Identifiers

PMID26637438
PMCPMC4691805
OpenAlexW2184712565

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.