Evidence map›Paper›PMID 27663133›Full record

ArticleTrends in cell biology2016

Novel Insights into PML-Dependent Oncosuppression.

Lorenzo Galluzzi

Abstract readComment
PubMed Publisher
In one paragraph

Article in Trends in cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 28% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Mitochondria-ER crosstalk via MAMS: Bridging cellular homeostasis and cancer progression.Apoptosis : an international journal on programmed cell death · 2026
    Review
  2. Review
  3. Review
  4. TRPC3 shapes the ER-mitochondria CaNature communications · 2022
    Article
  5. Endoplasmic Reticulum-Mitochondrial CaFrontiers in oncology · 2017
    Review
  6. IPFrontiers in oncology · 2017
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 2 countries.

Lorenzo GalluzziDepartment of Radiation Oncology, Weill Cornell Medical College, New York, NY 10065, USA; Equipe 11 Labellisée Ligue Contre le Cancer, Centre de Recherche des Cordeliers, 75006 Paris, France; INSERM, U1138, 75006 Paris, France; Université Paris Descartes/Paris V, Sorbonne Paris Cité, 75006 Paris, France; Université Pierre et Marie Curie/Paris VI, 75006 Paris, France; Gustave Roussy Comprehensive Cancer Institute, 94805 Villejuif, France. Electronic address: deadoc@vodafone.it.
Sorbonne Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

At odds with its nuclear counterpart, extranuclear promyelocytic leukemia constitutively inhibits autophagy, hence limiting cancer progression. These data raise the interesting possibility that some tumor suppressors have become specialized to operate at multiple subcellular compartments for counteracting different aspects of the oncogenic process.

Indexed as

Genes, Tumor SuppressorAnimalsHumansMiceModels, BiologicalPromyelocytic Leukemia ProteinTumor Suppressor Protein p53Promyelocytic Leukemia ProteinTumor Suppressor Protein p53autophagybeclin 1chloroquineMAMsp53regulated cell death

Identifiers

PMID27663133
OpenAlexW2523345792

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.