Evidence map›Paper›PMID 30836703›Full record

ReviewBiomolecules2019

Dual Role of the Alternative Reading Frame ARF Protein in Cancer.

Rosa Fontana, Michela Ranieri, Girolama La Mantia, Maria Vivo

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Driver mutation profiling by next-generation sequencing predicts survival and recurrence after curative-intent resection for pancreatic ductal adenocarcinoma: a genomic cohort study.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
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  6. Review
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  10. IncreasedMolecular & cellular oncology · 2025
    Article
  11. The journal of venomous animals and toxins including tropical diseases · 2025
    Article
  12. Review
  13. Microcephaly GeneInternational journal of molecular sciences · 2024
    Article
  14. Review
  15. Review
  16. Review
  17. Article
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  19. Article
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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 3 institutions in 2 countries.

Rosa FontanaDepartment of Pharmacology, Moores Cancer Center, University of California, San Diego, La Jolla, CA 92093, USA. rofontana@ucsd.edu.
Michela RanieriDivision of Hematology and Medical Oncology, Laura and Isaac Perlmutter Cancer Center, NYU Langone Medical Center, New York, NY 10016, USA. Michela.Ranieri@nyulangone.org.
Girolama La MantiaDepartment of Biology, University of Naples Federico II, 80126 Naples, Italy. lamantia@unina.it.
Maria VivoDepartment of Biology, University of Naples Federico II, 80126 Naples, Italy. maria.vivo@unina.it.
University of Naples Federico II · ITNYU Langone Health · USUniversity of California San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The CDKN2a/ARF locus expresses two partially overlapping transcripts that encode two distinct proteins, namely p14ARF (p19Arf in mouse) and p16INK4a, which present no sequence identity. Initial data obtained in mice showed that both proteins are potent tumor suppressors. In line with a tumor-suppressive role, ARF-deficient mice develop lymphomas, sarcomas, and adenocarcinomas, with a median survival rate of one year of age. In humans, the importance of ARF inactivation in cancer is less clear whereas a more obvious role has been documented for p16INK4a. Indeed, many alterations in human tumors result in the elimination of the entire locus, while the majority of point mutations affect p16INK4a. Nevertheless, specific mutations of p14ARF have been described in different types of human cancers such as colorectal and gastric carcinomas, melanoma and glioblastoma. The activity of the tumor suppressor ARF has been shown to rely on both p53-dependent and independent functions. However, novel data collected in the last years has challenged the traditional and established role of this protein as a tumor suppressor. In particular, tumors retaining ARF expression evolve to metastatic and invasive phenotypes and in humans are associated with a poor prognosis. In this review, the recent evidence and the molecular mechanisms of a novel role played by ARF will be presented and discussed, both in pathological and physiological contexts.

Indexed as

AdenocarcinomaAnimalsCyclin-Dependent Kinase Inhibitor p16HumansLymphomaMiceMice, KnockoutSarcomaTumor Suppressor Protein p14ARFCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16Tumor Suppressor Protein p14ARFactin cytoskeletonanoikisautophagyCDKN2a/ARF locuschemoresistanceFAK sumoylationtumor suppression

Identifiers

PMID30836703
PMCPMC6468759
OpenAlexW2918647555

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.