Evidence map›Paper›PMID 39966556›Full record

ReviewOncogene2025

Deletion of 17p in cancers: Guilt by (p53) association.

Francisca van Kampen, Abigail Clark, Jamie Soul, Aditi Kanhere, Mark A Glenn, Andrew R Pettitt, Nagesh Kalakonda, Joseph R Slupsky

Abstract readReview
In one paragraph

Review in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Frontiers in oncology · 2025
    Review
  12. Transcriptional rewiring in cancer driven byFrontiers in pharmacology · 2025
    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

8 authors.

Francisca van KampenDepartment of Molecular and Clinical Cancer Medicine, Institute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool, UK.
Abigail ClarkDepartment of Molecular and Clinical Cancer Medicine, Institute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool, UK.ORCID http://orcid.org/0009-0005-1688-6023
Jamie SoulComputational Biology Facility, University of Liverpool, Liverpool, UK.
Aditi KanhereDepartment of Molecular and Clinical Cancer Medicine, Institute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool, UK.ORCID http://orcid.org/0000-0001-5464-9006
Mark A GlennDepartment of Molecular and Clinical Cancer Medicine, Institute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool, UK.ORCID http://orcid.org/0009-0005-2490-2740
Andrew R PettittDepartment of Molecular and Clinical Cancer Medicine, Institute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool, UK.
Nagesh KalakondaDepartment of Molecular and Clinical Cancer Medicine, Institute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool, UK.ORCID http://orcid.org/0000-0002-5300-1360
Joseph R SlupskyDepartment of Molecular and Clinical Cancer Medicine, Institute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool, UK. jslupsky@liverpool.ac.uk.ORCID http://orcid.org/0000-0002-7410-9004

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Monoallelic deletion of the short arm of chromosome 17 (del17p) is a recurrent abnormality in cancers with poor outcomes. Best studied in relation to haematological malignancies, associated functional outcomes are attributed mainly to loss and/or dysfunction of TP53, which is located at 17p13.1, but the wider impact of deletion of other genes located on 17p is poorly understood. 17p is one of the most gene-dense regions of the genome and includes tumour suppressor genes additional to TP53, genes essential for cell survival and proliferation, as well as small and long non-coding RNAs. In this review we utilise a data-driven approach to demarcate the extent of 17p deletion in multiple cancers and identify a common loss-of-function gene signature. We discuss how the resultant loss of heterozygosity (LOH) and haploinsufficiency may influence cell behaviour but also identify vulnerabilities that can potentially be exploited therapeutically. Finally, we highlight how emerging animal and isogenic cell line models of del17p can provide critical biological insights for cancer cell behaviour.

Indexed as

Chromosome DeletionChromosomes, Human, Pair 17NeoplasmsTumor Suppressor Protein p53AnimalsHaploinsufficiencyHumansLoss of HeterozygositySmith-Magenis SyndromeTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID39966556
PMCPMC11876076

What OpenQuestion holds

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Registered trials

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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.