Evidence map›Paper›PMID 33050515›Full record

ArticleCancers2020

PARP1 Deficiency Reduces Tumour Growth by Decreasing E2F1 Hyperactivation: A Novel Mechanism in the Treatment of Cancer.

Pablo Iglesias, Marcos Seoane, Irene Golán, Isabel Castro-Piedras, Máximo Fraga, Víctor M Arce, Jose A Costoya

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. 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
0.3field-weighted citation impact, top 38% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. E2F1-induced upregulation ofHistology and histopathology · 2025
    Article
  4. Review
  5. Article
  6. PARP1 Promotes Heart Regeneration and Cardiomyocyte Proliferation.International journal of biological sciences · 2024
    Article
  7. Article
  8. Article
  9. 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

7 authors at 1 institution in 1 country.

Pablo IglesiasMolecular Oncology Laboratory MOL, Departamento de Fisioloxía, Centro Singular de Investigación en Medicina Molecular e Enfermidades Crónicas (CiMUS), Facultade de Medicina, Universidade de Santiago de Compostela, Instituto de Investigación Sanitaria de Santiago de Compostela (IDIS), 15782 Santiago de Compostela, Spain.ORCID 0000-0003-2506-5313
Marcos SeoaneMolecular Oncology Laboratory MOL, Departamento de Fisioloxía, Centro Singular de Investigación en Medicina Molecular e Enfermidades Crónicas (CiMUS), Facultade de Medicina, Universidade de Santiago de Compostela, Instituto de Investigación Sanitaria de Santiago de Compostela (IDIS), 15782 Santiago de Compostela, Spain.
Irene GolánMolecular Oncology Laboratory MOL, Departamento de Fisioloxía, Centro Singular de Investigación en Medicina Molecular e Enfermidades Crónicas (CiMUS), Facultade de Medicina, Universidade de Santiago de Compostela, Instituto de Investigación Sanitaria de Santiago de Compostela (IDIS), 15782 Santiago de Compostela, Spain.ORCID 0000-0003-3982-8748
Isabel Castro-PiedrasMolecular Oncology Laboratory MOL, Departamento de Fisioloxía, Centro Singular de Investigación en Medicina Molecular e Enfermidades Crónicas (CiMUS), Facultade de Medicina, Universidade de Santiago de Compostela, Instituto de Investigación Sanitaria de Santiago de Compostela (IDIS), 15782 Santiago de Compostela, Spain.
Máximo FragaDepartamento de Anatomía Patolóxica e Ciencias Forenses, Universidade de Santiago de Compostela, 15782 Santiago de Compostela, Spain.
Víctor M ArceMolecular Oncology Laboratory MOL, Departamento de Fisioloxía, Centro Singular de Investigación en Medicina Molecular e Enfermidades Crónicas (CiMUS), Facultade de Medicina, Universidade de Santiago de Compostela, Instituto de Investigación Sanitaria de Santiago de Compostela (IDIS), 15782 Santiago de Compostela, Spain.
Jose A CostoyaMolecular Oncology Laboratory MOL, Departamento de Fisioloxía, Centro Singular de Investigación en Medicina Molecular e Enfermidades Crónicas (CiMUS), Facultade de Medicina, Universidade de Santiago de Compostela, Instituto de Investigación Sanitaria de Santiago de Compostela (IDIS), 15782 Santiago de Compostela, Spain.ORCID 0000-0003-3691-6419
Universidade de Santiago de Compostela · ES

Funding

Consellería de Cultura, Educación e Ordenación Universitaria, Xunta de Galicia GPC2014/030Consellería de Cultura, Educación e Ordenación Universitaria, Xunta de Galicia INCITE08PXIB208091PRConsellería de Cultura, Educación e Ordenación Universitaria, Xunta de Galicia PRE/2011/131Consellería de Cultura, Educación e Ordenación Universitaria, Xunta de Galicia PXIB208091PREuropean Regional Development Fund ED431G/05Instituto de Salud Carlos III PI15/01129Ministerio de Ciencia e Innovación SAF2008-00543Ministerio de Ciencia e Innovación SAF2009-08629
6 · The paper itself

Abstract

In recent years, poly (ADP-ribose) polymerase (PARP) inhibitors have been evaluated for treating homologous recombination-deficient tumours, taking advantage of synthetic lethality. However, increasing evidence indicates that PARP1 exert several cellular functions unrelated with their role on DNA repair, including function as a co-activator of transcription through protein-protein interaction with E2F1. Since the RB/E2F1 pathway is among the most frequently mutated in many tumour types, we investigated whether the absence of PARP activity could counteract the consequences of E2F1 hyperactivation. Our results demonstrate that genetic ablation of

Indexed as

animal disease modelscell cycleE2F1 transcription factorgliomaneoplasmPoly (ADP-Ribose) Polymerase-1

Identifiers

PMID33050515
PMCPMC7599842
OpenAlexW3092193988

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.