Evidence map›Paper›PMID 31930277›Full record

ArticleGenetics and molecular biology2019

DNA repair genes in astrocytoma tumorigenesis, progression and therapy resistance.

Juliana Ferreira de Sousa, Rodolfo Bortolozo Serafim, Laura Marise de Freitas, Carla Raquel Fontana, Valeria Valente

Open access · goldAbstract read
In one paragraph

Article in Genetics and molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.3field-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

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Research progress on the role of the NEIL family in cancer.Frontiers in cell and developmental biology · 2025
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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

5 authors at 4 institutions in 3 countries.

Juliana Ferreira de SousaRadiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, U.S.A.
Rodolfo Bortolozo SerafimUniversidade de São Paulo, Faculdade de Medicina de Ribeirão Preto, Departamento de Biologia Celular e Molecular e Bioagentes Patogênicos, Universidade de São Paulo, Ribeirão Preto, SP, Brazil.
Laura Marise de FreitasUniversidade de São Paulo, Instituto de Química, Departamento de Bioquímica, São Paulo, SP, Brazil.
Carla Raquel FontanaUniversidade Estadual Paulista "Júlio de Mesquita Filho" (UNESP), Faculdade de Ciências Farmacêuticas, Departamento de Análises Clínicas, Araraquara, SP, Brazil.
Valeria ValenteUniversidade de São Paulo, Faculdade de Medicina de Ribeirão Preto, Departamento de Biologia Celular e Molecular e Bioagentes Patogênicos, Universidade de São Paulo, Ribeirão Preto, SP, Brazil.ORCID http://orcid.org/0000-0002-3942-7744
Universidade de Ribeirão Preto · BRNational Institutes of Health · USUniversidade de São Paulo · BRUniversidade Estadual Paulista (Unesp) · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is the most common and malignant type of primary brain tumor, showing rapid development and resistance to therapies. On average, patients survive 14.6 months after diagnosis and less than 5% survive five years or more. Several pieces of evidence have suggested that the DNA damage signaling and repair activities are directly correlated with GBM phenotype and exhibit opposite functions in cancer establishment and progression. The functions of these pathways appear to present a dual role in tumorigenesis and cancer progression. Activation and/or overexpression of ATRX, ATM and RAD51 genes were extensively characterized as barriers for GBM initiation, but paradoxically the exacerbated activity of these genes was further associated with cancer progression to more aggressive stages. Excessive amounts of other DNA repair proteins, namely HJURP, EXO1, NEIL3, BRCA2, and BRIP, have also been connected to proliferative competence, resistance and poor prognosis. This scenario suggests that these networks help tumor cells to manage replicative stress and treatment-induced damage, diminishing genome instability and conferring therapy resistance. Finally, in this review we address promising new drugs and therapeutic approaches with potential to improve patient survival. However, despite all technological advances, the prognosis is still dismal and further research is needed to dissect such complex mechanisms.

Identifiers

PMID31930277
PMCPMC7198033
OpenAlexW2996644410

What OpenQuestion holds

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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.