Evidence map›Paper›PMID 32932697›Full record

ReviewInternational journal of molecular sciences2020

Inhibition of DNA Repair in Cancer Therapy: Toward a Multi-Target Approach.

Samuele Lodovichi, Tiziana Cervelli, Achille Pellicioli, Alvaro Galli

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 49 citations in OpenAlex.

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  18. Inhibition of DNA Repair Enzymes as a Valuable Pharmaceutical Approach.International journal of molecular sciences · 2023
    Article
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  20. Article
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 2 institutions in 1 country.

Samuele LodovichiBioscience Department, University of Milan, Via Celoria 26, 20131 Milan, Italy.ORCID 0000-0002-6780-7410
Tiziana CervelliYeast Genetics and Genomics Group, Laboratory of Functional Genetics and Genomics, Institute of Clinical Physiology CNR, Via Moruzzi 1, 56125 Pisa, Italy.ORCID 0000-0002-9997-1741
Achille PellicioliBioscience Department, University of Milan, Via Celoria 26, 20131 Milan, Italy.ORCID 0000-0002-1528-9009
Alvaro GalliYeast Genetics and Genomics Group, Laboratory of Functional Genetics and Genomics, Institute of Clinical Physiology CNR, Via Moruzzi 1, 56125 Pisa, Italy.ORCID 0000-0002-9091-5639
Istituto di Fisiologia Clinica · ITUniversity of Milan · IT

Funding

Associazione Italiana per la Ricerca sul Cancro IG19917 to APFondazione Pisa 127/16
6 · The paper itself

Abstract

Alterations in DNA repair pathways are one of the main drivers of cancer insurgence. Nevertheless, cancer cells are more susceptible to DNA damage than normal cells and they rely on specific functional repair pathways to survive. Thanks to advances in genome sequencing, we now have a better idea of which genes are mutated in specific cancers and this prompted the development of inhibitors targeting DNA repair players involved in pathways essential for cancer cells survival. Currently, the pivotal concept is that combining the inhibition of mechanisms on which cancer cells viability depends is the most promising way to treat tumorigenesis. Numerous inhibitors have been developed and for many of them, efficacy has been demonstrated either alone or in combination with chemo or radiotherapy. In this review, we will analyze the principal pathways involved in cell cycle checkpoint and DNA repair focusing on how their alterations could predispose to cancer, then we will explore the inhibitors developed or in development specifically targeting different proteins involved in each pathway, underscoring the rationale behind their usage and how their combination and/or exploitation as adjuvants to classic therapies could help in patients clinical outcome.

Indexed as

AnimalsAntineoplastic AgentsCarcinogenesisCell Cycle CheckpointsCell SurvivalDNA DamageDNA RepairHumansNeoplasmsSignal TransductionAntineoplastic Agentscancer therapycell cycle checkpointDNA repairDNA repair inhibitorssynthetic lethality

Identifiers

PMID32932697
PMCPMC7554826
OpenAlexW3086680380

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.