Evidence map›Paper›PMID 32958072›Full record

ReviewJournal of hematology & oncology2020

A WEE1 family business: regulation of mitosis, cancer progression, and therapeutic target.

Andrea Ghelli Luserna di Rorà, Claudio Cerchione, Giovanni Martinelli, Giorgia Simonetti

Open access · goldAbstract readReview
In one paragraph

Review in Journal of hematology & oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 202 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
202citing papers in PubMed, 4 pooled it
16.6field-weighted citation impact, top 1% 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

202 citing papers in PubMed, 4 syntheses or guidelines pooled it, 299 citations in OpenAlex.

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142 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Andrea Ghelli Luserna di RoràBiosciences Laboratory (Onco-hematology Unit), Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Via P. Maroncelli 40, 47014, Meldola, FC, Italy.
Claudio CerchioneBiosciences Laboratory (Onco-hematology Unit), Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Via P. Maroncelli 40, 47014, Meldola, FC, Italy.
Giovanni MartinelliBiosciences Laboratory (Onco-hematology Unit), Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Via P. Maroncelli 40, 47014, Meldola, FC, Italy.
Giorgia SimonettiBiosciences Laboratory (Onco-hematology Unit), Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Via P. Maroncelli 40, 47014, Meldola, FC, Italy. giorgia.simonetti@irst.emr.it.ORCID 0000-0001-6954-969X
Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The inhibition of the DNA damage response (DDR) pathway in the treatment of cancer has recently gained interest, and different DDR inhibitors have been developed. Among them, the most promising ones target the WEE1 kinase family, which has a crucial role in cell cycle regulation and DNA damage identification and repair in both nonmalignant and cancer cells. This review recapitulates and discusses the most recent findings on the biological function of WEE1/PKMYT1 during the cell cycle and in the DNA damage repair, with a focus on their dual role as tumor suppressors in nonmalignant cells and pseudo-oncogenes in cancer cells. We here report the available data on the molecular and functional alterations of WEE1/PKMYT1 kinases in both hematological and solid tumors. Moreover, we summarize the preclinical information on 36 chemo/radiotherapy agents, and in particular their effect on cell cycle checkpoints and on the cellular WEE1/PKMYT1-dependent response. Finally, this review outlines the most important pre-clinical and clinical data available on the efficacy of WEE1/PKMYT1 inhibitors in monotherapy and in combination with chemo/radiotherapy agents or with other selective inhibitors currently used or under evaluation for the treatment of cancer patients.

Indexed as

Antineoplastic AgentsCell CycleCell Cycle ProteinsChemoradiotherapyDisease ProgressionDNA RepairDNA ReplicationDrug Resistance, NeoplasmDrug SynergismGenomic InstabilityHematologic NeoplasmsHumansMembrane ProteinsMitosisMutationNeoplasm ProteinsadavosertibAntineoplastic AgentsCell Cycle ProteinsMembrane ProteinsNeoplasm ProteinsPKMYT1 protein, humanProtein Kinase InhibitorsProtein Serine-Threonine KinasesProtein-Tyrosine KinasesPyrazolesPyrimidinonesTumor Suppressor ProteinsWEE1 protein, humanCell cycleDNA repairPKMYT1Pseudo-oncogeneTumor suppressorWEE1WEE1 family kinases

Identifiers

PMID32958072
PMCPMC7507691
OpenAlexW3087121815

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.