Evidence map›Paper›PMID 34981193›Full record

ReviewJournal of cancer research and clinical oncology2022

Dual-specificity phosphatases: therapeutic targets in cancer therapy resistance.

Zahra Zandi, Bahareh Kashani, Zivar Alishahi, Atieh Pourbagheri-Sigaroodi, Fatemeh Esmaeili, Seyed H Ghaffari, Davood Bashash, Majid Momeny

Open access · greenAbstract readReview
In one paragraph

Review in Journal of cancer research and clinical oncology, 2022. 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
3.8field-weighted citation impact, top 5% 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, 47 citations in OpenAlex.

  1. Review
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  9. DUSP8 as a regulator of glioblastoma stem-like cell contribution to tumor vascularization.Journal of experimental & clinical cancer research : CR · 2025
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  11. Review
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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

8 authors at 3 institutions in 1 country.

Zahra ZandiHematology/Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0000-0001-5504-2417
Bahareh KashaniHematology/Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Zivar AlishahiHematology/Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Atieh Pourbagheri-SigaroodiDepartment of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Fatemeh EsmaeiliHematology/Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Seyed H GhaffariHematology/Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Davood BashashDepartment of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Majid MomenyHematology/Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran. majid.momeny@hotmail.com.
Tehran University of Medical Sciences · IRShahid Beheshti University of Medical Sciences · IRStem Cell Technology Research Center · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTherapy resistance is the principal obstacle to achieving cures in cancer patients and its successful tackling requires a deep understanding of the resistance mediators. Increasing evidence indicates that tumor phosphatases are novel and druggable targets in translational oncology and their modulation may hinder tumor growth and motility and potentiate therapeutic sensitivity in various neoplasms via regulation of various signal transduction pathways. Dual-specificity phosphatases (DUSPs) are key players of cell growth, survival and death and have essential roles in tumor initiation, malignant progression and therapy resistance through regulation of the MAPK signaling pathway. In this review, different aspects of DUSPs are discussed.

methodsA comprehensive literature review was performed using various websites including PubMed.

resultsWe provide mechanistic insights into the roles of well-known DUSPs in resistance to a wide range of cancer therapeutic approaches including chemotherapy, radiation and molecular targeted therapy in human malignancies. Moreover, we discuss the development of DUSP modulators, with a focus on DUSP1 and 6 inhibitors. Ultimately, the preclinical investigations of small molecule inhibitors of DUSP1 and 6 are outlined.

conclusionEmerging evidence indicates that the DUSP family is aberrantly expressed in human malignancies and plays critical roles in determining sensitivity to a wide range of cancer therapeutic strategies through regulation of the MAPK signaling pathways. Consequently, targeting DUSPs and their downstream molecules can pave the way for more effective cancer therapies.

Indexed as

Antineoplastic AgentsBenzofuransCarcinogenesisDrug Resistance, NeoplasmDual Specificity Phosphatase 1Dual Specificity Phosphatase 6Gene Expression Regulation, NeoplasticHumansImidazolesJNK Mitogen-Activated Protein KinasesMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Molecular Targeted TherapyNeoplasmsp38 Mitogen-Activated Protein KinasesAntineoplastic AgentsBenzofuransDual Specificity Phosphatase 1Dual Specificity Phosphatase 6DUSP1 protein, humanDUSP6 protein, humanImidazolesJNK Mitogen-Activated Protein KinasesMAPK1 protein, humanMAPK3 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NSC 357756p38 Mitogen-Activated Protein KinasesCancer therapy resistanceDUSPSmall molecule DUSP inhibitors

Identifiers

PMID34981193
PMCPMC11800885
OpenAlexW4205972693

What OpenQuestion holds

Textmetadata
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.