Evidence map›Paper›PMID 32692487›Full record

ReviewCancer medicine2020

MASTL: A novel therapeutic target for Cancer Malignancy.

Iram Fatima, Amar B Singh, Punita Dhawan

Open access · goldAbstract readReview
In one paragraph

Review in Cancer medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. IL-22 regulates MASTL expression in intestinal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. The ATM-E6AP-MASTL axis mediates DNA damage checkpoint recovery.bioRxiv : the preprint server for biology · 2023
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  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

3 authors at 1 institution in 1 country.

Iram FatimaVA Nebraska-Western Iowa Health Care System, Omaha, NE, USA.
Amar B SinghVA Nebraska-Western Iowa Health Care System, Omaha, NE, USA.
Punita DhawanVA Nebraska-Western Iowa Health Care System, Omaha, NE, USA.ORCID 0000-0003-3434-8155
VA Nebraska Western Iowa Health Care System · US

Funding

UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Apar Kishor Ganti · 1985 to 2026
$55.0M
Mastl, a novel therapeutic target in Colon CancerR21CA216746 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI DHAWAN, PUNITA · 2018 to 2019
$358k
Role of Claudin-1 in Colon CancerI01BX002086 · VA · VETERANS HEALTH ADMINISTRATION · PI DHAWAN, PUNITA · 2013 to 2022
–
Role of Claudin-2 in Colon TumorigenesisI01BX002761 · VA · OMAHA VA MEDICAL CENTER · PI SINGH, AMAR B · 2016 to 2023
–
BLRD VA I01 BX002086BLRD VA I01 BX002761NCI NIH HHS P30 CA036727NCI NIH HHS R21 CA216746
6 · The paper itself

Abstract

Targeting mitotic kinases is an emerging anticancer approach with promising preclinical outcomes. Microtubule-associated serine/threonine kinase like (MASTL), also known as Greatwall (Gwl), is an important mitotic kinase that regulates mitotic progression of normal or transformed cells by blocking the activity of tumor suppressor protein phosphatase 2A (PP2A). MASTL upregulation has now been detected in multiple cancer types and associated with aggressive clinicopathological features. Apart, an aberrant MASTL activity has been implicated in oncogenic transformation through the development of chromosomal instability and alteration of key oncogenic signaling pathways. In this regard, recent publications have revealed potential role of MASTL in the regulation of AKT/mTOR and Wnt/β-catenin signaling pathways, which may be independent of its regulation of PP2A-B55 (PP2A holoenzyme containing a B55-family regulatory subunit). Taken together, MASTL kinase has emerged as a novel target for cancer therapeutics, and hence development of small molecule inhibitors of MASTL may significantly improve the clinical outcomes of cancer patients. In this article, we review the role of MASTL in cancer progression and the current gaps in this knowledge. We also discuss potential efficacy of MASTL expression for cancer diagnosis and therapy.

Indexed as

CDC2 Protein KinaseCell Transformation, NeoplasticChromosomal InstabilityCyclin B1Disease ProgressionDNA DamageDNA RepairGlycogen Synthase Kinase 3 betaHumansIntercellular Signaling Peptides and ProteinsMicrotubule-Associated ProteinsMitosisMolecular Targeted TherapyNeoplasmsPhosphoproteinsPhosphorylationCCNB1 protein, humanCDC2 Protein KinaseCDK1 protein, humancyclic AMP-regulated phosphoprotein 19Cyclin B1endosulfineGlycogen Synthase Kinase 3 betaGSK3B protein, humanIntercellular Signaling Peptides and ProteinsMASTL protein, humanMicrotubule-Associated ProteinsMTOR protein, humanPhosphoproteinsProtein Phosphatase 2Protein Serine-Threonine KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCANCERCELL cyclechemoresistanceMASTL

Identifiers

PMID32692487
PMCPMC7476815
OpenAlexW3044311628

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.