Evidence map›Paper›PMID 35272015›Full record

ReviewThe international journal of biochemistry & cell biology2022

Wnt antagonist as therapeutic targets in ovarian cancer.

Krithicaa Narayanaa Y, Naveen Kumar Perumalsamy, Sudha Warrier, Lakshmi R Perumalsamy, Arun Dharmarajan

Open access · greenAbstract readReview
In one paragraph

Review in The international journal of biochemistry & cell biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Wnt3a is a promising target in colorectal cancer.Medical oncology (Northwood, London, England) · 2023
    Review
  8. Review
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 3 institutions in 2 countries.

Krithicaa Narayanaa YDepartment of Biomedical Sciences, Faculty of Biomedical Sciences, Technology & Research, Sri Ramachandra Institute of Higher Education and Research (DU), Tamil Nadu 600116, India.
Naveen Kumar PerumalsamyDepartment of Biomedical Sciences, Faculty of Biomedical Sciences, Technology & Research, Sri Ramachandra Institute of Higher Education and Research (DU), Tamil Nadu 600116, India.
Sudha WarrierDivision of Cancer Stem Cells and Cardiovascular Regeneration, School of Regenerative Medicine, Manipal Academy of Higher Education (MAHE), Bangalore 560065, India; Cuor Stem Cellutions Pvt Ltd, Manipal Institute of Regenerative Medicine, Manipal Academy of Higher Education (MAHE), Bangalore 560065, India.
Lakshmi R PerumalsamyDepartment of Biomedical Sciences, Faculty of Biomedical Sciences, Technology & Research, Sri Ramachandra Institute of Higher Education and Research (DU), Tamil Nadu 600116, India. Electronic address: lakshmi.revathi@gmail.com.
Arun DharmarajanDepartment of Biomedical Sciences, Faculty of Biomedical Sciences, Technology & Research, Sri Ramachandra Institute of Higher Education and Research (DU), Tamil Nadu 600116, India; Stem Cell and Cancer Biology Laboratory, Curtin University, Perth, WA, Australia; School of Pharmacy and Biomedical Sciences, Curtin University, Perth, WA 6102, Australia; Curtin Health and Innovation Research Institute, Curtin University, Perth, WA 6102, Australia. Electronic address: a.dharmarajan@sriramachandra.edu.in.
Sri Ramachandra Institute of Higher Education and Research · INCurtin University · AUManipal Academy of Higher Education · IN

Funding

DBT-Wellcome Trust India Alliance IA/E/14/1/501793Wellcome Trust
6 · The paper itself

Abstract

Ovarian cancer is a fatal malignancy in women with a low survival rate that demands new therapeutic paradigms. Cancer cells acquire various exclusive alterations to proliferate, invade, metastasize, and escape cell death, acting independently of growth-inducing or growth-inhibiting signals. The nature of cellular signaling in tumorigenesis is interwoven. Wnt signaling is an evolutionarily conserved signaling cascade that has been shown to regulate ovarian cancer pathogenesis. The molecular mechanism of Wnt signaling underlying the development of ovarian cancer, drug resistance, and relapse is not completely understood. Extracellularly secreted Wnt signaling inhibitors are crucial regulators of ovarian cancer tumorigenesis and malignant properties of cancer stem cells. Wnt inhibitors arbitrated modifications affecting Wnt pathway proteins on the cell membranes, in the cytoplasm, and in the nucleus have been shown to span essential contributions in the initiation, progression, and chemoresistance of ovarian cancer. Although many extrinsic inhibitors developed targeting the downstream components of the Wnt signaling pathway, investigating the molecular mechanisms of endogenous secreted inhibitors might substantiate prognostic or therapeutic biomarkers development. Given the importance of Wnt signaling in ovarian cancer, more systematic studies combined with clinical studies are requisite to probe the precise mechanistic interactions of Wnt antagonists in ovarian cancer. This review outlines the latest progress on the Wnt antagonists and ovarian cancer-specific regulators such as micro-RNAs, small molecules, and drugs regulating these Wnt antagonists in ovarian tumourigenesis.

Indexed as

Neoplasm Recurrence, LocalOvarian NeoplasmsCarcinoma, Ovarian EpithelialCell Transformation, NeoplasticFemaleHumansWnt ProteinsWnt Signaling PathwayWnt ProteinsBiomarkerCancer stem cellNovel targetsOvarian cancerWnt antagonistsWnt signaling

Identifiers

PMID35272015
PMCPMC7616886
OpenAlexW4221077489

What OpenQuestion holds

Textmetadata
LicenceTDM
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.