Evidence map›Paper›PMID 33828085›Full record

ArticleCell death & disease2021

Silencing PTEN in the fallopian tube promotes enrichment of cancer stem cell-like function through loss of PAX2.

Angela Russo, Jose A Colina, Junlone Moy, Seth Baligod, Austin A Czarnecki, Peter Varughese, Daniel D Lantvit, Matthew J Dean, Joanna E Burdette

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Loss of phosphatase and tensin homolog (Cancer pathogenesis and therapy · 2025
    Article
  4. Navigating the Molecular Signaling: Deciphering Cancer Stem Cell Self-Renewal Pathways.International journal of molecular and cellular medicine · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
    Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. 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

9 authors at 2 institutions in 1 country.

Angela RussoDepartment of Pharmaceutical Sciences, University of Illinois at Chicago, Chicago, IL, 60607, USA. russoa@uic.edu.ORCID 0000-0002-7322-4190
Jose A ColinaDepartment of Pharmaceutical Sciences, University of Illinois at Chicago, Chicago, IL, 60607, USA.
Junlone MoyDepartment of Pharmaceutical Sciences, University of Illinois at Chicago, Chicago, IL, 60607, USA.ORCID 0000-0003-1117-3137
Seth BaligodDepartment of Pharmaceutical Sciences, University of Illinois at Chicago, Chicago, IL, 60607, USA.
Austin A CzarneckiDepartment of Pharmaceutical Sciences, University of Illinois at Chicago, Chicago, IL, 60607, USA.
Peter VarugheseDepartment of Pharmaceutical Sciences, University of Illinois at Chicago, Chicago, IL, 60607, USA.
Daniel D LantvitDepartment of Pharmaceutical Sciences, University of Illinois at Chicago, Chicago, IL, 60607, USA.
Matthew J DeanDepartment of Animal Sciences, University of Illinois Urbana-Champaign, Urbana, IL, 61801, USA.ORCID 0000-0001-5014-9311
Joanna E BurdetteDepartment of Pharmaceutical Sciences, University of Illinois at Chicago, Chicago, IL, 60607, USA.
University of Illinois Chicago · USUniversity of Illinois Urbana-Champaign · US

Funding

Microfluidic Models of Ovarian Cancer Preneoplastic LesionsR01CA240301 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI Joanna E Burdette, Jonathan Coppeta · 2019 to 2026
$4.6M
NCI NIH HHS R01 CA240301
6 · The paper itself

Abstract

High-grade serous ovarian cancer (HGSOC) is the most lethal gynecological malignancy that is primarily detected at the metastatic stage. Most HGSOC originates from the fallopian tube epithelium (FTE) and metastasizes to the ovary before invading the peritoneum; therefore, it is crucial to study disease initiation and progression using FTE-derived models. We previously demonstrated that loss of PTEN from the FTE leads to ovarian cancer. In the present study, loss of PTEN in FTE led to the enrichment of cancer stem cell markers such as LGR5, WNT4, ALDH1, CD44. Interestingly, loss of the transcription factor PAX2, which is a common and early alteration in HGSOC, played a pivotal role in the expression of cancer stem-like cells (CSC) markers and cell function. In addition, loss of PTEN led to the generation of two distinct subpopulations of cells with different CSC marker expression, tumorigenicity, and chemoresistance profiles. Taken together, these data suggest that loss of PTEN induces reprogramming of the FTE cells into a more stem-like phenotype due to loss of PAX2 and provides a model to study early events during the FTE-driven ovarian cancer tumor formation.

Indexed as

Biomarkers, TumorCarcinogenesisCarcinoma, Ovarian EpithelialFallopian TubesFemaleHumansNeoplastic Stem CellsPAX2 Transcription FactorPTEN PhosphohydrolaseBiomarkers, TumorPAX2 protein, humanPAX2 Transcription FactorPTEN Phosphohydrolase

Identifiers

PMID33828085
PMCPMC8027874
OpenAlexW3140265563

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.