Evidence map›Paper›PMID 26973247›Full record

ArticleOncogene2016

Effects of Kras activation and Pten deletion alone or in combination on MUC1 biology and epithelial-to-mesenchymal transition in ovarian cancer.

L Zhang, T Ma, J Brozick, K Babalola, R Budiu, G Tseng, A M Vlad

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. The multifaced role and therapeutic regulation of autophagy in ovarian cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  7. Article
  8. Resistance to mutant KRASExperimental cell research · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
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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

7 authors at 2 institutions in 1 country.

L ZhangDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.
T MaDepartment of Biostatistics, University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA, USA.
J BrozickMagee-Womens Research Institute, Pittsburgh, PA, USA.
K BabalolaDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.
R BudiuDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.
G TsengDepartment of Biostatistics, University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA, USA.
A M VladDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.
University of Pittsburgh · USMagee-Womens Research Institute · US

Funding

MUC1 Roles in ovarian cancer pathogenesis and immune therapyR01CA163462 · NCI · MAGEE-WOMEN'S RES INST AND FOUNDATION · PI VLAD, ANDA M · 2012 to 2016
$1.4M
NCI NIH HHS R01 CA163462
6 · The paper itself

Abstract

Mucin1 (MUC1) is an epithelial glycoprotein overexpressed in ovarian cancer and actively involved in tumor cell migration and metastasis. Using novel in vitro and in vivo MUC1-expressing conditional (Cre-loxP) ovarian tumor models, we focus here on MUC1 biology and the roles of Kras activation and Pten deletion during cell transformation and epithelial-to-mesenchymal transition (EMT). We generated several novel murine ovarian cancer cell lines derived from the ovarian surface epithelia (OSE) of mice with conditional mutations in Kras, Pten or both. In addition, we also generated several tumor-derived new cell lines that reproduce the original tumor phenotype in vivo and mirror late stage metastatic disease. Our results demonstrate that de novo activation of oncogenic Kras does not trigger increased proliferation, cellular transformation or EMT, and prevents MUC1 upregulation. In contrast, Pten deletion accelerates cell proliferation, triggers cellular transformation in vitro and in vivo, and stimulates MUC1 expression. Ovarian tumor-derived cell lines MKP-Liver and MKP-Lung cells reproduce in vivo EMT and represent the first immune competent mouse model for distant hematogenous spread. Whole genome microarray expression analysis using tumor and OSE-derived cell lines reveal a 121 gene signature associated with EMT and metastasis. When applied to n=542 cases from The Cancer Genome Atlas (TCGA) ovarian cancer dataset, the gene signature identifies a patient subset with decreased survival (P=0.04). Using an extensive collection of novel murine cell lines we have identified distinct roles for Kras and Pten on MUC1 and EMT in vivo and in vitro. The data has implications for future design of combination therapies targeting Kras mutations, Pten deletions and MUC1 vaccines.

Indexed as

AnimalsCell Line, TumorCell ProliferationDisease Models, AnimalEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMiceMucin-1Ovarian NeoplasmsProto-Oncogene Proteins p21(ras)PTEN PhosphohydrolaseHras protein, mousemuc1 protein, mouseMucin-1Proto-Oncogene Proteins p21(ras)PTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID26973247
PMCPMC5023457
OpenAlexW2295196607

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.