Evidence map›Paper›PMID 29958137›Full record

ArticleNeoplasia (New York, N.Y.)2018

Cooperation Between Pten and Smad4 in Murine Salivary Gland Tumor Formation and Progression.

Yu Cao, Han Liu, Liwei Gao, Ling Lu, Li Du, Han Bai, Jiang Li, Sherif Said, Xiao-Jing Wang, John Song and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neoplasia (New York, N.Y.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Current State of Knowledge on Salivary Gland Cancers.Critical reviews in oncogenesis · 2018
    Review
  9. 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

14 authors at 5 institutions in 2 countries.

Yu CaoLaboratory of Precision Oncology, School of Pharmacy, China Medical University, Shenyang, Liaoning, China; Department of Otolaryngology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Han LiuDepartment of Oral Pathology, Dalian Medical University, Dalian, Liaoning, China.
Liwei GaoDepartment of Radiation Oncology, China Japan Friendship Hospital, Beijing, China.
Ling LuDepartment of Otolaryngology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Li DuDepartment of Otolaryngology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Department of Otolaryngology, The Fourth Affiliated Hospital, China Medical University, Shenyang, Liaoning, China.
Han BaiDepartment of Oral Pathology, Dalian Medical University, Dalian, Liaoning, China.
Jiang LiDepartment of Oral Pathology, 9th People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Key Laboratory of Stomatology, Shanghai, China.
Sherif SaidDepartment of Pathology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Xiao-Jing WangDepartment of Pathology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
John SongDepartment of Otolaryngology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Natalie SerkovaDepartment of Anesthesiology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Minjie WeiLaboratory of Precision Oncology, School of Pharmacy, China Medical University, Shenyang, Liaoning, China.
Jing XiaoDepartment of Oral Pathology, Dental School, China Medial University, Shenyang, Liaoning, China; Department of Oral Pathology, Dalian Medical University, Dalian, Liaoning, China. Electronic address: xiaoj@dlmedu.edu.cn.
Shi-Long LuDepartment of Otolaryngology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Laboratory of Precision Oncology, School of Pharmacy, China Medical University, Shenyang, Liaoning, China; Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Department of Dermatology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA. Electronic address: shi-long.lu@ucdenver.edu.
University of Colorado Anschutz Medical Campus · USChina Medical University · CNDalian Medical University · CNChina-Japan Friendship Hospital · CNShanghai Jiao Tong University · CN

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Transgenic and Gene Targeting CoreP30AR057212 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI NORRIS, DAVID A. · 2009 to 2018
$6.2M
The Role of PI3K Pathway in Head and Neck Cancer Invasion and MetastasisR01DE021788 · NIDCR · UNIVERSITY OF COLORADO DENVER · PI LU, SHI-LONG · 2011 to 2015
$1.8M
NIAMS NIH HHS P30 AR057212NIDCR NIH HHS R01 DE021788
6 · The paper itself

Abstract

Salivary gland tumor (SGT) is a rare tumor type, which exhibits broad-spectrum phenotypic, biological, and clinical heterogeneity. Currently, the molecular mechanisms that cause SGT pathogenesis remain poorly understood. A lack of animal models that faithfully recapitulate the naturally occurring process of human SGTs has hampered research progress on this field. In this report, we developed an inducible keratin 5-driven conditional knockout mouse model to delete gene(s) of interest in murine salivary gland upon local RU486 delivery. We have deleted two major tumor suppressors, Pten, a negative regulator of the PI3K pathway, and Smad4, the central signaling mediator of TGFβ pathway, in the murine salivary gland. Our results have shown that deletion of either Pten or Smad4 in murine salivary gland resulted in pleomorphic adenomas, the most common tumor in human SGT patients. Deletion of both Pten and Smad4 in murine salivary gland developed several malignancies, with salivary adenoid cystic carcinoma (SACC) being the most frequently seen. Molecular characterization showed that SACC exhibited mTOR activation and TGFβ1 overexpression. Examination of human SGT clinical samples revealed that loss of Pten and Smad4 is common in human SACC samples, particularly in the most aggressive solid form, and is correlated with survival of SACC patients, highlighting the human relevance of the murine models. In summary, our results offer significant insight into synergistic role of Pten and Smad4 in SGT, providing a rationale for targeting mTOR and/or TGFβ signaling to control SGT formation and progression.

Indexed as

AnimalsCarcinoma, Adenoid CysticDisease ProgressionHumansMiceMice, Inbred C57BLMifepristonePhosphatidylinositol 3-KinasesPTEN PhosphohydrolaseSalivary Gland NeoplasmsSalivary GlandsSignal TransductionSmad4 ProteinTOR Serine-Threonine KinasesTransforming Growth Factor betaMifepristonePhosphatidylinositol 3-KinasesPTEN PhosphohydrolasePten protein, mouseSmad4 ProteinSmad4 protein, mouseTOR Serine-Threonine KinasesTransforming Growth Factor beta

Identifiers

PMID29958137
PMCPMC6031150
OpenAlexW2809951856

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.