Evidence map›Paper›PMID 24784716›Full record

ArticleReproductive sciences (Thousand Oaks, Calif.)2014

Telomerase expression abrogates rapamycin-induced irreversible growth arrest of uterine fibroid smooth muscle cells.

Guangli Suo, Anil Sadarangani, Wingchung Tang, Bryan D Cowan, Jean Y J Wang

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Reproductive sciences (Thousand Oaks, Calif.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03500367 (Efficacy and Safety of Rapamycin), which is not on this map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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.

NCT03500367 phase4unknown statusnot on this mapstarted 2018, after this paper: background citation

Efficacy and Safety of Rapamycin (Sirolimus) in the Treatment of Symptomatic Uterine Fibroids and Leiomyomatosis

TypeinterventionalSponsorPeking Union Medical College HospitalRan2018 to 2022Enrolled25ConditionsUterine FibroidsArmsrapamycin
3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. 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

5 authors at 3 institutions in 1 country.

Guangli SuoDepartment of Medicine, Division of Hematology/Oncology, Moores Cancer Center, University of California, San Diego School of Medicine, La Jolla, CA, USA glsuo2013@sinano.ac.cn.
Anil SadaranganiDepartment of Medicine, Division of Hematology/Oncology, Moores Cancer Center, University of California, San Diego School of Medicine, La Jolla, CA, USA.
Wingchung TangDepartment of Medicine, Division of Hematology/Oncology, Moores Cancer Center, University of California, San Diego School of Medicine, La Jolla, CA, USA.
Bryan D CowanDepartment of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson, MS, USA.
Jean Y J WangDepartment of Medicine, Division of Hematology/Oncology, Moores Cancer Center, University of California, San Diego School of Medicine, La Jolla, CA, USA jywang@ucsd.edu.
University of California, San Diego · USMoores Cancer CenterUniversity of Mississippi Medical Center · US

Funding

VIRAL MALIGNANCYP30CA023100 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DIANE M SIMEONE · 1985 to 2026
$124.9M
Protein Tyrosine Kinases in Leiomyomata UteriR01HD046225 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI WANG, JEAN Y.J. · 2003 to 2007
$1.9M
NCI NIH HHS P30 CA023100NICHD NIH HHS R01 HD046225
6 · The paper itself

Abstract

Uterine fibroids are the most common solid tumors found in women of reproductive age. It has been reported that deregulation of the mammalian target of rapamycin (mTOR) pathway plays an important role in the etiology of leiomyoma. Here, we investigated the effect of rapamycin, an inhibitor of mTORC1, on the growth of primary fibroid smooth muscle cells (fSMCs) and human telomerase reverse transcriptase (hTERT)-transduced and immortalized fSMCs. With the primary fSMCs, a 24-hour treatment with rapamycin was sufficient to trigger a growth arrest that was not reversible upon drug removal. By contrast, the growth inhibitory effect of rapamycin on the hTERT-transduced fSMCs was readily reversible, as these cells resumed proliferation upon the withdrawal of the drug. These results suggest that rapamycin-induced irreversible growth arrest of fSMCs is dependent on the senescence barrier that is abrogated by the ectopic expression of telomerase.

Indexed as

AnimalsCell Cycle CheckpointsCell Line, TransformedCells, CulturedFemaleGrowth InhibitorsHumansLeiomyomaMechanistic Target of Rapamycin Complex 1MiceMice, KnockoutMultiprotein ComplexesMyocytes, Smooth MuscleSirolimusTelomeraseTOR Serine-Threonine KinasesGrowth InhibitorsMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesSirolimusTelomeraseTERT protein, humanTOR Serine-Threonine Kinasesleiomyomarapamycintelomerase

Identifiers

PMID24784716
PMCPMC4212341
OpenAlexW1989879220

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.