Evidence map›Paper›PMID 27409646›Full record

ReviewEndocrinology2016

Minireview: Lymphangioleiomyomatosis (LAM): The "Other" Steroid-Sensitive Cancer.

Hen Prizant, Stephen R Hammes

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Endocrinology, 2016. 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 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  8. Review
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  16. Review
  17. Review
  18. Article
  19. New Insights into the Regulation of mTOR Signaling via CaInternational journal of molecular sciences · 2023
    Review
  20. Lymphangioleiomyomatosis: a metastatic lung disease.American journal of physiology. Cell physiology · 2023
    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

2 authors at 1 institution in 1 country.

Hen PrizantDepartments of Medicine and Pharmacology, University of Rochester Medical Center, Rochester, New York 14642.
Stephen R HammesDepartments of Medicine and Pharmacology, University of Rochester Medical Center, Rochester, New York 14642.
University of Rochester Medical Center · US

Funding

Estrogen Signaling in a Mouse Model for LymphangioleiomyomatosisR01CA193583 · NCI · UNIVERSITY OF ROCHESTER · PI HAMMES, STEPHEN R. · 2016 to 2020
$1.7M
NCI NIH HHS R01 CA193583
6 · The paper itself

Abstract

Lymphangioleiomyomatosis (LAM) is a devastating rare lung disease affecting primarily childbearing age women in which tumors consisting of abnormal smooth-muscle-like cells grow within the lungs and progressively lead to loss of pulmonary function. LAM cells metastasize to the lungs, predominantly through the lymphatics; however, the source of the LAM cell is still unknown. LAM cells contain inactivating mutations in genes encoding tuberous sclerosis 1 or 2, proteins that normally limit cell growth through suppression of mammalian target of rapamycin complex 1. As of today, sirolimus (an mammalian target of rapamycin complex 1 inhibitor) is the only treatment, available for LAM patients that is approved by the Food and Drug Administration; however, this drug and others in its class provide stabilization but not remission of LAM. One of the biggest problems in treating LAM is that both the origin of the LAM cells and the mechanism of the sexual dimorphism in LAM are still not understood. LAM cells express estrogen and progesterone receptors, and lung function declines during periods of high circulating estrogen levels. Moreover, numerous basic research studies find that estrogen is a key driving force in LAM cell proliferation, migration, and metastasis. In this review, we highlight recent insights regarding the role of steroid hormones in LAM and discuss possible explanations for the profound female sexual dimorphism of LAM.

Indexed as

Cathepsin KEstrogensFemaleHumansLeiomyomaLeukocyte ElastaseLungLymphangioleiomyomatosisLymphatic MetastasisMatrix MetalloproteinasesProgesteroneSelective Estrogen Receptor ModulatorsSex CharacteristicsUterine NeoplasmsUterusCathepsin KEstrogensLeukocyte ElastaseMatrix MetalloproteinasesProgesteroneSelective Estrogen Receptor Modulators

Identifiers

PMID27409646
PMCPMC5007898
OpenAlexW2507477761

What OpenQuestion holds

Textmetadata
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.