Evidence map›Paper›PMID 27698899›Full record

ReviewJournal of Cancer2016

Is mTOR Inhibitor Good Enough for Treatment All Tumors in TSC Patients?

Samy L Habib, Noor Y Al-Obaidi, Maciej Nowacki, Katarzyna Pietkun, Barbara Zegarska, Tomasz Kloskowski, Wojciech Zegarski, Tomasz Drewa, Edward A Medina, Zhenze Zhao and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Journal of Cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

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  14. Evolving Treatment Paradigms in Non-clear Cell Kidney Cancer.Current treatment options in oncology · 2018
    Review
  15. Inhibiting 4EBP1 in Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Review
  16. 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

11 authors at 1 institution in 1 country.

Samy L HabibGeriatric Research Education and Clinical Center, South Texas, Veterans Healthcare System; Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, Texas 78229, USA.
Noor Y Al-ObaidiDepartment of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, Texas 78229, USA.
Maciej NowackiCollegium Medicum, Bydgoszcz and Nicolaus Copernicus University, Torun, Poland.
Katarzyna PietkunCollegium Medicum, Bydgoszcz and Nicolaus Copernicus University, Torun, Poland.
Barbara ZegarskaCollegium Medicum, Bydgoszcz and Nicolaus Copernicus University, Torun, Poland.
Tomasz KloskowskiCollegium Medicum, Bydgoszcz and Nicolaus Copernicus University, Torun, Poland.
Wojciech ZegarskiCollegium Medicum, Bydgoszcz and Nicolaus Copernicus University, Torun, Poland.
Tomasz DrewaCollegium Medicum, Bydgoszcz and Nicolaus Copernicus University, Torun, Poland.
Edward A MedinaDepartment of Pathology.
Zhenze ZhaoDepartment of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, Texas 78229, USA.
Sitai LiangDepartment of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, Texas 78229, USA.
The University of Texas Health Science Center at San Antonio · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tuberous sclerosis complex (TSC) is an autosomal dominant and multi-system genetic disorder in humans. TSC affects around 25,000 to 40,000 individuals in the United States and about 1 to 2 million individuals worldwide, with an estimated prevalence of one in 6,000 newborns. TSC occurs in all races and ethnic groups, and in both genders. TSC is caused by defects or mutations in two genes, TSC1 and TSC2. Loss of TSC1/TSC2 leads to dysregulation of mTOR, resulting in aberrant cell differentiation and development, and abnormal enlargement of cells. TSC is characterized by the development of benign and/or malignant tumors in several organs including renal/liver angiomyolipomas, facial angiofibroma, lymphangiomyomatosis, cardiac rhabdomyomas, retinal astrocytic, renal cell carcinoma, and brain subependymal giant cell astrocytomas (SEGA). In addition, TSC disease causes disabling neurologic disorders, including epilepsy, mental retardation and autism. Particularly problematic are the development of renal angiomyolipomas, which tend to be larger, bilateral, multifocal and present at a younger age compared with sporadic forms. In addition, SEGA block the flow of fluid within the brain, causing a buildup of fluid and pressure that leads to blurred vision and seizures. In the current review, we describe the pathology of TSC disease in key organs and summarize the use of mTOR inhibitors to treat tumors in TSC patients.

Indexed as

AMLLAMmTOR inhibitorsSEGA.TSC

Identifiers

PMID27698899
PMCPMC5039383
OpenAlexW2517842918

What OpenQuestion holds

Textmetadata
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.