Evidence map›Paper›PMID 30086763›Full record

ReviewMolecular cancer2018

FBXW7: a critical tumor suppressor of human cancers.

Chien-Hung Yeh, Marcia Bellon, Christophe Nicot

Open access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 344 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
344citing papers in PubMed, 2 pooled it
20.5field-weighted citation impact, top 1% 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

344 citing papers in PubMed, 2 syntheses or guidelines pooled it, 520 citations in OpenAlex.

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284 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Chien-Hung YehDepartment of Pathology and Laboratory Medicine, Center for Viral Pathogenesis, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS, 66160, USA.
Marcia BellonDepartment of Pathology and Laboratory Medicine, Center for Viral Pathogenesis, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS, 66160, USA.
Christophe NicotDepartment of Pathology and Laboratory Medicine, Center for Viral Pathogenesis, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS, 66160, USA. cnicot@kumc.edu.ORCID 0000-0001-5927-2869
University of Kansas Medical Center · US

Funding

How HTLV-I Tax and HBZ control telomerase activity to induce adult T-cell leukemiaR01CA201309 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI NICOT, CHRISTOPHE P · 2016 to 2020
$1.7M
NCI NIH HHS R01 CA201309
6 · The paper itself

Abstract

The ubiquitin-proteasome system (UPS) is involved in multiple aspects of cellular processes, such as cell cycle progression, cellular differentiation, and survival (Davis RJ et al., Cancer Cell 26:455-64, 2014; Skaar JR et al., Nat Rev Drug Discov 13:889-903, 2014; Nakayama KI and Nakayama K, Nat Rev Cancer 6:369-81, 2006). F-box and WD repeat domain containing 7 (FBXW7), also known as Sel10, hCDC4 or hAgo, is a member of the F-box protein family, which functions as the substrate recognition component of the SCF E3 ubiquitin ligase. FBXW7 is a critical tumor suppressor and one of the most commonly deregulated ubiquitin-proteasome system proteins in human cancer. FBXW7 controls proteasome-mediated degradation of oncoproteins such as cyclin E, c-Myc, Mcl-1, mTOR, Jun, Notch and AURKA. Consistent with the tumor suppressor role of FBXW7, it is located at chromosome 4q32, a genomic region deleted in more than 30% of all human cancers (Spruck CH et al., Cancer Res 62:4535-9, 2002). Genetic profiles of human cancers based on high-throughput sequencing have revealed that FBXW7 is frequently mutated in human cancers. In addition to genetic mutations, other mechanisms involving microRNA, long non-coding RNA, and specific oncogenic signaling pathways can inactivate FBXW7 functions in cancer cells. In the following sections, we will discuss the regulation of FBXW7, its role in oncogenesis, and the clinical implications and prognostic value of loss of function of FBXW7 in human cancers.

Indexed as

MutationF-Box-WD Repeat-Containing Protein 7Gene Expression Regulation, NeoplasticHumansMicroRNAsNeoplasmsPrognosisProteasome Endopeptidase ComplexRNA, Long NoncodingSignal TransductionF-Box-WD Repeat-Containing Protein 7FBXW7 protein, humanMicroRNAsProteasome Endopeptidase ComplexRNA, Long NoncodingCancerCDC4C-mycCyclin EFBXW7HTLVJunmcl-1mTORNotch

Identifiers

PMID30086763
PMCPMC6081812
OpenAlexW2887067858

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.