Evidence map›Paper›PMID 35346215›Full record

ReviewMolecular cancer2022

Clinical significance of FBXW7 loss of function in human cancers.

Jingyi Fan, Marcia Bellon, Mingyi Ju, Lin Zhao, Minjie Wei, Liwu Fu, Christophe Nicot

Open access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 1 pooled it
10.7field-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

104 citing papers in PubMed, 1 synthesis or guideline pooled it, 129 citations in OpenAlex.

  1. Pooled it
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  13. Crotonylation impedes c-Myc oncogenic activity.Proceedings of the National Academy of Sciences of the United States of America · 2026
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44 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

7 authors at 3 institutions in 4 countries.

Jingyi FanState Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, Guangdong Esophageal Cancer Institute; Sun Yat-sen University Cancer Center, Guangzhou, 510060, Guangdong Province, China.
Marcia BellonDepartment of Pathology and Laboratory Medicine, Center for Viral Pathogenesis, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS, 66160, USA.
Mingyi JuDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, 110122, China.
Lin ZhaoDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, 110122, China.
Minjie WeiDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, 110122, China.
Liwu FuState Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, Guangdong Esophageal Cancer Institute; Sun Yat-sen University Cancer Center, Guangzhou, 510060, Guangdong Province, China. Fulw@mail.sysu.edu.cn.
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
Ministry of Education · KNSun Yat-sen University · CNUniversity 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

FBXW7 (F-Box and WD Repeat Domain Containing 7) (also referred to as FBW7 or hCDC4) is a component of the Skp1-Cdc53 / Cullin-F-box-protein complex (SCF/β-TrCP). As a member of the F-box protein family, FBXW7 serves a role in phosphorylation-dependent ubiquitination and proteasome degradation of oncoproteins that play critical role(s) in oncogenesis. FBXW7 affects many regulatory functions involved in cell survival, cell proliferation, tumor invasion, DNA damage repair, genomic instability and telomere biology. This thorough review of current literature details how FBXW7 expression and functions are regulated through multiple mechanisms and how that ultimately drives tumorigenesis in a wide array of cell types. The clinical significance of FBXW7 is highlighted by the fact that FBXW7 is frequently inactivated in human lung, colon, and hematopoietic cancers. The loss of FBXW7 can serve as an independent prognostic marker and is significantly correlated with the resistance of tumor cells to chemotherapeutic agents and poorer disease outcomes. Recent evidence shows that genetic mutation of FBXW7 differentially affects the degradation of specific cellular targets resulting in a distinct and specific pattern of activation/inactivation of cell signaling pathways. The clinical significance of FBXW7 mutations in the context of tumor development, progression, and resistance to therapies as well as opportunities for targeted therapies is discussed.

Indexed as

F-Box-WD Repeat-Containing Protein 7NeoplasmsHumansLoss of Function MutationUbiquitinationF-Box-WD Repeat-Containing Protein 7FBXW7 protein, humanAneuploidyApoptosisCancerCDC4Cell cycleCentrosomeChromosome instabilitycircRNACyclin EDNA repairDrug resistanceEpigeneticFBW7FBXW7ImmunotherapyLncRNAMCL-1miRNAMutationMYCNon-coding RNANOTCHTumor suppressor

Identifiers

PMID35346215
PMCPMC8962602
OpenAlexW4220690241

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.