Evidence map›Paper›PMID 32041464›Full record

ReviewCancer biology & therapy2020

Harnessing the vulnerabilities of p53 mutants in lung cancer - Focusing on the proteasome: a new trick for an old foe?

Eziafa I Oduah, Steven R Grossman

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer biology & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

14 citing papers in PubMed, 15 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Eziafa I OduahDepartment of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Steven R GrossmanDepartment of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Virginia Commonwealth University · US

Funding

The Role of p53-inducible Sesn1 and Sesn2 genes in lung carcinogenesisR01CA172660 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI GROSSMAN, STEVEN R. · 2013 to 2017
$1.5M
NCI NIH HHS R01 CA172660
6 · The paper itself

Abstract

Gain-of-function (GOF) p53 mutations occur commonly in human cancer and lead to both loss of p53 tumor suppressor function and acquisition of aggressive cancer phenotypes. The oncogenicity of GOF mutant p53 is highly related to its abnormal protein stability relative to wild type p53, and overall stoichiometric excess. We provide an overview of the mechanisms of dysfunction and abnormal stability of GOF p53 specifically in lung cancer, the leading cause of cancer-related mortality, where, depending on histologic subtype, 33-90% of tumors exhibit GOF p53 mutations. As a distinguishing feature and oncogenic mechanism in lung and many other cancers, GOF p53 represents an appealing and cancer-specific therapeutic target. We review preclinical evidence demonstrating paradoxical depletion of GOF p53 by proteasome inhibitors, as well as preclinical and clinical studies of proteasome inhibition in lung cancer. Finally, we provide a rationale for a reexamination of proteasome inhibition in lung cancer, focusing on tumors expressing GOF p53 alleles.

Indexed as

MutationAnimalsHumansLung NeoplasmsProteasome Endopeptidase ComplexTumor Suppressor Protein p53Proteasome Endopeptidase ComplexTP53 protein, humanTumor Suppressor Protein p53gain-of-functionlung cancerP53 mutationproteasomeproteasome inhibitorsstability

Identifiers

PMID32041464
PMCPMC7515531
OpenAlexW3006291572

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.