Evidence map›Paper›PMID 29383129›Full record

ArticleOncotarget2017

CKS protein overexpression renders tumors susceptible to a chemotherapeutic strategy that protects normal tissues.

John Tat, Céline Loriot, Martha Henze, Charles Spruck, Brunhilde H Felding, Steven I Reed

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 79% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

6 authors at 3 institutions in 1 country.

John TatDepartment of Molecular Medicine, The Scripps Research Institute, CA 92037, La Jolla, San Diego, USA.
Céline LoriotDepartment of Molecular Medicine, The Scripps Research Institute, CA 92037, La Jolla, San Diego, USA.
Martha HenzeDepartment of Molecular Medicine, The Scripps Research Institute, CA 92037, La Jolla, San Diego, USA.
Charles SpruckTumor Initiation and Maintenance Program, Cancer Center, Sanford-Burnham-Prebys Medical Discovery Institute, La Jolla, 92037, CA, San Diego, USA.
Brunhilde H FeldingDepartment of Molecular Medicine, The Scripps Research Institute, CA 92037, La Jolla, San Diego, USA.
Steven I ReedDepartment of Molecular Medicine, The Scripps Research Institute, CA 92037, La Jolla, San Diego, USA.
Scripps Research Institute · USSanford Burnham Prebys Medical Discovery Institute · USUniversity of California, San Diego · US

Funding

Scripps Translational Science InstituteUL1TR001114 · NCATS · SCRIPPS RESEARCH INSTITUTE, THE · PI TOPOL, ERIC JEFFREY · 2013 to 2017
$24.0M
The role of Cyclin E in growth control and tumorogenesisR01CA078343 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI REED, STEVEN I · 1998 to 2019
$8.1M
Normalizing Breast Cancer Metabolism to Prevent Progression and Recurrence (PQ21)R01CA170737 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI FELDING, BRUNIE H. · 2012 to 2015
$2.1M
The Role of Cks Proteins in Mammalian MeiosisR01HD049539 · NICHD · SIDNEY KIMMEL CANCER CENTER · PI SPRUCK, CHARLES H. · 2006 to 2010
$1.9M
Vascular mechanisms regulating breast cancer brain metastasisR01CA170140 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ELICEIRI, BRIAN P, FELDING, BRUNIE H. · 2012 to 2016
$1.8M
Scripps Translational Science InstituteTL1TR001113 · NCATS · SCRIPPS RESEARCH INSTITUTE, THE · PI TOPOL, ERIC JEFFREY · 2013 to 2017
$1.0M
Antibody Fingerprinting of Triple Negative Breast Cancer by High Throughput FACSR21CA198595 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI FELDING, BRUNIE H., SMIDER, VAUGHN VASIL · 2015 to 2016
$457k
NCATS NIH HHS TL1 TR001113NCATS NIH HHS UL1 TR001114NCI NIH HHS R01 CA078343NCI NIH HHS R01 CA170140NCI NIH HHS R01 CA170737NCI NIH HHS R21 CA198595NICHD NIH HHS R01 HD049539
6 · The paper itself

Abstract

The cyclin-dependent kinase-interacting proteins Cyclin-dependent Kinase Subunit 1 and 2 (CKS1 and 2) are frequently overexpressed in cancer and linked to increased aggressiveness and poor prognoses. We previously showed that CKS protein overexpression overrides the replication stress checkpoint activated by oncoproteins. Since CKS overexpression and oncoprotein activation/overexpression are often observed in the same tumors, we have hypothesized that CKS-mediated checkpoint override could enhance the ability of premalignant cells experiencing oncoprotein-induced replication stress to expand. This tumor advantage, however, could represent a vulnerability to exploit therapeutically. Here, we first show

Indexed as

cancer chemotherapycyclin-dependent kinasecyclin-dependent kinase subunitreplication stressreplication stress checkpoint

Identifiers

PMID29383129
PMCPMC5777741
OpenAlexW2772506892

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.