Evidence map›Paper›PMID 34461089›Full record

ReviewThe Journal of biological chemistry2021

New strategies for targeting kinase networks in cancer.

Ali E Yesilkanal, Gary L Johnson, Alexandre F Ramos, Marsha Rich Rosner

Open access · goldAbstract readReview
In one paragraph

Review in The Journal of biological chemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

36 citing papers in PubMed, 52 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

4 authors at 4 institutions in 2 countries.

Ali E YesilkanalBen May Department for Cancer Research, University of Chicago, Chicago, Illinois, USA. Electronic address: aeyesilkanal@gmail.com.
Gary L JohnsonDepartment of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Alexandre F RamosInstituto do Câncer do Estado de São Paulo, Faculdade de Medicina and Escola de Artes, Ciências e Humanidades, University of São Paulo, Brazil.
Marsha Rich RosnerBen May Department for Cancer Research, University of Chicago, Chicago, Illinois, USA. Electronic address: m-rosner@uchicago.edu.
Instituto do Câncer do Estado de São Paulo · BRMay Institute · USUniversity of Chicago · USUniversity of North Carolina at Chapel Hill · US

Funding

Tissue Procurement & PathologyP50CA058223 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BENJAMIN CARLISLE CALHOUN · 1992 to 2026
$59.3M
Regulation of RKIP FunctionR01GM121735 · NIGMS · UNIVERSITY OF CHICAGO · PI ROSNER, MARSHA R · 2017 to 2020
$1.6M
NCI NIH HHS P50 CA058223NIGMS NIH HHS R01 GM121735
6 · The paper itself

Abstract

Targeted strategies against specific driver molecules of cancer have brought about many advances in cancer treatment since the early success of the first small-molecule inhibitor Gleevec. Today, there are a multitude of targeted therapies approved by the Food and Drug Administration for the treatment of cancer. However, the initial efficacy of virtually every targeted treatment is often reversed by tumor resistance to the inhibitor through acquisition of new mutations in the target molecule, or reprogramming of the epigenome, transcriptome, or kinome of the tumor cells. At the core of this clinical problem lies the assumption that targeted treatments will only be efficacious if the inhibitors are used at their maximum tolerated doses. Such aggressive regimens create strong selective pressure on the evolutionary progression of the tumor, resulting in resistant cells. High-dose single agent treatments activate alternative mechanisms that bypass the inhibitor, while high-dose combinatorial treatments suffer from increased toxicity resulting in treatment cessation. Although there is an arsenal of targeted agents being tested clinically and preclinically, identifying the most effective combination treatment plan remains a challenge. In this review, we discuss novel targeted strategies with an emphasis on the recent cross-disciplinary studies demonstrating that it is possible to achieve antitumor efficacy without increasing toxicity by adopting low-dose multitarget approaches to treatment of cancer and metastasis.

Indexed as

Neoplasm ProteinsNeoplasmsAnimalsHumansImatinib MesylateProtein Kinase InhibitorsProtein KinasesImatinib MesylateNeoplasm ProteinsProtein Kinase InhibitorsProtein Kinasescancer therapycell signalingcombination therapydrug resistanceinhibitorkinase networkmathematical modelingmitogen-activated protein kinase (MAPK)receptor tyrosine kinasestargeted therapy

Identifiers

PMID34461089
PMCPMC8449055
OpenAlexW3196809995

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.