Evidence map›Paper›PMID 28303264›Full record

ReviewTrends in cancer2017

The Strange Case of CDK4/6 Inhibitors: Mechanisms, Resistance, and Combination Strategies.

Erik S Knudsen, Agnieszka K Witkiewicz

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Trends in cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05156450 (Phase Ib/II Clinical Study of TQB3616 Capsules in Combination With Abiraterone Acetate Plus Prednisone in Patients With Metastatic Castration-Resistant Prostate Cancer), which is not on this map. Cited by 168 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
168citing papers in PubMed, 2 pooled it
22.1field-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.

NCT05156450 phase2unknown statusnot on this mapstarted 2022, after this paper: background citation

Phase Ib/II Clinical Study of TQB3616 Capsules in Combination With Abiraterone Acetate Plus Prednisone in Patients With Metastatic Castration-Resistant Prostate Cancer

TypeinterventionalSponsorWest China HospitalRan2022 to 2024Enrolled30ConditionsProstatic Neoplasms, Castration-Resistant, Drug Therapy, CombinationArmsTQB3616 Capsules Combined With Abiraterone Acetate Plus Prednisone
3 · Its place in the literature

Who cites it

168 citing papers in PubMed, 2 syntheses or guidelines pooled it, 280 citations in OpenAlex.

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  5. A Phase 0 Trial of Ribociclib in Recurrent Glioblastoma Patients Incorporating a Tumor Pharmacodynamic- and Pharmacokinetic-Guided Expansion Cohort.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
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108 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

2 authors at 1 institution in 1 country.

Erik S KnudsenUniversity of Arizona Cancer Center; Department of Medicine, University of Arizona.
Agnieszka K WitkiewiczUniversity of Arizona Cancer Center; Department of Medicine, University of Arizona; Department of Pathology, University of Arizona.
University of Arizona Cancer Center

Funding

Common Genetically Altered Pathways as Targets for Therapy in Pancreatic CancerR01CA211878 · NCI · UNIVERSITY OF ARIZONA · PI KNUDSEN, ERIK, WITKIEWICZ, AGNIESZKA · 2017 to 2021
$1.9M
Action of RB Pathway in Breast Cancer TherapyR01CA129134 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI KNUDSEN, ERIK · 2010 to 2014
$1.7M
Pathway Heterogeneity: Etiology and Treatment of TNBCR01CA188650 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI KNUDSEN, ERIK · 2014 to 2018
$1.7M
Impact of ErbB2 and RB Pathways on DCIS Progression and TreatmentR01CA163863 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI WITKIEWICZ, AGNIESZKA · 2012 to 2016
$1.6M
NCI NIH HHS R01 CA129134NCI NIH HHS R01 CA163863NCI NIH HHS R01 CA188650NCI NIH HHS R01 CA211878
6 · The paper itself

Abstract

CDK4/6 inhibitors have emerged as a powerful class of agents with clinical activity in a number of malignancies. Targeting the cell cycle represents a core attack on a defining feature of cancer. However, the mechanisms through which selective CDK4/6 targeted agents act has few parallels in the current pharmaceutical armamentarium against cancer. Notably, CDK4/6 inhibitors act downstream of most mitogenic signaling cascades, which have implications both related to clinical efficacy and resistance. Core knowledge of cell cycle processes has provided insights into mechanisms of intrinsic resistance to CDK4/6 inhibitors; however, the basis of acquired resistance versus durable response is only beginning to emerge. This review focuses on the mechanism of action and biomarkers to direct the precision use of CDK4/6 inhibitors and rationally-developed combination therapies.

Indexed as

AnimalsAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsCell CycleCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6Drug Resistance, NeoplasmHumansNeoplasmsProtein Kinase InhibitorsAntineoplastic AgentsCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6Protein Kinase InhibitorsBreast CancerCell CycleCyclin D1E2FRB

Identifiers

PMID28303264
PMCPMC5347397
OpenAlexW2568050301

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.