Evidence map›Paper›PMID 28580868›Full record

ReviewJournal of clinical oncology : official journal of the American Society of Clinical Oncology2017

Cell-Cycle Therapeutics Come of Age.

Matthew Ingham, Gary K Schwartz

Open access · greenAbstract readReview
In one paragraph

Review in Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 182 papers.

0numbers the graph read from it
0cells of the map it votes in
182citing papers in PubMed
25.6field-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

182 citing papers in PubMed, 392 citations in OpenAlex.

  1. Trial
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  7. The preliminary study on the effect of PSEN1 on the proliferation and invasion of breast cancer cells.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2026
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  8. Review
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  20. Regulating Astrocytes via Short Fibers for Spinal Cord Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article

122 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.

Matthew InghamAll authors: Columbia University School of Medicine, New York, NY.
Gary K SchwartzAll authors: Columbia University School of Medicine, New York, NY.
Columbia University · US

Funding

Molecular Oncology Training ProgramT32CA203703 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Katherine D Crew, DAWN HERSHMAN · 2016 to 2026
$4.1M
NCI NIH HHS T32 CA203703
6 · The paper itself

Abstract

The ability to sustain unscheduled proliferation is a hallmark of cancer. The normal process of cell division occurs via the cell cycle, a series of highly regulated steps that are orchestrated at the molecular level by specific cyclins that act in association with cyclin-dependent kinases (CDKs). Cyclin D and CDK4/6 play a key role in cell-cycle progression by phosphorylating and inactivating the retinoblastoma protein, a tumor suppressor that restrains G1- to S-phase progression. The first-generation CDK inhibitors demonstrated broad activity upon several CDKs, which likely explains their considerable toxicities and limited efficacy. Palbociclib, ribociclib, and abemaciclib represent a new class of highly specific ATP-competitive CDK4/6 inhibitors that induce reversible G1-phase cell-cycle arrest in retinoblastoma-positive tumor models. Both palbociclib and ribociclib have been approved in combination with hormone-based therapy for the treatment of naïve hormone receptor-positive advanced breast cancer on the basis of an improvement in progression-free survival. In general, CDK4/6 inhibitors are cytostatic as monotherapy but demonstrate favorable tolerability, which has prompted interest in combination approaches. Combinations with phosphatidylinositol 3-kinase and mammalian target of rapamycin inhibitors in breast cancer, and inhibitors of the RAS/RAF/mitogen-activated protein kinase pathway in RAS-mutant cancers are particularly promising approaches that are currently being evaluated. Although the subject of intense preclinical study, predictive biomarkers for response and resistance to these drugs remain largely undefined. CDK4/6 inhibitors have emerged as the most promising of the cell-cycle therapeutics and intense efforts are now underway to expand the reach of this paradigm.

Indexed as

AnimalsCell CycleCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6HumansNeoplasmsProtein Kinase InhibitorsCDK4 protein, humanCDK6 protein, humanCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6Protein Kinase Inhibitors

Identifiers

PMID28580868
PMCPMC6075824
OpenAlexW2621171915

What OpenQuestion holds

Textmetadata
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.