Evidence map›Paper›PMID 30038670›Full record

ReviewTherapeutic advances in medical oncology2018

CDK4/6 inhibition in breast cancer: current practice and future directions.

Sonia Pernas, Sara M Tolaney, Eric P Winer, Shom Goel

Registry-linked trialOpen access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Therapeutic advances in medical oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06599216 (Adebrelimab Combined With Dalpicicliband Standard Endocrine Therapy for HR + / HER 2-breast Cancer), which is not on this map. Cited by 176 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
176citing papers in PubMed, 3 pooled it
30.4field-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.

NCT06599216 phase2active not recruitingnot on this mapstarted 2024, after this paper: background citation

Adebrelimab Combined With Dalpicicliband Standard Endocrine Therapy for HR + / HER 2-breast Cancer:A Single-center,Open-label,Single-arm Clinical Trial

TypeinterventionalSponsorHarbin Medical UniversityRan2024 to 2027Enrolled30ConditionsBreast Cancer, HR+/HER2- Breast CancerArmsAdebrelimab+Dalpciclib+Standard Endocrine Therapy
3 · Its place in the literature

Who cites it

176 citing papers in PubMed, 3 syntheses or guidelines pooled it, 311 citations in OpenAlex.

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116 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Sonia PernasDepartment of Medical Oncology, Breast Cancer Unit, Institut Català d'Oncologia (ICO)-H.U.Bellvitge-IDIBELL, L'Hospitalet, Barcelona, Spain Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA.ORCID https://orcid.org/0000-0002-1485-5080
Sara M TolaneyDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA.
Eric P WinerDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA.
Shom GoelDepartment of Medical Oncology, Dana-Farber Cancer Institute, 450 Brookline Avenue, Boston, MA 02215, USA Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA.
Dana-Farber Cancer Institute · USInstitut d'Investigació Biomédica de Bellvitge · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cyclin D/cyclin-dependent kinases 4 and 6 (CDK4/6)-retinoblastoma protein (RB) pathway plays a key role in the proliferation of both normal breast epithelium and breast cancer cells. A strong rationale for inhibiting CDK4/6 in breast cancers has been present for many years. However, potent and selective CDK4/6 inhibitors have only recently become available. These agents prevent phosphorylation of the RB tumor suppressor, thereby invoking cancer cell cycle arrest in G1. CDK4/6 inhibitors have transited rapidly from preclinical studies to the clinical arena, and three have already been approved for the treatment of advanced, estrogen receptor (ER)-positive breast cancer patients on account of striking clinical trial results demonstrating substantial improvements in progression-free survival. ER-positive breast cancers harbor several molecular features that would predict their sensitivity to CDK4/6 inhibitors. As physicians gain experience with using these agents in the clinic, new questions arise: are CDK4/6 inhibitors likely to be useful for patients with other subtypes of breast cancer? Are there other agents that could be effectively combined with CDK4/6 inhibitors, beyond endocrine therapy? Is there a rationale for combining CDK4/6 inhibitors with novel immune-based therapies? In this review, we describe not only the clinical data available to date, but also the biology of the CDK4/6 pathway and discuss answers to these questions. In particular, we highlight that CDK4 and CDK6 govern much more than the cancer cell cycle, and that their optimal use in the clinic depends on a deeper understanding of the less well characterized effects of these enzymes.

Indexed as

breast cancerCDK4/6 inhibitorsHER2-positiveimmune checkpoint blockadePI3K inhibitorspredictors of response/resistancetriple-negative breast cancer

Identifiers

PMID30038670
PMCPMC6050811
OpenAlexW2883670730

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.