Evidence map›Paper›PMID 37779425›Full record

ArticleCancer research2023

Distinct Mechanisms of Resistance to CDK4/6 Inhibitors Require Specific Subsequent Treatment Strategies: One Size Does Not Fit All.

Hannah F Wingate, Khandan Keyomarsi

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In one paragraph

Article in Cancer research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

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  7. METTL1-mediated tRNA mJournal of experimental & clinical cancer research : CR · 2024
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Hannah F WingateDepartment of Breast Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-1055-8935
Khandan KeyomarsiDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-5440-0849

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclin-dependent kinase (CDK) 4/6 inhibitors have transformed the treatment landscape of patients with hormone receptor-positive breast cancers. However, despite improvements in clinical outcomes, the approximately 70% of patients with tumors that are not intrinsically resistant to a CDK4/6 inhibitor still ultimately acquire resistance, which leads to a dilemma for clinicians when deciding which treatment to offer patients when they demonstrate disease progression on a CDK4/6 inhibitor. As such, many groups have sought to understand the mechanisms of resistance to CDK4/6 inhibitors, mostly focusing on genetic alterations associated with resistance. Though several recurrent mutations have been described, they are not consistent enough to guide clinical practice or generate novel rational treatment options. Two recent publications have used transcriptomic analysis to unravel distinct mechanisms driving resistance to individual CDK4/6 inhibitors and in doing so have identified biomarkers that could potentially help identify the next course of treatment for patients following disease progression.

Indexed as

Antineoplastic AgentsBreast NeoplasmsCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6Disease ProgressionFemaleHumansProtein Kinase InhibitorsAntineoplastic AgentsCDK4 protein, humanCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6Protein Kinase Inhibitors

Identifiers

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.