Evidence map›Paper›PMID 36900131›Full record

ReviewDiagnostics (Basel, Switzerland)2023

Mechanisms of Resistance to CDK4/6 Inhibitors and Predictive Biomarkers of Response in HR+/HER2-Metastatic Breast Cancer-A Review of the Literature.

Ioana-Miruna Stanciu, Andreea Ioana Parosanu, Cristina Orlov-Slavu, Ion Cristian Iaciu, Ana Maria Popa, Cristina Mihaela Olaru, Cristina Florina Pirlog, Radu Constantin Vrabie, Cornelia Nitipir

Full text readReview
In one paragraph

Review in Diagnostics (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
–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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
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  18. Targeting CDK2 to combat drug resistance in cancer therapy.Future oncology (London, England) · 2024
    Review
  19. Article
  20. Palbociclib as an Antitumor Drug: A License to Kill.Molecules (Basel, Switzerland) · 2024
    Review
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

9 authors.

Ioana-Miruna StanciuDepartment of Oncology, "Carol Davila" University of Medicine and Pharmacy, 020021 Bucharest, Romania.ORCID 0009-0003-5937-0778
Andreea Ioana ParosanuDepartment of Oncology, "Carol Davila" University of Medicine and Pharmacy, 020021 Bucharest, Romania.
Cristina Orlov-SlavuDepartment of Oncology, "Carol Davila" University of Medicine and Pharmacy, 020021 Bucharest, Romania.
Ion Cristian IaciuDepartment of Oncology, "Carol Davila" University of Medicine and Pharmacy, 020021 Bucharest, Romania.
Ana Maria PopaDepartment of Oncology, "Carol Davila" University of Medicine and Pharmacy, 020021 Bucharest, Romania.
Cristina Mihaela OlaruDepartment of Oncology, "Carol Davila" University of Medicine and Pharmacy, 020021 Bucharest, Romania.
Cristina Florina PirlogDepartment of Oncology, "Carol Davila" University of Medicine and Pharmacy, 020021 Bucharest, Romania.
Radu Constantin VrabieDepartment of Oncology, "Carol Davila" University of Medicine and Pharmacy, 020021 Bucharest, Romania.
Cornelia NitipirDepartment of Oncology, "Carol Davila" University of Medicine and Pharmacy, 020021 Bucharest, Romania.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The latest and newest discoveries for advanced and metastatic hormone receptor-positive (HR+) and human epidermal growth factor receptor 2-negative (HER2-) breast cancer are the three cyclin-dependent kinases 4 and 6 inhibitors (CDK4/6i) in association with endocrine therapy (ET). However, even if this treatment revolutionized the world and continued to be the first-line treatment choice for these patients, it also has its limitations, caused by de novo or acquired drug resistance which leads to inevitable progression after some time. Thus, an understanding of the overview of the targeted therapy which represents the gold therapy for this subtype of cancer is essential. The full potential of CDK4/6i is yet to be known, with many trials ongoing to expand their utility to other breast cancer subtypes, such as early breast cancer, and even to other cancers. Our research establishes the important idea that resistance to combined therapy (CDK4/6i + ET) can be due to resistance to endocrine therapy, to treatment with CDK4/6i, or to both. Individuals' responses to treatment are based mostly on genetic features and molecular markers, as well as the tumor's hallmarks; therefore, a future perspective is represented by personalized treatment based on the development of new biomarkers, and strategies to overcome drug resistance to combinations of ET and CDK4/6 inhibitors. The aim of our study was to centralize the mechanisms of resistance, and we believe that our work will have utility for everyone in the medical field who wants to deepen their knowledge about ET + CDK4/6 inhibitors resistance.

Indexed as

advanced/metastatic breast cancerbiomarkers of responseCDK4/6 inhibitorsendocrine therapyprogression on CDK4/6 inhibitorsresistance mechanisms

Identifiers

PMID36900131
PMCPMC10000620

What OpenQuestion holds

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LicenceCC BY
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identifiers read8
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.