Evidence map›Paper›PMID 35917168›Full record

ReviewThe oncologist2022

Targeting CDK4 and 6 in Cancer Therapy: Emerging Preclinical Insights Related to Abemaciclib.

Seth A Wander, Neil O'Brien, Lacey M Litchfield, Declan O'Dea, Claudia Morato Guimaraes, Dennis J Slamon, Shom Goel

Open access · goldAbstract readReview
In one paragraph

Review in The oncologist, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Abemaciclib Inhibits Retinoblastoma Tumor Growth by Targeting CDK1/2.Investigative ophthalmology & visual science · 2026
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Palbociclib as an Antitumor Drug: A License to Kill.Molecules (Basel, Switzerland) · 2024
    Review
  16. Article
  17. Article
  18. Review
  19. Slower CDK4 and faster CDK2 activation in the cell cycle.Structure (London, England : 1993) · 2024
    Article
  20. Article
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

7 authors at 5 institutions in 3 countries.

Seth A WanderDepartment of Medical Oncology, Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA, USA.
Neil O'BrienDepartment of Medicine, Division of Hematology/Oncology, Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Lacey M LitchfieldEli Lilly and Company, Indianapolis, IN, USA.
Declan O'DeaEli Lilly and Company, Cork, Ireland.ORCID 0000-0002-1029-0596
Claudia Morato GuimaraesEli Lilly and Company, Indianapolis, IN, USA.
Dennis J SlamonDepartment of Medicine, Division of Hematology/Oncology, Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Shom GoelDepartment of Cancer Medicine, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.
Eli Lilly (United States) · USUniversity of California, Los Angeles · USEli Lilly (Ireland) · IEHarvard University · USThe University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pharmacologic inhibitors of cyclin-dependent kinases 4 and 6 (CDK4 and 6) are approved for the treatment of subsets of patients with hormone receptor positive (HR+) breast cancer (BC). In metastatic disease, strategies involving endocrine therapy combined with CDK4 and 6 inhibitors (CDK4 and 6i) improve clinical outcomes in HR+ BCs. CDK4 and 6i prevent retinoblastoma tumor suppressor protein phosphorylation, thereby blocking the transcription of E2F target genes, which in turn inhibits both mitogen and estrogen-mediated cell proliferation. In this review, we summarize preclinical data pertaining to the use of CDK4 and 6i in BC, with a particular focus on several of the unique chemical, pharmacologic, and mechanistic properties of abemaciclib. As research efforts elucidate the novel mechanisms underlying abemaciclib activity, potential new applications are being identified. For example, preclinical studies have demonstrated abemaciclib can exert antitumor activity against multiple tumor types and can cross the blood-brain barrier. Abemaciclib has also demonstrated distinct activity as a monotherapeutic in the treatment of BC. Accordingly, we also discuss how a greater understanding of mechanisms related to CDK4 and 6 blockade highlight abemaciclib's unique in-class properties, and could pave new avenues for enhancing its therapeutic efficacy.

Indexed as

Breast NeoplasmsMitogensAminopyridinesBenzimidazolesCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6EstrogensFemaleHumansProtein Kinase InhibitorsTumor Suppressor ProteinsabemaciclibAminopyridinesBenzimidazolesCDK4 protein, humanCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6EstrogensMitogensProtein Kinase InhibitorsTumor Suppressor Proteinsabemaciclibantitumorbreast neoplasmsCDK4 and 6preclinical

Identifiers

PMID35917168
PMCPMC9526495
OpenAlexW4289519304

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.