Evidence map›Paper›PMID 40856900›Full record

ReviewMedical oncology (Northwood, London, England)2025

The landscape of cyclin-dependent kinase 4/6 inhibitors in solid malignancies: emphasis on immunotherapy combinatorial strategies.

Sara A Hussein, Ahmed H Saadawy, Eman Badr, Maha R A Abdollah, Neamtullah Wael, Rasha M Allam, Ahmed M Al-Abd, Ana Maria Roncero Sanchez, Mai F Tolba

Abstract readReview
In one paragraph

Review in Medical oncology (Northwood, London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

9 authors.

Sara A HusseinDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Ain Shams University, Abbassia, 11566, Cairo, Egypt.
Ahmed H SaadawyDepartment of Biological Sciences, Dornsife College of Letters, Arts and Sciences, University of Southern California, Los Angeles, CA, USA.
Eman BadrBiomedical Sciences Program, University of Science and Technology, Zewail City, Giza, 12578, Egypt.
Maha R A AbdollahDepartment of Pharmacology, Faculty of Pharmacy, The British University in Egypt, El Sherouk City, Cairo, Egypt.
Neamtullah WaelCenter for Drug Discovery Research and Development, Ain Shams University, Cairo, Egypt.
Rasha M AllamDepartment of Pharmacology, Medical and Clinical Research Institute, National Research Centre, Cairo, Egypt.
Ahmed M Al-AbdDepartment of Pharmacology, Medical and Clinical Research Institute, National Research Centre, Cairo, Egypt.
Ana Maria Roncero SanchezCNIO-Spanish National Cancer Research Center, Melchor Fernández Almagro, Madrid, Spain.
Mai F TolbaDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Ain Shams University, Abbassia, 11566, Cairo, Egypt. tolba.mf@pharma.asu.edu.eg.

Funding

the Egyptian Academy of Scientific Research and Technology (ASRT) . RESPECT grant (ID:10073)
6 · The paper itself

Abstract

Given the pivotal role of CDK4/6 deregulation in the pathogenesis of various malignancies, CDK4/6 inhibitors have been incorporated into cancer treatment protocols. Beyond their antiproliferative effects, these inhibitors exhibit prominent immunomodulatory properties. Preclinical data indicated that CDK4/6 inhibitors enhance the tumor cell antigen presentation capacity and restrict the proliferation of immunosuppressive regulatory T-cells. Furthermore, studies showed that CDK4/6 inhibitors could enhance the development of memory T-cell in vivo in melanoma mouse models and in the clinical setting in breast cancer (BC) patients. In silico analysis identified 225 protein targets for CDK4/6 inhibitors involved in 57 immune-related pathways which further supported the immune-modulatory potential of these inhibitors in innate immunity, cytokine signaling, and adaptive immunity. Furthermore, 24 targets exhibited significantly higher protein expression in immune cell types compared to non-immune cell types, as indicated by data from the Human Protein Atlas. The favorable modulation of T-cell immunity by CDK4/6 inhibitors could complement the antitumor effect of immunotherapies, such as immune checkpoint inhibitors (ICIs), which hamper PD-1 /PD-L1 signaling and result in the reactivation of the antitumor T-cell response. Herein, we explore the clinical portfolio of CDK4/6 inhibitors across various solid malignancies, with emphasis on emerging combinations with ICIs.

Indexed as

Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6ImmunotherapyNeoplasmsProtein Kinase InhibitorsAnimalsHumansImmune Checkpoint InhibitorsCDK4 protein, humanCDK6 protein, humanCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6Immune Checkpoint InhibitorsProtein Kinase InhibitorsCDK4/6 inhibitorsClinical trialsImmune checkpoint inhibitorsImmunotherapySolid tumors

Identifiers

PMID40856900
PMCPMC12380978

What OpenQuestion holds

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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.