ReviewPharmaceutics2021
Oncogenic and Tumor Suppressive Components of the Cell Cycle in Breast Cancer Progression and Prognosis.
Review in Pharmaceutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- The Value of Dysregulated LncRNAs on Clinicopathology and Survival in Non-Small-Cell LungFrontiers in genetics · 2022Pooled it
- SDC4 silencing promotes cell cycle arrest at the restriction point (R point) in anoikis-resistant endothelial cells.Cytotechnology · 2026Article
- Integrated transcriptomic and functional characterization of Claudin-1 reveals its oncogenic and immunomodulatory roles in pancreatic ductal adenocarcinoma.Tissue barriers · 2026Article
- Therapeutic evaluation of paclitaxel co-loaded PLGA nanoparticles with imatinib, protamine-imatinib, and gefitinib: comparative in vitro studies in MDA-MB-231 breast cancer cells and in vivo investigations in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- JOINT IDENTIFICATION OF SPATIALLY VARIABLE GENES VIA A NETWORK-ASSISTED BAYESIAN REGULARIZATION APPROACH.The annals of applied statistics · 2025Article
- Antineoplastic effect of anastrozole-loaded polymer nanocapsules on malignant human breast cancer cells (MCF-7).Scientific reports · 2025Article
- Aberrant expression of CNTRL was associated with poor prognosis, immune response and progression in glioma.Discover oncology · 2025Article
- Article
- Expression characteristics, molecular mechanisms, and clinical significance of DICER1 in breast cancer.Frontiers in genetics · 2025Article
- Review
- p27 Cell Cycle Inhibitor and Survival in Luminal-Type Breast Cancer: Gene Ontology, Machine Learning, and Drug Screening Analysis.Journal of breast cancer · 2024Article
- Curdepsidone A Induces Intrinsic Apoptosis and Inhibits Protective Autophagy via the ROS/PI3K/AKT Signaling Pathway in HeLa Cells.Marine drugs · 2024Article
- P53 together with ferroptosis: a promising strategy leaving cancer cells without escape.Acta biochimica et biophysica Sinica · 2024Article
- Advances in the mechanism of CDK4/6 inhibitor resistance in HR+/HER2- breast cancer.Therapeutic advances in medical oncology · 2024Review
- Correlation Between Messenger RNA Expression and Clinicopathological Features of Breast Cancer: A systematic review.Journal of Cancer · 2024Article
- ACAT1 promotes proliferation and metastasis of bladder cancer via AKT/GSK3β/c-Myc signaling pathway.Journal of Cancer · 2024Article
- Potential Antitumor Effect of α-Mangostin against Rat Mammary Gland Tumors Induced by LA7 Cells.International journal of molecular sciences · 2023Article
- Novel Anticancer Strategies II.Pharmaceutics · 2023Article
- Catechol-O-methyl transferase suppresses cell invasion and interplays with MET signaling in estrogen dependent breast cancer.Scientific reports · 2023Article
- Design and synthesis of chromone-nitrogen mustard derivatives and evaluation of anti-breast cancer activity.Journal of enzyme inhibition and medicinal chemistry · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer, a disease of inappropriate cell proliferation, is strongly interconnected with the cell cycle. All cancers consist of an abnormal accumulation of neoplastic cells, which are propagated toward uncontrolled cell division and proliferation in response to mitogenic signals. Mitogenic stimuli include genetic and epigenetic changes in cell cycle regulatory genes and other genes which regulate the cell cycle. This suggests that multiple, distinct pathways of genetic alterations lead to cancer development. Products of both oncogenes (including cyclin-dependent kinase (CDKs) and cyclins) and tumor suppressor genes (including cyclin-dependent kinase inhibitors) regulate cell cycle machinery and promote or suppress cell cycle progression, respectively. The identification of cyclins and CDKs help to explain and understand the molecular mechanisms of cell cycle machinery. During breast cancer tumorigenesis, cyclins A, B, C, D1, and E; cyclin-dependent kinase (CDKs); and CDK-inhibitor proteins p16, p21, p27, and p53 are known to play significant roles in cell cycle control and are tightly regulated in normal breast epithelial cells. Following mitogenic stimuli, these components are deregulated, which promotes neoplastic transformation of breast epithelial cells. Multiple studies implicate the roles of both types of components-oncogenic CDKs and cyclins, along with tumor-suppressing cyclin-dependent inhibitors-in breast cancer initiation and progression. Numerous clinical studies have confirmed that there is a prognostic significance for screening for these described components, regarding patient outcomes and their responses to therapy. The aim of this review article is to summarize the roles of oncogenic and tumor-suppressive components of the cell cycle in breast cancer progression and prognosis.
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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.