ReviewCancer science2012
Novel regulation of checkpoint kinase 1: Is checkpoint kinase 1 a good candidate for anti-cancer therapy?
Review in Cancer science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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
35 citing papers in PubMed, 60 citations in OpenAlex.
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- Identification and Validation of Prognostic Biomarker Signatures Associated with Overall Survival in Colorectal Cancer: Evidence from Bioinformatics Analysis and an in vivo Study.Asian Pacific journal of cancer prevention : APJCP · 2026Article
- Multi-omics analysis and functional validation of CHEK1 as an independent prognostic biomarker in Pancreatic cancer.PloS one · 2026Article
- SLAYER: a computational framework for identifying synthetic lethal interactions through integrated analysis of cancer dependencies.NAR genomics and bioinformatics · 2025Article
- Combination of S-1 and the oral ATR inhibitor ceralasertib is effective against pancreatic cancer cells.Cancer chemotherapy and pharmacology · 2024Article
- Network pharmacology and molecular docking reveal the mechanisms of curcumin activity against esophageal squamous cell carcinoma.Frontiers in pharmacology · 2024Article
- AZD6738 promotes the tumor suppressive effects of trifluridine in colorectal cancer cells.Oncology reports · 2023Article
- Gastric Cancer Pre-Stage Detection and Early Diagnosis of Gastritis Using Serum Protein Signatures.Molecules (Basel, Switzerland) · 2022Article
- ATR inhibitor AZD6738 increases the sensitivity of colorectal cancer cells to 5‑fluorouracil by inhibiting repair of DNA damage.Oncology reports · 2022Article
- Development and Validation of a Novel Circadian Rhythm-Related Signature to Predict the Prognosis of the Patients with Hepatocellular Carcinoma.BioMed research international · 2022Article
- Identification of 9 Gene Signatures by WGCNA to Predict Prognosis for Colon Adenocarcinoma.Computational intelligence and neuroscience · 2022Article
- Review
- A Case Report of Metastatic Castration-Resistant Prostate Cancer Harboring aFrontiers in oncology · 2021Article
- Bcl-2/Bcl-xL inhibitor navitoclax increases the antitumor effect of Chk1 inhibitor prexasertib by inducing apoptosis in pancreatic cancer cells via inhibition of Bcl-xL but not Bcl-2.Molecular and cellular biochemistry · 2020Article
- Modulation of DNA Damage Response by Sphingolipid Signaling: An Interplay that Shapes Cell Fate.International journal of molecular sciences · 2020Review
- Article
- The role of CDC25C in cell cycle regulation and clinical cancer therapy: a systematic review.Cancer cell international · 2020Review
- Hypoxia-targeted drug delivery.Chemical Society reviews · 2019Review
- Estrogen-dependent disruption of intracellular iron metabolism augments the cytotoxic effects of doxorubicin in select breast and ovarian cancer cells.Cancer management and research · 2019Article
- Checkpoint Kinase 1 Expression Predicts Poor Prognosis in Nigerian Breast Cancer Patients.Molecular diagnosis & therapy · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA-damaging strategies, such as radiotherapy and the majority of chemotherapeutic therapies, are the most frequently used non-surgical anti-cancer therapies for human cancers. These therapies activate DNA damage/replication checkpoints, which induce cell-cycle arrest to provide the time needed to repair DNA damage. Due to genetic defect(s) in the ATM (ataxia-telangiectasia mutated)-Chk2-p53 pathway, an ATR (ATM- and Rad3-related)-Chk1-Cdc25 route is the sole checkpoint pathway in a majority of cancer cells. Chk1 inhibitors are expected to selectively induce the mitotic cell death (mitotic catastrophe) of cancer cells. However, recent new findings have pointed out that Chk1 is essential for the maintenance of genome integrity even during unperturbed cell-cycle progression, which is controlled by a variety of protein kinases. These observations have raised concerns about a possible risk of Chk1 inhibitors on the clinics. In this review, we summarize recent advances in Chk1 regulation by phosphorylation, and discuss Chk1 as a molecular target for cancer therapeutics.
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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.