ReviewCell cycle (Georgetown, Tex.)2010
Targeting the checkpoint kinase Chk1 in cancer therapy.
Review in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 81 citations in OpenAlex.
- Preclinical analyses and phase I evaluation of LY2603618 administered in combination with pemetrexed and cisplatin in patients with advanced cancer.Investigational new drugs · 2014Trial
- CHK1 targets spleen tyrosine kinase (L) for proteolysis in hepatocellular carcinoma.The Journal of clinical investigation · 2012Trial
- Cancer Vulnerabilities Through Targeting the ATR/Chk1 and ATM/Chk2 Axes in the Context of DNA Damage.Cells · 2025Review
- Characterization of G2/M checkpoint classifier for personalized treatment in uterine corpus endometrial carcinoma.Cancer cell international · 2025Article
- Advancing cancer therapy: new frontiers in targeting DNA damage response.Frontiers in pharmacology · 2024Review
- The Combination of ATM and Chk1 Inhibitors Induces Synthetic Lethality in Colorectal Cancer Cells.Cancers · 2023Article
- FGFR2 loss sensitizes MYCN-amplified neuroblastoma CHP134 cells to CHK1 inhibitor-induced apoptosis.Cancer science · 2022Article
- Exploiting DNA repair pathways for tumor sensitization, mitigation of resistance, and normal tissue protection in radiotherapy.Cancer drug resistance (Alhambra, Calif.) · 2021Article
- UBE2T-regulated H2AX monoubiquitination induces hepatocellular carcinoma radioresistance by facilitating CHK1 activation.Journal of experimental & clinical cancer research : CR · 2020Article
- Role for Metallothionein-3 in the Resistance of Human U87 Glioblastoma Cells to Temozolomide.ACS omega · 2020Article
- MicroRNA-708 Suppresses Cell Proliferation and Enhances Chemosensitivity of Cervical Cancer Cells to cDDP by Negatively Targeting Timeless.OncoTargets and therapy · 2020Article
- Co-Inhibition of the DNA Damage Response and CHK1 Enhances Apoptosis of Neuroblastoma Cells.International journal of molecular sciences · 2019Article
- MTH1 deficiency selectively increases non-cytotoxic oxidative DNA damage in lung cancer cells: more bad news than good?BMC cancer · 2018Article
- Paths from DNA damage and signaling to genome rearrangements via homologous recombination.Mutation research · 2017Review
- Translational research in radiation-induced DNA damage signaling and repair.Translational cancer research · 2017Article
- A novel Chk1-binding peptide that enhances genotoxic sensitivity through the cellular redistribution of nuclear Chk1.International journal of molecular medicine · 2016Article
- DNA Damage Signalling and Repair Inhibitors: The Long-Sought-After Achilles' Heel of Cancer.Biomolecules · 2015Review
- TIPIN depletion leads to apoptosis in breast cancer cells.Molecular oncology · 2015Article
- Checkpoint kinase1 (CHK1) is an important biomarker in breast cancer having a role in chemotherapy response.British journal of cancer · 2015Article
- Untangling the ATR-CHEK1 network for prognostication, prediction and therapeutic target validation in breast cancer.Molecular oncology · 2015Article
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 2 institutions in 2 countries.
Funding
Abstract
A paramount objective of the eukaryotic cell division cycle is to overcome numerous internal and external insults to faithfully duplicate the genetic information once per every cycle. This is carried out by elaborate networks of genome surveillance signaling pathways, termed replication checkpoints. Central to replication checkpoints are two protein kinases, the upstream kinase ATR, and its downstream target kinase, Chk1. When the DNA replication process is interrupted, the ATR-Chk1 pathway transmits signals to delay cell cycle progression, and to maintain fork viability so that DNA duplication can resume after the initial damage is corrected. Previous studies showed that replicative stress not only activated Chk1, but also triggered the ubiquitin-dependent destruction of Chk1 in cultured human cells. In a recent study, we identified the F-box protein, Fbx6, as the mediator that regulates Chk1 ubiquitination and degradation in both normally cycling cells and during replication stress. We further showed that expression levels of Chk1 and Fbx6 exhibited an overall inverse correlation in both cultured cancer cell lines and in breast tumor tissues, and that defects in Chk1 degradation, for instance, due to reduced expression of Fbx6, rendered tumor cells resistant to anticancer treatment. Here we highlight those findings and their implications in the replication checkpoint and cellular sensitivity to cancer therapies.
Indexed as
Identifiers
What OpenQuestion holds
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.