ArticleMolecular pharmacology2009
Cisplatin-induced DNA damage activates replication checkpoint signaling components that differentially affect tumor cell survival.
Article in Molecular pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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
68 citing papers in PubMed, 134 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
- Article
- Exploring new quinoxaline, quinoline, and naphthalene carboxamides as HDAC-targeted anticancer agents: Cytotoxicity, enzymatic HDAC evaluation, and in silico studies.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Article
- High-throughput spheroid-based assay for functional breast cancer precision medicine facilitated by deep learning.Communications medicine · 2026Article
- Curcumin Derivative CU4c Exhibits HDAC-Inhibitory and Anticancer Activities Against Human Lung Cancer Cells In Vitro and in Mouse Xenograft Models.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Cardamom synergizes with cisplatin against human osteosarcoma cells by mTOR-mediated autophagy.Cancer gene therapy · 2025Article
- KW2478 and Cisplatin Synergistically Anti-colorectal Cancer by Targeting PI3K/AKT/mTOR Pathway.Anti-cancer agents in medicinal chemistry · 2025Article
- The microbiome and lung cancer: microbial effects on host immune responses and treatment outcomes.Frontiers in microbiomes · 2025Review
- The ATR inhibitor berzosertib acts as a radio- and chemosensitizer in head and neck squamous cell carcinoma cell lines.Investigational new drugs · 2023Article
- The Gold(I) Complex with Plant Hormone Kinetin Shows Promising In Vitro Anticancer and PPARγ Properties.International journal of molecular sciences · 2023Article
- Article
- TFAP2C Knockdown Sensitizes Bladder Cancer Cells to Cisplatin Treatment via Regulation of EGFR and NF-κB.Cancers · 2022Article
- Loss of NSE-4 Perturbs Genome Stability and DNA Repair inInternational journal of molecular sciences · 2022Article
- The Employment of GeneraNutrients · 2022Review
- Pharmacologic inhibition of ataxia telangiectasia and Rad3-related (ATR) in the treatment of head and neck squamous cell carcinoma.Molecular carcinogenesis · 2022Review
- Article
- A Novel Copper(II) Indenoisoquinoline Complex Inhibits Topoisomerase I, Induces G2 Phase Arrest, and Autophagy in Three Adenocarcinomas.Frontiers in oncology · 2022Article
- Palmitate Enhances the Efficacy of Cisplatin and Doxorubicin against Human Endometrial Carcinoma Cells.International journal of molecular sciences · 2021Article
- DNA Topoisomerase 3α Is Involved in Homologous Recombination Repair and Replication Stress Response inFrontiers in cell and developmental biology · 2021Article
- Microbiome dysbiosis in lung cancer: from composition to therapy.NPJ precision oncology · 2020Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cisplatin and other platinating agents are some of the most widely used chemotherapy agents. These drugs exert their antiproliferative effects by creating intrastrand and interstrand DNA cross-links, which block DNA replication. The cross-links mobilize signaling and repair pathways, including the Rad9-Hus1-Rad1-ATR-Chk1 pathway, a pathway that helps tumor cells survive the DNA damage inflicted by many chemotherapy agents. Here we show that Rad9 and ATR play critical roles in helping tumor cells survive cisplatin treatment. However, depleting Chk1 with small interfering RNA or inhibiting Chk1 with 3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide (AZD7762) did not sensitize these cells to cisplatin, oxaliplatin, or carboplatin. Moreover, when Rad18, Rad51, BRCA1, BRCA2, or FancD2 was disabled, Chk1 depletion did not further sensitize the cells to cisplatin. In fact, Chk1 depletion reversed the sensitivity seen when Rad18 was disabled. Collectively, these studies suggest that the pharmacological manipulation of Chk1 may not be an effective strategy to sensitize tumors to platinating agents.
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.