ReviewCellular and molecular life sciences : CMLS2010
Targeting abnormal DNA double strand break repair in cancer.
Review in Cellular and molecular life sciences : CMLS, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed.
- Inhibitors of phosphoinositide 3-kinase (PI3K) and phosphoinositide 3-kinase-related protein kinase family (PIKK).Journal of enzyme inhibition and medicinal chemistry · 2023Review
- The role of peptides in reversing chemoresistance of breast cancer: current facts and future prospects.Frontiers in pharmacology · 2023Review
- Article
- Dual mTOR/DNA-PK Inhibitor CC-115 Induces Cell Death in Melanoma Cells and Has Radiosensitizing Potential.International journal of molecular sciences · 2020Article
- Partnering with PARP inhibitors in acute myeloid leukemia with FLT3-ITD.Cancer letters · 2019Review
- Induction of HRR genes and inhibition of DNMT1 is associated with anthracycline anti-tumor antibiotic-tolerant breast carcinoma cells.Molecular and cellular biochemistry · 2019Article
- Article
- DNA polymerase beta participates in DNA End-joining.Nucleic acids research · 2018Article
- Enhancing the Cytotoxic Effects of PARP Inhibitors with DNA Demethylating Agents - A Potential Therapy for Cancer.Cancer cell · 2016Article
- Scaffold attachment factor A (SAF-A) and Ku temporally regulate repair of radiation-induced clustered genome lesions.Oncotarget · 2016Article
- DNA polymerase θ (POLQ), double-strand break repair, and cancer.DNA repair · 2016Review
- Article
- High-Fidelity Reprogrammed Human IPSCs Have a High Efficacy of DNA Repair and Resemble hESCs in Their MYC Transcriptional Signature.Stem cells international · 2016Article
- Human DNA ligase III bridges two DNA ends to promote specific intermolecular DNA end joining.Nucleic acids research · 2015Article
- Aromatase Inhibitor-Mediated Downregulation of INrf2 (Keap1) Leads to Increased Nrf2 and Resistance in Breast Cancer.Molecular cancer therapeutics · 2015Article
- c-MYC Generates Repair Errors via Increased Transcription of Alternative-NHEJ Factors, LIG3 and PARP1, in Tyrosine Kinase-Activated Leukemias.Molecular cancer research : MCR · 2015Article
- Expression of a novel peptide derived from PCNA damages DNA and reverses cisplatin resistance.Cancer chemotherapy and pharmacology · 2014Article
- Mechanism of suppression of chromosomal instability by DNA polymerase POLQ.PLoS genetics · 2014Article
- Mechanisms of injury to normal tissue after radiotherapy: a review.Plastic and reconstructive surgery · 2014Review
- Effect of EME1 exon variant Ile350Thr on risk and early onset of breast cancer in southern Chinese women.Journal of biomedical research · 2013Article
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.
Funding
Abstract
A major challenge in cancer treatment is the development of therapies that target cancer cells with little or no toxicity to normal tissues and cells. Alterations in DNA double strand break (DSB) repair in cancer cells include both elevated and reduced levels of key repair proteins and changes in the relative contributions of the various DSB repair pathways. These differences can result in increased sensitivity to DSB-inducing agents and increased genomic instability. The development of agents that selectively inhibit the DSB repair pathways that cancer cells are more dependent upon will facilitate the design of therapeutic strategies that exploit the differences in DSB repair between normal and cancer cells. Here, we discuss the pathways of DSB repair, alterations in DSB repair in cancer, inhibitors of DSB repair and future directions for cancer therapies that target DSB repair.
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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.