ReviewCurrent oncology reports2007
The role of DNA repair in chronic lymphocytic leukemia pathogenesis and chemotherapy resistance.
Review in Current oncology reports, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 15 citations in OpenAlex.
- Involvement of classic and alternative non-homologous end joining pathways in hematologic malignancies: targeting strategies for treatment.Experimental hematology & oncology · 2021Review
- HMGB1 interacts with XPA to facilitate the processing of DNA interstrand crosslinks in human cells.Nucleic acids research · 2016Article
- Poly(ADP-ribose) polymerase inhibitor CEP-8983 synergizes with bendamustine in chronic lymphocytic leukemia cells in vitro.Leukemia research · 2014Article
- Telomerase contributes to fludarabine resistance in primary human leukemic lymphocytes.PloS one · 2013Article
- Article
- Targeting and processing of site-specific DNA interstrand crosslinks.Environmental and molecular mutagenesis · 2010Review
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
No grant is acknowledged in the PubMed record.
Abstract
Front-line therapy for chronic lymphocytic leukemia (CLL) with alkylating agents is associated with low rates of complete remission and no improvement in overall survival. The ability of CLL cells to efficiently repair alkylator-induced damage to DNA might explain this lack of response. Novel strategies that inhibit DNA repair, such as combinations of alkylating agents, purine nucleoside analogues, and immunotherapy, have produced durable clinical and molecular remission in both untreated and relapsed CLL. This review evaluates the contribution of DNA repair processes in the development of resistance to chemotherapy and the impact of therapies that exploit the DNA repair capacity of CLL cells to therapeutic advantage.
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.