ArticlePloS one2012
Dose dependent effects on cell cycle checkpoints and DNA repair by bendamustine.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Bendamustine supercharge plus brentuximab vedotin as early salvage therapy following failure to obtain complete metabolic remission after two cycles of adriamycin-bleomycin-vinblastine-dacarbazine for classic Hodgkin lymphoma in patients aged ≤ 60 years: Long-term efficacy results of a retrospective multicentre study.British journal of haematology · 2025Article
- Article
- Article
- Bendamustine: A review of pharmacology, clinical use and immunological effects (Review).Oncology reports · 2022Review
- Review
- Autophagy Inhibition Potentiates the Anticancer Effects of a Bendamustine Derivative NL-101 in Acute T Lymphocytic Leukemia.BioMed research international · 2020Article
- Brentuximab vedotin followed by bendamustine supercharge for refractory or relapsed Hodgkin lymphoma.Blood advances · 2019Article
- Thymine DNA glycosylase as a novel target for melanoma.Oncogene · 2019Article
- Long-term outcomes, secondary malignancies and stem cell collection following bendamustine in patients with previously treated non-Hodgkin lymphoma.British journal of haematology · 2017Observational
- Screening with an NMNAT2-MSD platform identifies small molecules that modulate NMNAT2 levels in cortical neurons.Scientific reports · 2017Article
- Inhibition of STAT3 by Anticancer Drug Bendamustine.PloS one · 2017Article
- Pixantrone induces cell death through mitotic perturbations and subsequent aberrant cell divisions.Cancer biology & therapy · 2015Article
- Re-purposing clinical kinase inhibitors to enhance chemosensitivity by overriding checkpoints.Cell cycle (Georgetown, Tex.) · 2014Article
- Article
- Gallotannin imposes S phase arrest in breast cancer cells and suppresses the growth of triple-negative tumors in vivo.PloS one · 2014Article
- A synthetic lethal screen identifies the Vitamin D receptor as a novel gemcitabine sensitizer in pancreatic cancer cells.Cell cycle (Georgetown, Tex.) · 2014Article
- Centromere fragmentation is a common mitotic defect of S and G2 checkpoint override.Cell cycle (Georgetown, Tex.) · 2013Article
- Chemotherapy induced DNA damage response: convergence of drugs and pathways.Cancer biology & therapy · 2013Review
- Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Bendamustine (BDM) is an active chemotherapeutic agent approved in the U. S. for treating chronic lymphocytic leukemia and non-Hodgkin lymphoma. Its chemical structure suggests it may have alkylator and anti-metabolite activities; however the precise mechanism of action is not well understood. Here we report the concentration-dependent effects of BDM on cell cycle, DNA damage, checkpoint response and cell death in HeLa cells. Low concentrations of BDM transiently arrested cells in G2, while a 4-fold higher concentration arrested cells in S phase. DNA damage at 50, but not 200 µM, was efficiently repaired after 48 h treatment, suggesting a difference in DNA repair efficiency at the two concentrations. Indeed, perturbing base-excision repair sensitized cells to lower concentrations of BDM. Timelapse studies of the checkpoint response to BDM showed that inhibiting Chk1 caused both the S- and G2-arrested cells to prematurely enter mitosis. However, whereas the cells arrested in G2 (low dose BDM) entered mitosis, segregated their chromosomes and divided normally, the S-phase arrested cells (high dose BDM) exhibited a highly aberrant mitosis, whereby EM images showed highly fragmented chromosomes. The vast majority of these cells died without ever exiting mitosis. Inhibiting the Chk1-dependent DNA damage checkpoint accelerated the time of killing by BDM. Our studies suggest that BDM may affect different biological processes depending on drug concentration. Sensitizing cells to killing by BDM can be achieved by inhibiting base-excision repair or disrupting the DNA damage checkpoint pathway.
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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.