ArticleExperimental and therapeutic medicine2012
Lymphoma cells with increased anti-oxidant defenses acquire chemoresistance.
Article in Experimental and therapeutic medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 29 citations in OpenAlex.
- Review of various NAMPT inhibitors for the treatment of cancer.Frontiers in pharmacology · 2022Review
- The E3 Ubiquitin Ligase NEDD4-1 Mediates Temozolomide-Resistant Glioblastoma through PTEN Attenuation and Redox Imbalance in Nrf2-HO-1 Axis.International journal of molecular sciences · 2021Article
- NAD- and NADPH-Contributing Enzymes as Therapeutic Targets in Cancer: An Overview.Biomolecules · 2020Review
- Article
- PGC1α induced by reactive oxygen species contributes to chemoresistance of ovarian cancer cells.Oncotarget · 2017Article
- Knockdown of PKM2 and GLS1 expression can significantly reverse oxaliplatin-resistance in colorectal cancer cells.Oncotarget · 2017Article
- Redox Regulating Enzymes and Connected MicroRNA Regulators Have Prognostic Value in Classical Hodgkin Lymphomas.Oxidative medicine and cellular longevity · 2017Article
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- Redox Control of Multidrug Resistance and Its Possible Modulation by Antioxidants.Oxidative medicine and cellular longevity · 2016Review
- Fasting induces anti-Warburg effect that increases respiration but reduces ATP-synthesis to promote apoptosis in colon cancer models.Oncotarget · 2015Article
- Copper-zinc superoxide dismutase-mediated redox regulation of bortezomib resistance in multiple myeloma.Redox biology · 2015Article
- Mitochondria and redox homoeostasis as chemotherapeutic targets.Biochemical Society transactions · 2014Review
- The copper chelator ATN-224 induces peroxynitrite-dependent cell death in hematological malignancies.Free radical biology & medicine · 2013Article
- Clinical efficacy of CyberKnife combined with chemotherapy and hyperthermia for advanced non-small cell lung cancer.Molecular and clinical oncology · 2013Article
- Stalling the engine of resistance: targeting cancer metabolism to overcome therapeutic resistance.Cancer research · 2013Review
- Efficacy study of CyberKnife stereotactic radiosurgery combined with CIK cell immunotherapy for advanced refractory lung cancer.Experimental and therapeutic medicine · 2013Article
- Mitochondrial adaptations to oxidative stress confer resistance to apoptosis in lymphoma cells.International journal of molecular sciences · 2012Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Chronic inflammation increases lymphoma risk. Chronic inflammation exposes cells to increased reactive oxygen species (ROS). Constant exposure to ROS selects for oxidative stress-resistant cells with upregulated anti-oxidant defense enzymes. The impact of oxidative stress resistance on the redox biology and chemotherapy response in lymphoma has not been rigorously tested. To measure the effect of antioxidant defense enzyme upregulation in lymphoid cells, we created oxidative stress-resistant WEHI7.2 thymic lymphoma cell variants. We selected a population of WEHI7.2 cells for resistance to hydrogen peroxide and constructed catalase-overexpressing WEHI7.2 transfectants. The WEHI7.2 variants had: i) increased catalase and total superoxide dismutase activities; ii) an altered GSSG/2GSH redox potential; iii) a more oxidized NADP(+)/NADPH pool; and iv) increased phase 2 enzymes, NAD(P)H:quinone oxidoreductase and glutathione S-transferases μ and π. Regression analysis showed a correlation between the GSSG/2GSH redox potential and the increased phase 2 enzyme activities. As predicted from the anti-oxidant defense enzyme profile, the variants were more resistant to the oxidants hydrogen peroxide and paraquat. The variants exhibited resistance to the common lymphoma chemotherapeutics, cyclophosphamide, doxorubicin, vincristine and glucocorticoids. These data indicate that chronic ROS exposure results in lymphoid cells with multiple changes in their redox biology and a chemoresistance phenotype. These data further suggest that lymphomas that arise at the site of chronic inflammation develop chemoresistance due to a combination of drug detoxification and removal of ROS.
Identifiers
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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.