scholarly journals Radiation therapy-induced reactive oxygen species specifically eliminates CD19+ IgA+ B cells in nasopharyngeal carcinoma

2019 ◽  
Vol Volume 11 ◽  
pp. 6299-6309 ◽  
Author(s):  
Weiwei Li ◽  
Luman Wang ◽  
Chunying Shen ◽  
Tingting Xu ◽  
Yiwei Chu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Radiation Therapy ◽  
B Cells ◽  
Nasopharyngeal Carcinoma ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Role of Natural Radiosensitizers and Cancer Cell Radioresistance: An Update

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Arif Malik ◽  
Misbah Sultana ◽  
Aamer Qazi ◽  
Mahmood Husain Qazi ◽  
Gulshan Parveen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Radiation Therapy ◽  
Cancer Stem Cells ◽  
Ionizing Radiation ◽  
Malignant Tumors ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Ros Scavenging

Cancer originates from genetic mutations accumulation. Cancer stem cells have been depicted as tumorigenic cells that can differentiate and self-renew. Cancer stem cells are thought to be resistant to conventional therapy like chemotherapy and radiation therapy. Radiation therapy and chemotherapy damage carcinomic DNA cells. Because of the ability of cancer stem cells to self-renew and reproduce malignant tumors, they are the subject of intensive research. In this review, CSCs radioresistant mechanisms which include DNA damage response and natural radiosensitizers have been summed up. Reactive oxygen species play an important role in different physiological processes. ROS scavenging is responsible for regulation of reactive oxygen species generation. A researcher has proved that microRNAs regulate tumor radiation resistance. Ionizing radiation does not kill the cancer cells; rather, IR just slows down the signs and symptoms. Ionizing radiation damages DNA directly/indirectly. IR is given mostly in combination with other chemo/radiotherapies. We briefly described here the behavior of cancer stem cells and radioresistance therapies in cancer treatment. To overcome radioresistance in treatment of cancer, strategies like fractionation modification, treatment in combination, inflammation modification, and overcoming hypoxic tumor have been practiced. Natural radiosensitizers, for example, curcumin, genistein, and quercetin, are more beneficial than synthetic compounds.

scholarly journals Synergistically Enhancing the Therapeutic Effect of Radiation Therapy with Radiation Activatable and Reactive Oxygen Species-Releasing Nanostructures

ACS Nano ◽  
2018 ◽  
Vol 12 (5) ◽  
pp. 4946-4958 ◽  
Author(s):  
Kai Cheng ◽  
Michael Sano ◽  
Cesare H. Jenkins ◽  
Guanglei Zhang ◽  
Don Vernekohl ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Radiation Therapy ◽  
Therapeutic Effect ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals 4440 Enhanced radiation therapy using chlorin-e6 conjugated gold nanoparticles

2020 ◽  
Vol 4 (s1) ◽  
pp. 107-107
Author(s):  
Samir V Jenkins ◽  
Robert J. Griffin
Keyword(s):  
Reactive Oxygen Species ◽  
Gold Nanoparticles ◽  
Radiation Therapy ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Cell Killing ◽  
Chlorin E6 ◽  
List Type ◽  
Oxygen Species ◽  
Vis Spectroscopy

OBJECTIVES/GOALS: Development of gold nanoparticles covalently linked to a photosensitizer for use to enhance radiation therapy. The particles will be thoroughly characterized structurally and mechanistically. The gold particles should enhance radiation activity by closer proximity to the photosensitizer and by increasing particle accumulation in the tumor.METHODS/STUDY POPULATION: Gold nanoparticles were synthesized and coated with amine-terminated poly(ethylene) glycol, then covalently conjugated to chlorin e6, a known FDA-approved photosensitizer. The system was characterized using UV-Vis spectroscopy, transmission electron microscopy, and nanoparticle tracking analysis. The generation of reactive oxygen species was measured after X-irradiation. Enhanced cell killing was evaluated clonogenically in addition to assessment of in vivo efficacy and tumor pathology.RESULTS/ANTICIPATED RESULTS: Conjugation of the particle to the photosensitizer was achieved, and the molecule was detected by UV-Vis spectroscopy. TEM and NTA showed no aggregation of the particles, and an increase in reactive oxygen species generation was observed. The conjugates increased cell killing during radiation treatment, whereas neither the particle alone nor the photosensitizer significantly affected clonogenic survival at the same concentrations. Breast tumors grown in immunocompetent mice showed increased necrotic tissue after a single 20 gy treatment in the presence of the conjugate.DISCUSSION/SIGNIFICANCE OF IMPACT: Radiation therapy is widely used clinically, but dosage is limited largely to prevent injury to adjacent normal tissue. By increasing the local effect of radiation therapy, our gold conjugate has the potential to augment the effective radiation dose in the tumor, thereby reducing damage to healthy tissue and providing a more effective therapy.

Green Tea Component, Catechin, Induces Apoptosis of Human Malignant B Cells via Production of Reactive Oxygen Species

2005 ◽  
Vol 11 (16) ◽  
pp. 6040-6049 ◽  
Author(s):  
Tomonori Nakazato ◽  
Keisuke Ito ◽  
Yasuo Ikeda ◽  
Masahiro Kizaki
Keyword(s):  
Reactive Oxygen Species ◽  
B Cells ◽  
Green Tea ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Ibrutinib Selects for Cells with Elevated Reactive Oxygen Species and Downregulated Phosphatases

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 3795-3795
Author(s):  
Nathan Camp ◽  
Meghan Garrett ◽  
Ajay K. Gopal ◽  
Richard James
Keyword(s):  
Reactive Oxygen Species ◽  
B Cells ◽  
B Cell ◽  
Cell Lines ◽  
Cell Lymphoma ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Oxygen Species

Signals from the B-cell receptor are inappropriately activated in B-cell malignancies, including Chronic lymphocytic leukemia (CLL), Mantle cell lymphoma (MCL), and Diffuse large B-cell lymphoma (DLBCL). In CLL, 90% of patients respond to treatment with ibrutinib, an inhibitor of Bruton's Tyrosine Kinase (BTK), with a mean three-year progression free survival rate of approximately 60%. Despite these promising numbers, patients who do not initially respond to ibrutinib have extremely poor outcomes, and nearly all patients eventually become resistant to ibrutinib due to mutations in BTK and its downstream effector Phospholipase C gamma 2 (PLCG2), with a median survival time of 23 months. In order to identify salvage therapies for ibrutinib-resistant patients, we employed several quantitative proteomic methods to identify signaling pathways and proteins that are essential in ibrutinib-resistant patient cells and cell lines. Total proteomic analysis of lymphoma cell lines selected with ibrutinib in vitro revealed that multiple mitochondrial proteins are increased in B cells exposed to ibrutinib. Next, we found that ibrutinib-treated B cells also exhibited increases in reactive oxygen species (ROS), which potently inhibit several protein phosphatases, including B cell receptor signaling regulators PTPN6 and INPP5D. We next looked at tyrosine phosphorylation in patient B cells collected at several time points during ibrutinib treatment and found decreased phosphorylation of both PTPN6 (Y536) and INPP5D (Y944 and Y865) during treatment. Furthermore, total levels of PTPN6 are decreased in patients within 3 months of initiating treatment, and disruption of PTPN6 in cell lines by CRISPR provided a selective advantage in ibrutinib-treated cell populations. Finally, we found that ibrutinib-treated and ibrutinib-naïve primary CLL cells are sensitive to compounds that prevent reactive oxygen species generation (SOD and PHOX inhibitors). Combined, we propose a mechanism by which ibrutinib treatment leads to increased levels of ROS and decreased phosphatase activity, ultimately leading to a growth advantage in the presence of ibrutinib without concomitant mutations in PLCG2 and BTK. We hypothesize that targeting proteins important for reactive oxygen species generation would also be useful in patients and could result in regained disease control and/or prevention of acquired resistance. Disclosures Gopal: Seattle Genetics, Pfizer, Janssen, Gilead, Sanofi, Spectrum, Amgen, Aptevo, BRIM bio, Acerta, I-Mab-pharma, Takeda, Compliment, Asana Bio, and Incyte.: Consultancy; Teva, Bristol-Myers Squibb, Merck, Takeda, Seattle Genetics, Pfizer, Janssen, Takeda, and Effector: Research Funding; Seattle Genetics, Pfizer, Janssen, Gilead, Sanofi, Spectrum, Amgen, Aptevo, BRIM bio, Acerta, I-Mab-pharma, Takeda, Compliment, Asana Bio, and Incyte: Honoraria.

scholarly journals Differential Effects of Reactive Oxygen Species on IgG versus IgM Levels in TLR-Stimulated B Cells

2020 ◽  
Vol 204 (8) ◽  
pp. 2133-2142 ◽  
Author(s):  
Karin Margaretha Gilljam ◽  
Kristine Lillebø Holm ◽  
Muhammad Zahoor ◽  
Federica Grazia Centonze ◽  
Hesso Farhan ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
B Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Differential Effects
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