scholarly journals Melatonin as a Radio-Sensitizer in Cancer

Biomedicines ◽  
2020 ◽  
Vol 8 (8) ◽  
pp. 247
Author(s):  
Carolina Alonso-González ◽  
Alicia González ◽  
Javier Menéndez-Menéndez ◽  
Carlos Martínez-Campa ◽  
Samuel Cos
Keyword(s):  
Side Effects ◽  
Tumor Cells ◽  
Cancer Growth ◽  
Therapeutic Effects ◽  
Oxygen Species ◽  
Normal Cells ◽  
Normal Tissues ◽  
Species Production ◽  
Estrogen Biosynthesis ◽  
Stimulation Of

Radiotherapy is one of the treatments of choice in many types of cancer. Adjuvant treatments to radiotherapy try, on one hand, to enhance the response of tumor cells to radiation and, on the other hand, to reduce the side effects to normal cells. Radiosensitizers are agents that increase the effect of radiation in tumor cells by trying not to increase side effects in normal tissues. Melatonin is a hormone produced mainly by the pineal gland which has an important role in the regulation of cancer growth, especially in hormone-dependent mammary tumors. Different studies have showed that melatonin administered with radiotherapy is able to enhance its therapeutic effects and can protect normal cells against side effects of this treatment. Several mechanisms are involved in the radiosensitization induced by melatonin: increase of reactive oxygen species production, modulation of proteins involved in estrogen biosynthesis, impairment of tumor cells to DNA repair, modulation of angiogenesis, abolition of inflammation, induction of apoptosis, stimulation of preadipocytes differentiation and modulation of metabolism. At this moment, there are very few clinical trials that study the therapeutic usefulness to associate melatonin and radiotherapy in humans. All findings point to melatonin as an effective adjuvant molecule to radiotherapy in cancer treatment.

NADPH Oxidase as a Target for Modulation of Radiation Response; Implications to Carcinogenesis and Radiotherapy

2019 ◽  
Vol 12 (1) ◽  
pp. 50-60 ◽  
Author(s):  
Keywan Mortezaee ◽  
Nasser Hashemi Goradel ◽  
Peyman Amini ◽  
Dheyauldeen Shabeeb ◽  
Ahmed Eleojo Musa ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Nadph Oxidase ◽  
Tumor Cells ◽  
Normal Tissue ◽  
Therapeutic Effects ◽  
Radiation Toxicity ◽  
Ros Production ◽  
Normal Tissues ◽  
Increased Risk ◽  
Stimulation Of

Background:Radiotherapy is a treatment modality for cancer. For better therapeutic efficiency, it could be used in combination with surgery, chemotherapy or immunotherapy. In addition to its beneficial therapeutic effects, exposure to radiation leads to several toxic effects on normal tissues. Also, it may induce some changes in genomic expression of tumor cells, thereby increasing the resistance of tumor cells. These changes lead to the appearance of some acute reactions in irradiated organs, increased risk of carcinogenesis, and reduction in the therapeutic effect of radiotherapy.Discussion:So far, several studies have proposed different targets such as cyclooxygenase-2 (COX-2), some toll-like receptors (TLRs), mitogen-activated protein kinases (MAPKs) etc., for the amelioration of radiation toxicity and enhancing tumor response. NADPH oxidase includes five NOX and two dual oxidases (DUOX1 and DUOX2) subfamilies that through the production of superoxide and hydrogen peroxide, play key roles in oxidative stress and several signaling pathways involved in early and late effects of ionizing radiation. Chronic ROS production by NOX enzymes can induce genomic instability, thereby increasing the risk of carcinogenesis. Also, these enzymes are able to induce cell death, especially through apoptosis and senescence that may affect tissue function. ROS-derived NADPH oxidase causes apoptosis in some organs such as intestine and tongue, which mediate inflammation. Furthermore, continuous ROS production stimulates fibrosis via stimulation of fibroblast differentiation and collagen deposition. Evidence has shown that in contrast to normal tissues, the NOX system induces tumor resistance to radiotherapy through some mechanisms such as induction of hypoxia, stimulation of proliferation, and activation of macrophages. However, there are some contradictory results. Inhibition of NADPH oxidase in experimental studies has shown promising results for both normal tissue protection and tumor sensitization to ionizing radiation.Conclusion:In this article, we aimed to review the role of different subfamilies of NADPH oxidase in radiation-induced early and late normal tissue toxicities in different organs.

scholarly journals Enzyme-Responsive Materials as Carriers for Improving Photodynamic Therapy

2021 ◽  
Vol 9 ◽  
Author(s):  
Houhe Liu ◽  
Fanwen Yang ◽  
Wenjie Chen ◽  
Teng Gong ◽  
Yi Zhou ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Photodynamic Therapy ◽  
Side Effects ◽  
Clinical Application ◽  
Smart Materials ◽  
Therapeutic Effects ◽  
Oxygen Species ◽  
Responsive Materials ◽  
Normal Tissues ◽  
Tumor Tissues

Photodynamic therapy (PDT) is a mini-invasive therapy on malignancies via reactive oxygen species (ROS) induced by photosenitizer (PS) upon light irradiation. However, poor target of PS to tumor limits the clinical application of PDT. Compared with normal tissues, tumor tissues have a unique enzymatic environment. The unique enzymatic environment in tumor tissues has been widely used as a target for developing smart materials to improve the targetability of drugs to tumor. Enzyme-responsive materials (ERM) as a smart material can respond to the enzymes in tumor tissues to specifically deliver drugs. In PDT, ERM was designed to react with the enzymes highly expressed in tumor tissues to deliver PS in the target site to prevent therapeutic effects and avoid its side-effects. In the present paper, we will review the application of ERM in PDT and discuss the challenges of ERM as carriers to deliver PS for further boosting the development of PDT in the management of malignancies.

The Role of Reactive Oxygen Species in Tumor Treatment and its Impact on Bone Marrow Hematopoiesis

2020 ◽  
Vol 21 (5) ◽  
pp. 477-498
Author(s):  
Yongfeng Chen ◽  
Xingjing Luo ◽  
Zhenyou Zou ◽  
Yong Liang
Keyword(s):  
Reactive Oxygen Species ◽  
Bone Marrow ◽  
Oxidative Damage ◽  
Tumor Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tumor Treatment ◽  
Normal Cells ◽  
Treatment And Prevention

Reactive oxygen species (ROS), an important molecule inducing oxidative stress in organisms, play a key role in tumorigenesis, tumor progression and recurrence. Recent findings on ROS have shown that ROS can be used to treat cancer as they accelerate the death of tumor cells. At present, pro-oxidant drugs that are intended to increase ROS levels of the tumor cells have been widely used in the clinic. However, ROS are a double-edged sword in the treatment of tumors. High levels of ROS induce not only the death of tumor cells but also oxidative damage to normal cells, especially bone marrow hemopoietic cells, which leads to bone marrow suppression and (or) other side effects, weak efficacy of tumor treatment and even threatening patients’ life. How to enhance the killing effect of ROS on tumor cells while avoiding oxidative damage to the normal cells has become an urgent issue. This study is a review of the latest progress in the role of ROS-mediated programmed death in tumor treatment and prevention and treatment of oxidative damage in bone marrow induced by ROS.

scholarly journals Targeting Engineered Nanoparticles for Breast Cancer Therapy

Pharmaceutics ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 1829
Author(s):  
Kumar Ganesan ◽  
Yan Wang ◽  
Fei Gao ◽  
Qingqing Liu ◽  
Chen Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Side Effects ◽  
Exploratory Study ◽  
Engineered Nanoparticles ◽  
Therapeutic Effects ◽  
Breast Cancer Therapy ◽  
Normal Tissues ◽  
Therapeutic Drugs ◽  
Common Cancer ◽  
Important Approach

Breast cancer (BC) is the second most common cancer in women globally after lung cancer. Presently, the most important approach for BC treatment consists of surgery, followed by radiotherapy and chemotherapy. The latter therapeutic methods are often unsuccessful in the treatment of BC because of their various side effects and the damage incurred to healthy tissues and organs. Currently, numerous nanoparticles (NPs) have been identified and synthesized to selectively target BC cells without causing any impairments to the adjacent normal tissues or organs. Based on an exploratory study, this comprehensive review aims to provide information on engineered NPs and their payloads as promising tools in the treatment of BC. Therapeutic drugs or natural bioactive compounds generally incorporate engineered NPs of ideal sizes and shapes to enhance their solubility, circulatory half-life, and biodistribution, while reducing their side effects and immunogenicity. Furthermore, ligands such as peptides, antibodies, and nucleic acids on the surface of NPs precisely target BC cells. Studies on the synthesis of engineered NPs and their impact on BC were obtained from PubMed, Science Direct, and Google Scholar. This review provides insights on the importance of engineered NPs and their methodology for validation as a next-generation platform with preventive and therapeutic effects against BC.

scholarly journals Nano-Therapies for Glioblastoma Treatment

Cancers ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 242 ◽  
Author(s):  
Alphandéry
Keyword(s):  
Tumor Cells ◽  
Immune Cells ◽  
Treg Cells ◽  
Oxygen Species ◽  
Radical Oxygen Species ◽  
Cancer Treatments ◽  
Therapeutic Drugs ◽  
Anti Cancer ◽  
Stimulation Of ◽  
Apoptotic Mechanism

Traditional anti-cancer treatments are inefficient against glioblastoma, which remains one of the deadliest and most aggressive cancers. Nano-drugs could help to improve this situation by enabling: (i) an increase of anti-glioblastoma multiforme (GBM) activity of chemo/gene therapeutic drugs, notably by an improved diffusion of these drugs through the blood brain barrier (BBB), (ii) the sensibilization of radio-resistant GBM tumor cells to radiotherapy, (iii) the removal by surgery of infiltrating GBM tumor cells, (iv) the restoration of an apoptotic mechanism of GBM cellular death, (v) the destruction of angiogenic blood vessels, (vi) the stimulation of anti-tumor immune cells, e.g., T cells, NK cells, and the neutralization of pro-tumoral immune cells, e.g., Treg cells, (vii) the local production of heat or radical oxygen species (ROS), and (viii) the controlled release/activation of anti-GBM drugs following the application of a stimulus. This review covers these different aspects.

scholarly journals Stimulation of P2X7 receptors causes Ca2+‐ and PKC‐mediated reactive oxygen species production in murine macrophages

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Guadalupe Martel‐Gallegos ◽  
Griselda Casas‐Pruneda ◽  
Filiberta Ortega ◽  
Sergio Sanchez‐Armass ◽  
Patricia Perez‐Cornejo ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
P2x7 Receptors ◽  
Murine Macrophages ◽  
Species Production ◽  
Stimulation Of

scholarly journals The Role of Mirk Kinase in Sarcomas

Sarcoma ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Eileen Friedman
Keyword(s):  
Tumor Cells ◽  
Gastrointestinal Stromal Tumors ◽  
Oxygen Species ◽  
Chemotherapeutic Drugs ◽  
Antioxidant Genes ◽  
Tumor Cell Apoptosis ◽  
Stromal Tumors ◽  
Normal Tissues ◽  
Low Levels

Targeting the tyrosine kinase KIT in gastrointestinal stromal tumors has led to improved treatment. Other kinases might serve as therapeutic targets in the more common forms of sarcoma. The kinase Mirk/dyrk1B is highly expressed in the vast majority of osteosarcomas and rhabdomyosarcomas and mediates their growth, as depletion of Mirk led to tumor cell apoptosis. Mirk is known to increase the expression of a series of antioxidant genes, which scavenge reactive oxygen species (ROS) within various tumor cells, mediating their survival. As a result, depleting Mirk led to increased levels of damaging ROS. Tumor cells depleted of Mirk were also sensitized to low levels of chemotherapeutic drugs that increase ROS levels. In contrast, Mirk expression is quite low in most normal cells, and Mirk depletion or embryonic knockout of Mirk did not detectably affect cell survival. Thus targeting Mirk for intervention in sarcomas might spare most normal tissues.

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