“…In oncology, surgery, image-guided ablation, local radiation therapy (RT), and systemic chemotherapeutics are the four clinical treatment modalities, but all are accompanied by significant adverse effects [13,14]. RT commonly used in the management of head and neck tumors causes skin burns and affects voice, jawbone, and teeth [15].…”
Purpose
High-intensity focused ultrasound (HIFU/FUS) has expanded as a noninvasive quantifiable option for hyperthermia (HT). HT in a temperature range of 40–47 °C (thermal dose CEM43 ≥ 25) could work as a sensitizer to radiation therapy (RT). Here, we attempted to understand the tumor radiosensitization effect at the cellular level after a combination treatment of FUS+RT.
Methods
An in vitro FUS system was developed to induce HT at frequencies of 1.147 and 1.467 MHz. Human head and neck cancer (FaDU), glioblastoma (T98G), and prostate cancer (PC-3) cells were exposed to FUS in ultrasound-penetrable 96-well plates followed by single-dose X‑ray irradiation (10 Gy). Radiosensitizing effects of FUS were investigated by cell metabolic activity (WST‑1 assay), apoptosis (annexin V assay, sub-G1 assay), cell cycle phases (propidium iodide staining), and DNA double-strand breaks (γH2A.X assay).
Results
The FUS intensities of 213 (1.147 MHz) and 225 W/cm2 (1.467 MHz) induced HT for 30 min at mean temperatures of 45.20 ± 2.29 °C (CEM43 = 436 ± 88) and 45.59 ± 1.65 °C (CEM43 = 447 ± 79), respectively. FUS improves the effect of RT significantly by reducing metabolic activity in T98G cells 48 h (RT: 96.47 ± 8.29%; FUS+RT: 79.38 ± 14.93%; p = 0.012) and in PC-3 cells 72 h (54.20 ± 10.85%; 41.01 ± 11.17%; p = 0.016) after therapy, but not in FaDu cells. Mechanistically, FUS+RT leads to increased apoptosis and enhancement of DNA double-strand breaks compared to RT alone in T98G and PC-3 cells.
Conclusion
Our in vitro findings demonstrate that FUS has good potential to sensitize glioblastoma and prostate cancer cells to RT by mainly enhancing DNA damage.
“…In oncology, surgery, image-guided ablation, local radiation therapy (RT), and systemic chemotherapeutics are the four clinical treatment modalities, but all are accompanied by significant adverse effects [13,14]. RT commonly used in the management of head and neck tumors causes skin burns and affects voice, jawbone, and teeth [15].…”
Purpose
High-intensity focused ultrasound (HIFU/FUS) has expanded as a noninvasive quantifiable option for hyperthermia (HT). HT in a temperature range of 40–47 °C (thermal dose CEM43 ≥ 25) could work as a sensitizer to radiation therapy (RT). Here, we attempted to understand the tumor radiosensitization effect at the cellular level after a combination treatment of FUS+RT.
Methods
An in vitro FUS system was developed to induce HT at frequencies of 1.147 and 1.467 MHz. Human head and neck cancer (FaDU), glioblastoma (T98G), and prostate cancer (PC-3) cells were exposed to FUS in ultrasound-penetrable 96-well plates followed by single-dose X‑ray irradiation (10 Gy). Radiosensitizing effects of FUS were investigated by cell metabolic activity (WST‑1 assay), apoptosis (annexin V assay, sub-G1 assay), cell cycle phases (propidium iodide staining), and DNA double-strand breaks (γH2A.X assay).
Results
The FUS intensities of 213 (1.147 MHz) and 225 W/cm2 (1.467 MHz) induced HT for 30 min at mean temperatures of 45.20 ± 2.29 °C (CEM43 = 436 ± 88) and 45.59 ± 1.65 °C (CEM43 = 447 ± 79), respectively. FUS improves the effect of RT significantly by reducing metabolic activity in T98G cells 48 h (RT: 96.47 ± 8.29%; FUS+RT: 79.38 ± 14.93%; p = 0.012) and in PC-3 cells 72 h (54.20 ± 10.85%; 41.01 ± 11.17%; p = 0.016) after therapy, but not in FaDu cells. Mechanistically, FUS+RT leads to increased apoptosis and enhancement of DNA double-strand breaks compared to RT alone in T98G and PC-3 cells.
Conclusion
Our in vitro findings demonstrate that FUS has good potential to sensitize glioblastoma and prostate cancer cells to RT by mainly enhancing DNA damage.
“…Anthracycline treatment witnessed clinically significant cardiac toxicity due to a generic polymorphism in CELF4, RARG, SLC28A3, and UGT1A6 genes responsible for alterations in anatomical and physiological characteristics of the sarcomere, the expression of topoisomerase-2β, the transportation of drugs, and the biotransformation of drugs, respectively [ 155 ].…”
Section: Genes’ Susceptibility To Cardiotoxicity Induced By Chemotherapeutic Agentsmentioning
The advancement in therapy has provided a dramatic improvement in the rate of recovery among cancer patients. However, this improved survival is also associated with enhanced risks for cardiovascular manifestations, including hypertension, arrhythmias, and heart failure. The cardiotoxicity induced by chemotherapy is a life-threatening consequence that restricts the use of several chemotherapy drugs in clinical practice. This article addresses the prevalence of cardiotoxicity mediated by commonly used chemotherapeutic and immunotherapeutic agents. The role of susceptible genes and radiation therapy in the occurrence of cardiotoxicity is also reviewed. This review also emphasizes the protective role of antioxidants and future perspectives in anticancer drug-induced cardiotoxicities.
“…Although strong evidence and clinical data to guide post-RT cardiac surveillance is lacking and recommendations are based on expert opinions, comprehensive screening and long-term routine follow-up for RIHD, especially of high-risk patients, seem to be prudent, given the high prevalence and long latency period between exposure and onset of the disease [75]. The above is reflected in the consensus statement by the European Association of Cardiovascular Imaging, the American Society of Echocardiography [69], and the guidelines published by the American Society of Clinical Oncology (ASCO), the Canadian Cardiovascular Society, and the European Society of Cardiology (ESC) [13, 76, 77].…”
Despite the advancements of modern radiotherapy, radiation-induced heart disease remains a common cause of morbidity and mortality amongst cancer survivors. This review outlines the basic mechanism, clinical presentation, risk stratification, early detection, possible mitigation, and treatment of this condition.
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