scholarly journals The Role of Radiotherapy towards Pediatric Cancer

2021 ◽  
Vol 11 (2) ◽  
pp. 57-65
Author(s):  
Agustinus Darmadi Hariyanto ◽  
Hari Murti Wijaya ◽  
Jellyca Anton ◽  
Seize Edwiena Yanuarta ◽  
Steven Octavianus ◽  
...  
Keyword(s):  
Pediatric Cancer

ACE2/Angiotensin-(1-7)/Mas Receptor Axis in Human Cancer: Potential Role for Pediatric Tumors

2020 ◽  
Vol 21 (9) ◽  
pp. 892-901 ◽  
Author(s):  
Ana Luiza Ataide Carneiro de Paula Gonzaga ◽  
Vitória Andrade Palmeira ◽  
Thomas Felipe Silva Ribeiro ◽  
Larissa Braga Costa ◽  
Karla Emília de Sá Rodrigues ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Angiotensin Ii ◽  
Pediatric Cancer ◽  
Pediatric Patients ◽  
Human Cancer ◽  
Experimental Studies ◽  
At1 Receptor ◽  
Pediatric Tumors ◽  
Mas Receptor

Background: Pediatric tumors remain the highest cause of death in developed countries. Research on novel therapeutic strategies with lesser side effects is of utmost importance. In this scenario, the role of Renin-Angiotensin System (RAS) axes, the classical one formed by angiotensinconverting enzyme (ACE), Angiotensin II and AT1 receptor and the alternative axis composed by ACE2, Angiotensin-(1-7) and Mas receptor, have been investigated in cancer. Objective: This review aimed to summarize the pathophysiological role of RAS in cancer, evidence for anti-tumor effects of ACE2/Angiotensin-(1-7)/Mas receptor axis and future therapeutic perspectives for pediatric cancer. Methods: Pubmed, Scopus and Scielo were searched in regard to RAS molecules in human cancer and pediatric patients. The search terms were “RAS”, “ACE”, “Angiotensin-(1-7)”, “ACE2”, “Angiotensin II”, “AT1 receptor”, “Mas receptor”, “Pediatric”, “Cancer”. Results: Experimental studies have shown that Angiotensin-(1-7) inhibits the growth of tumor cells and reduces local inflammation and angiogenesis in several types of cancer. Clinical trials with Angiotensin-( 1-7) or TXA127, a pharmaceutical grade formulation of the naturally occurring peptide, have reported promising findings, but not enough to recommend medical use in human cancer. In regard to pediatric cancer, only three articles that marginally investigated RAS components were found and none of them evaluated molecules of the alternative RAS axis. Conclusion: Despite the potential applicability of Angiotensin-(1-7) in pediatric tumors, the role of this molecule was never tested. Further clinical trials are necessary, also including pediatric patients, to confirm safety and efficiency and to define therapeutic targets.

The Emerging Role of Ras Pathway Signaling in Pediatric Cancer

2020 ◽  
Vol 80 (23) ◽  
pp. 5155-5163
Author(s):  
Gina M. Ney ◽  
Laura McKay ◽  
Carl Koschmann ◽  
Rajen Mody ◽  
Qing Li
Keyword(s):  
Pediatric Cancer ◽  
Ras Pathway

ROLE OF AYURVEDA IN PREVENTION OF PEDIATRIC CANCER

2020 ◽  
Vol 8 (10) ◽  
pp. 4788-4793
Author(s):  
Pavan Kumar U.B ◽  
Susheel Shetty
Keyword(s):  
Pediatric Cancer ◽  
Preventive Measures ◽  
Indian Council ◽  
Dna Mutations ◽  
The World ◽  
Total Cancer ◽  
Risk Of Cancer ◽  
Cancer In Children

Cancer is one of the deadliest diseases spreading drastically in 21st century, as now officially became the most dangerous killer in the world according to WHO. Cancer in children constitutes 5.5% of total cancer cases in India according to the Indian Council for Medical Research. Based on the AdhyatmikaVyadhi classification of disease pediatric cancer can be studied under three headings mainly, pre-conception, during pregnancy and after birth. In the contemporary system it is said that Inherent DNA mutations from parents would increase the risk of Cancer in children, which is the result of DNA changes that happen early in the child’s life. Ayurveda explains about some of the measures for prevention such as Dinacharya, Ritucharya, Rasayana, Vajeekarana, Shodhana, GarbhiniParicharya. Hence here an attempt is made to study the role of these preventive measures in pediatric cancer.

“Limiting Anthracycline-Induced Cardiotoxicity Using Amrubicin in Leukemia Systems”.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 3760-3760
Author(s):  
Joy Marie Fulbright ◽  
Joya Chandra
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cancer Patients ◽  
Dna Fragmentation ◽  
Pediatric Cancer ◽  
Small Cell ◽  
Jurkat Cells ◽  
Leukemia Cells ◽  
Pediatric Cancer Patients

Abstract Abstract 3760 Poster Board III-696 The overall survival of pediatric cancer patients has greatly improved over the last forty years in part due to the introduction of anthracyclines into therapeutic regimens. However, a significant limitation of anthracyline use is cardiotoxicity by this class of drugs. The mechanism most often cited as contributing to anthracycline cardiotoxicity is the production of reactive oxygen species (ROS) and subsequent damage to mitochondria, resulting in activation of the apoptotic cascade. Because heart tissue contains more mitochondria than other organ sites, this mechanism is particularly damaging to this organ site. Newer, less toxic anthracyclines are being developed and amrubicin, a completely synthetic anthracycline with potent topoisomerase II inhibition, is one such compound and is approved in Japan for the treatment of small cell and non-small cell lung cancer. In animal studies amrubicin has demonstrated decreased cardiotoxicity compared to doxorubicin, and in Phase I/II clinical trials in lymphomas and solid tumors has demonstrated single agent activity and an improved early cardiotoxicity profile. Our goal was to elucidate the role of ROS in the decreased cardiotoxicity observed with amrubicin exposure and to test the ability of amrubicin to promote cell death in leukemia cells. We used a rat cardiomyocyte cell line model (H9c2 cells) to quantify oxidative stress after exposure to amrubicin or other anthracyclines. Flow cytometry was used to evaluate superoxide levels after the cells were treated for 24 hours and stained with hydroethidium (HE). Interestingly, at equimolar doses (500 nM, 1 μM, 2 μM and 3 μM), cardiomyocytes treated with amrubicin produced less superoxide than cells treated with an equivalent dose of daunorubicin. These results suggest that ROS-mediated damage to cardiomyocytes is less after amrubicin exposure as compared to daunorubicin. The anti-leukemia efficacy of amrubicin was also evaluated as compared to other anthracyclines. Apoptosis induction in three different acute lymphocytic and myelocytic leukemia cell lines; Jurkat, ML-1 and KG-1 was measured using propidium iodide staining followed by flow cytometric analysis to yield cell cycle distributions. The percentage of the population with subdiploid amounts of DNA were representative of cells undergoing apoptotic DNA fragmentation. Using this method, we found that all three anthracyclines caused cell death after 24 hours of exposure. In order to assess the role of oxidative stress in anthracycline mediated cell death in leukemia cells, we measured ROS levels using equipotent doses of the drugs that elicited a 50% increase in the subdiploid population at 24 hours. In Jurkat and ML-1 cells both daunorubicin and doxorubicin significantly increased superoxide levels compared to control. Amrubicin also increased superoxide levels in Jurkat cells compared to cells treated with diluent alone. To establish a relationship between the observed oxidative stress and DNA fragmentation, we treated Jurkat cells with daunorubicin and doxorubicin with and without pretreatment with NAC (N-acetyl-cysteine), an antioxidant. NAC pretreatment significantly decreased superoxide levels, but did not abrogate the anthracyclines' promotion of apoptotic DNA fragmentation. These results suggest that ROS may not be essential for anthracycline cytotoxicity in leukemia cells. Since ROS are promoting cardiotoxic effects, yet appear dispensible for anti-leukemia effects, anthracyclines that cause less ROS, such as amrubicin, may prove to be better treatment options in pediatric cancer patients for whom anthracycline exposure is indicated. Furthermore, our data raises the possibility that amrubicin's decreased cardiotoxicity could be enhanced by administering antioxidants to patients without compromising the drug's anti-tumor effects. Disclosures: Chandra: Pharmion Corporation: Research Funding.

Sign in / Sign up

Export Citation Format

Share Document