Siew Lian Leong1, Nathorn Chaiyakunapruk2, Wichittra Tassaneeyakul3, Poukwan Arunmanakul4, Surakit Nathisuwan5, Shaun Wen Huey Lee6. 1. School of Pharmacy, Monash University Malaysia, Selangor, Malaysia; Faculty of Pharmacy, Cyberjaya University College of Medical Sciences, Selangor, Malaysia. 2. School of Pharmacy, Monash University Malaysia, Selangor, Malaysia; Center of Pharmaceutical Outcomes Research (CPOR), Department of Pharmacy Practice, Faculty of Pharmaceutical Sciences, Naresuan University, Phitsanulok, Thailand; School of Pharmacy, University of Wisconsin, Madison, USA; Asian Centre for Evidence Synthesis in Population, Implementation and Clinical Outcomes (PICO), Health and Well-being Cluster, Global Asia in the 21st Century (GA21) Platform, Monash University Malaysia, Selangor, Malaysia. 3. Department of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand. 4. Pharmaceutical Care Department, Faculty of Pharmacy, Chiang Mai University, Chiang Mai, Thailand. 5. Division of Clinical Pharmacy, Department of Pharmacy, Faculty of Pharmacy, Mahidol University, Bangkok, Thailand. 6. School of Pharmacy, Monash University Malaysia, Selangor, Malaysia; Asian Centre for Evidence Synthesis in Population, Implementation and Clinical Outcomes (PICO), Health and Well-being Cluster, Global Asia in the 21st Century (GA21) Platform, Monash University Malaysia, Selangor, Malaysia; School of Pharmacy, Taylor's University Lakeside Campus, Jalan Taylors, 47500 Subang Jaya, Selangor, Malaysia. Electronic address: shaun.lee@monash.edu.
Abstract
BACKGROUND: Exploration on genetic roles in antineoplastic-related cardiovascular toxicity has increased with the advancement of genotyping technology. However, knowledge on the extent of genetic determinants in affecting the susceptibility to the cardiovascular toxicities of antineoplastic is limited. This study aims to identify potential single nucleotide polymorphism (SNP) in predicting non-anthracycline antineoplastic-related cardiovascular toxicity. METHODS: We systematically searched for original research in PubMed, Cochrane Central Register of Controlled Studies, CINAHL Plus, EMBASE and HuGE Navigator from database inception until January 2018. Studies on association between polymorphism and antineoplastic-induced cardiovascular toxicity in patients treated for cancer of all antineoplastic agents were included except for anthracycline. Case reports, conference abstracts, reviews and non-patient studies were excluded. Data extracted by two independent reviewers were combined with random-effects model and reported according to PRISMA and MOOSE guidelines. RESULTS: The 35 studies included examined a total of 219 SNPs in 80 genes, 11 antineoplastic and 5 types of cardiovascular toxicities. Meta-analyses showed that human epidermal growth factor receptor 2 (HER2) rs1136201, a risk variants (pooled OR: 2.43; 1.17-5.06, p = 0.018) is a potential predictors for trastuzumab-related cardiotoxicity. Gene dose effect analysis showed number of variant allele may contribute to the risk too. CONCLUSIONS: This review found that HER2 rs1136201 can have the potential in predicting trastuzumab-related heart failure. As such, further studies are needed to confirm the validity of these results as well as determine the economic aspect of using SNPs prior to its implementation as a clinical practice.
BACKGROUND: Exploration on genetic roles in antineoplastic-related cardiovascular toxicity has increased with the advancement of genotyping technology. However, knowledge on the extent of genetic determinants in affecting the susceptibility to the cardiovascular toxicities of antineoplastic is limited. This study aims to identify potential single nucleotide polymorphism (SNP) in predicting non-anthracycline antineoplastic-related cardiovascular toxicity. METHODS: We systematically searched for original research in PubMed, Cochrane Central Register of Controlled Studies, CINAHL Plus, EMBASE and HuGE Navigator from database inception until January 2018. Studies on association between polymorphism and antineoplastic-induced cardiovascular toxicity in patients treated for cancer of all antineoplastic agents were included except for anthracycline. Case reports, conference abstracts, reviews and non-patient studies were excluded. Data extracted by two independent reviewers were combined with random-effects model and reported according to PRISMA and MOOSE guidelines. RESULTS: The 35 studies included examined a total of 219 SNPs in 80 genes, 11 antineoplastic and 5 types of cardiovascular toxicities. Meta-analyses showed that humanepidermal growth factor receptor 2 (HER2) rs1136201, a risk variants (pooled OR: 2.43; 1.17-5.06, p = 0.018) is a potential predictors for trastuzumab-related cardiotoxicity. Gene dose effect analysis showed number of variant allele may contribute to the risk too. CONCLUSIONS: This review found that HER2rs1136201 can have the potential in predicting trastuzumab-related heart failure. As such, further studies are needed to confirm the validity of these results as well as determine the economic aspect of using SNPs prior to its implementation as a clinical practice.
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