Science Advances : Significant progress! For the first time, Yu Ying of Shanghai University of Science and Technology has established genetic evidence of cardiovascular risk caused by anti-tumor drugs.

Cardiovascular dysfunction is one of the most common complications of long-term cancer treatment.
evidence that anti-tumor drugs increase cardiovascular risk during cancer treatment and seriously affect patient survival.
, little is known about the genetic factors associated with the cardiovascular risk of anti-tumor drugs.
October 14, 2020, Yu Ying of Shanghai University of Science and Technology/Tianjin Medical University and Li Jun of Tianjin Medical University jointly published a research paper entitled "The Support of Genetics for Cardiovascular Risk Induced by antineoplastic drugs" online in Advances, which establishes a compilation of genetic evidence to support the risk of cardiovascular disease caused by anti-tumor drugs.
genetic evidence is largely due to causal allegations that alter gene expression in cardiovascular disease.
study found significant increases in levels of anti-tumor drugs expected to induce cardiovascular risk in drugs associated with adverse cardiovascular reactions, including many first-line cancer treatments.
tests have shown that vitamin A X-like aortics can reduce triglyceride delysion, thereby regulating cardiovascular risk.
, the findings establish a link between causal allegens of cardiovascular disease genes and pharmacological regulation, which can facilitate the discovery of cancer drugs and clinical trial design.
advances in medicine and treatment strategies have led to increased survival rates for cancer patients, complications that increase morbidity and mortality have also been widely observed.
cardiovascular disease (CVD) is one of the most common complications in cancer treatment and can lead to premature morbidity and death in long-term cancer survivors.
For example, chemotherapy can improve the disease-free and total survival of breast cancer patients, but it has long been noted that cyclic drugs such as amycin can cause dose-dependent heart toxicity through redox circulation and mediated free-forming.
another common cardiovascular side effect of anti-tumor drugs was observed during the treatment of metastasis human skin growth factor 2 (HER2)-positive breast cancer using herceptin.
cardiovascular risk associated with anti-tumor drugs has prompted researchers to develop possible factors that can accurately predict heart toxicity.
Compared to clinically relevant conditions and outcomes, reliance on biomarker assessments, including genetics, metagenetics, and other molecular esopeological assessments, can facilitate the development of evidence-based methods to accurately assess the risk of anti-tumor drugs to cardiovascular disease.
Since the adgenomic association study (GWASs) and next-generation sequencing (NGS), remarkable progress has been made in identifying genetic variants that affect cardiovascular risk and prognostication, greatly contributing to their widespread use.
a normative finding is that a non-synonymic variant of RARG gives sensitivity to cardiac toxicity in childhood caused by cyclocyclytic drugs by changing the expression of TOP2B.
a recent study by NGS showed that rare genetic variants of the TTN gene are susceptible to cancer-treated cardiomyopathy in adult and pediatric cancer patients.
such examples and rapid advances in genetic understanding of CVD in large populations raise the question of how best to link the genetic association of CVD to the potential cardiac toxicity of existing anti-tumor drugs, guide treatment options and dissect potential mechanisms for side effects.
the study established a compilation of genetic evidence to support the risk of cardiovascular disease caused by anti-tumor drugs.
genetic evidence is largely due to causal allegations that alter gene expression in cardiovascular disease.
study found significant increases in levels of anti-tumor drugs expected to induce cardiovascular risk in drugs associated with adverse cardiovascular reactions, including many first-line cancer treatments.
tests have shown that vitamin A X-like aortics can reduce triglyceride delysion, thereby regulating cardiovascular risk.
the findings establish a link between causal allegant genes in cardiovascular disease genes and pharmacological regulatory directions, which can facilitate the discovery of cancer drugs and clinical trial design.
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