最新刊期
卷 32 ， 期 10 ， 2022
- 摘要：Background and objective: Cardio-oncology that focuses on the management of cardiovascular toxicity associated with cancer therapy, has grown rapidly worldwide as an emerging interdisciplinary discipline over the past decade. This study aimed to summarize the hot spots and development trends of cardio-oncology to provide a reference for scientific researchers in related fields based on bibliometrics. Methods: CiteSpace was employed to conduct the visualized analysis of annual publications, authors, countries, citations and keywords of the related papers from 2012 to 2022 in the Web of Science Core Collection and China National Knowledge Infrastructure (CNKI). Results: A total of 4 287 English articles and 1 165 Chinese articles were included after screening. At present, the number of foreign literature in the field of cardio-oncology, showed a trend of rapid growth, while our country has "slow development period" and "rapid development period" with 2016 as the boundary. The United States is the country with the largest number of publications in Web of Science, accounting for about 34.21% of the total, followed by China, Italy and other countries. The institutions with the largest number of publications at home and abroad are the University of Texas MD Anderson Cancer Center and the First Affiliated Hospital of Dalian Medical University. Bonnie KY, Ana Barac, Paaladinesh Thavendiranathan are the main contributors abroad, and Xia Yunlong, Zhang Yuhui and Cheng Leilei are the main contributors in China. The most frequently cited literature is the position statement on cancer treatment and cardiovascular toxicity from the European Society of Cardiology. The most frequently used keywords abroad were "heart failure", "breast cancer" and "cardiotoxicity", while the most frequently used keywords in China were "cardiotoxicity", "cardiac tumor" and "doxorubicin". Keywords with the strongest citation bursts at home and abroad in recent three years are "immune checkpoint inhibitors". Conclusion: The research hotspots mainly focus on cardiotoxicity caused by antineoplastic therapy, prevention and treatment, screening and diagnosis of cardiovascular toxicity associated with cancer therapy, etc. Establishing a multidisciplinary diagnosis and treatment model and paying attention to the immune checkpoint inhibitor-related myocarditis and whole process management of cardio-oncology are the directions of future development.关键词：Cardio-oncology;Cardiotoxicity;Bibliometrics;CiteSpace29|2529|0更新时间：2025-12-31
- 摘要：Background and purpose: Adriamycin, also named as doxorubicin, is an effective antineoplastic anthracycline drug used worldwide. However, its cardiotoxicities characterized as dilated cardiomyopathy and congestive heart failure have limited its clinical application. This study aimed to compare the effects of benazepril, atorvastatin, sacubitril/valsartan and carvedilol on the protection of adriamycin-induced cardiomyopathy, which are commonly used as cardioprotective agents for hypertension, hyperlipidemia and cardiomyopathy, and then preliminarily explored the underlying mechanisms. Methods: Adult male C57BL/6 mice were divided into saline, adriamycin, adriamycin+atorvastatin, adriamycin+benazepril, adriamycin+sacubitril/valsartan and adriamycin+carvedilol groups. In addition to the saline group, adriamycin solution (4 mg/kg per week) was injected intraperitoneally for 5 weeks to establish the dox-induced cardiomyopathy model in vivo. Different groups were pretreated with different cardioprotective agents 0.2 mL per day for each mouse by gavage for a total of 6 weeks. The dose was: atorvastatin 10 mg/kg per day, benazepril 10 mg/kg per day, sakubactro/valsartan 60 mg/kg per day (sakubactro 28.8 mg/kg per day, valsartan 31.2 mg/kg per day) and carvedilol 5 mg/kg per day, respectively. Two-dimensional echocardiography, cell apoptosis, fibrosis and inflammation markers were analyzed in these mice. Real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) was used to detect the total mRNA in cardiomyocytes, and Western blot was used to detect the expression levels of Bax and Bcl-2. Among BALB/c mice inoculated with 4T1 breast tumor cells, the tumor volume and mass were studied before and after treatments with different cardioprotective drugs to evaluate the effects of cardioprotective drugs on tumor growth. Results: The data revealed that all these four cardioprotective agents effectively inhibited adriamycin-induced left ventricular dysfunction, ameliorated histopathological damage, suppressed adriamycin-induced cell apoptosis and modulated the expressions of Bcl-2 and Bax proteins. They also attenuated adriamycin-mediated expressions of proinflammatory cytokines, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) in the myocardium. Furthermore, sacubitril/valsartan not only enormously improved left ventricular ejection fraction (LVEF) (65.1%±3.8%, 63.5%±4.6%, 61.6%±4.1% and 62.1%±5.2%, P<0.05) and fractional shortening (FS) (34.2%±3.7%, 33.9%±3.3%, 32.6%±2.8% and 33.0%±3.6%, P<0.05), but also alleviated cardiac fibrosis compared with the other three medicaments. Benazepril and sacubitril/valsartan manifested curative effect in limiting the size of the heart, the ratio of heart weight to tibia length (HW/TL), and cardiomyocyte cross-sectional area (CSA). Atorvastatin owned a moderate level of anti-apoptotic and anti-inflammatory properties. Among these medications, carvedilol provided the best anti-inflammatory effects. Conclusion: We compared different agents for their effects on the protection of adriamycin-induced cardiomyopathy and preliminarily explored underlying mechanisms. In the future, large-scale clinical studies could further explore the potential of different cardioprotective drugs at the patient level to alleviate adriamycin-induced cardiotoxicities.关键词：Adriamycin;Cardiotoxicity;Cardiomyopathy;Apoptosis;Fibrosis;Inflammation14|3788|0更新时间：2025-12-31
- 摘要：Background and purpose: Adriamycin also named as doxorubicin, is one of the most widely used cytotoxic chemotherapeutic agents for clinical practice for the treatment of various tumors, and belongs to anthracycline antitumor drugs. Unfortunately, this drug will cause serious side effects, especially dose-dependent cardiotoxicity, which has become a concern in the field of onco-cardiology. At present, there is no universally recognized, unified and robust method to construct Doxorubicin-induced cardiomyopathy model. This experiment was designed to explore the optimal dose and frequency of doxorubicin-induced cardiomyopathy in a mouse model.Methods: Forty 8-10-week-old male C57BL/6J mice were randomly divided into 4 groups (control group and 3 model groups). The model group was divided into model 1 (M1) group (15 mg/kg, single dose) and M2 group (5 mg/ kg, once a day for 3 days continuously) and M3 group (7.5 mg/kg, twice on alternate days). General vital signs (body weight change and survival rate), echocardiography, body surface electrocardiogram (ECG), N-terminal pro-B-type natriuretic peptide (NT-proBNP), cardiac troponin I (cTnI) and myocardial tissue morphological changes were evaluated comprehensively.Results: Compared with the control group, the body weight of mice in M1, M2 and M3 groups decreased significantly (P<0.001); M3 group had higher survival rate than M1 and M2 group (80% vs 40% and 50%, P<0.05). Compared with the control group, M1 group and M2 group, the body surface ECG showed that the PR interval of M3 group [(0.064 2±0.003 8)s vs (0.042 3±0.000 9)s, (0.052 7±0.007 9) s and (0.062 0±0.001 2)s, P<0.05] and QT interval [(0.047 5±0.000 2)s vs (0.022 0±0.000 9)s, (0.038 6±0.004 4)s and (0.044 4±0.003 0)s, P<0.05] were significantly prolonged. Cardiac ultrasound showed that M3 ejection fraction decreased significantly (40.40%±2.24% vs 54.72%±1.64%, 46.00%±4.41% and 54.68%±3.38%, P<0.05). M3 short-axis shortening rate decreased significantly (19.40%±1.20% vs 27.88%±1.05%, 22.57%±2.50% and 27.86%±2.20%, P<0.05). Cardiac markers showed that compared with CON, the serum NT-proBNP levels of M1, M2 and M3 in adriamycin group were significantly increased [(638.13±12.69) pg/mL vs (1 271.36±11.76) pg/mL, (1 270.85±36.19) pg/mL and (1 225.26±24.19) pg/ mL, P<0.05]. Histomorphology showed that the vacuoles in cardiomyocyte of M3 group was significantly increased compared with CON, M1 and M2 group (81/field vs 3/field, 65/field and 34/field, P<0.05).Conclusion: Intraperitoneal injection of adriamycin in acute heart failure model is simple and reliable. The model in which adriamycin is administered by intraperitoneal injection at a dose of 7.5 mg/ kg, twice on alternate days, with cumulative dose of 15 mg/kg is optimal.关键词：Adriamycin-induced cardiotoxicity;Cardiomyopathy;Onco-cardiology;Model19|2920|0更新时间：2025-12-31
Specialists'Article
- 摘要：Pancreatic cancer is a highly dismal malignancy and has a poor response to major treatments. Patients with pancreatic cancer usually have poor prognosis. Precision therapy has a great potential to improve the outcome of pancreatic cancer. Over 25% of patients have druggable targets, which mainly involve in KRAS mutation status, homologous recombination repair deficiency, gene fusions, and immunotherapy related pathways. Patients with familial or personal history of malignancy, younger patients, or patients with acinar cell carcinoma may benefit from precision therapy. However, only 4% of patients have received precision therapy, and thus precision therapy is still not a major therapeutic method for pancreatic cancer. It is common that genetic/molecular reports are lack of critical information, such as KRAS mutation status, tumor cell content, fusions and germline mutations. It is necessary to promote precision therapy from streamlet towards mainstream by formulating detection technique, establishing expertise team and stressing cooperation to accumulate evidence, thereby providing benefits for the patients. Recent reports have shown that precision treatments could improve the outcome and survival of patients with pancreatic cancer. In 2019, The New England Journal of Medicine published the POLO study which investigated olaparib, an inhibitor of poly (ADP-ribose) polymerase (PARP), in patients with metastatic pancreatic cancer and BRCA1 or BRCA2 germline mutation. This is the first clinical trial of precision therapy based on therapeutic targets in pancreatic cancer. In 2020, Pishvaian et al. from the University of Texas MD Anderson Cancer Center published the results of “Know Your Tumor (KYT)”. In this study, among 1 856 patients with pancreatic cancer, patients with actionable molecular alterations who received a matched therapy (n = 46, 2.58 years) had longer median overall survival than did those patients who only received unmatched therapies [n = 143; 1.51 years; hazard ratio (HR) was 0.42, P = 0.004]. The patients who received a matched therapy also had longer overall survival compared with the patients who did not have an actionable molecular alteration (n=488; 1.32 years; HR was 0.34, P<0.000 1). This real-world study indicates that matched treatments for patients with pancreatic cancer and actionable molecular alterations could prolong the overall survival of patients for more than one year. To date, therapeutic targets in pancreatic cancer include KRAS mutation status (KRAS wild-type and KRAS G12C mutation), homologous recombination repair deficiency (BRCA1/2, PALB2, ATM/ATR/ATRX, CHEK2, CDK12, RAD51, NBN, BLM, FANC, RAD51/51C, RAD50, BAP1, BARD1, BRIP1, MRE11), gene fusions (NTRK, NRG1, ALK, RAF, RET, MET, FGFR2/3, ROS), immunotherapy related pathways [MSI-H, TMB, MMR-D (MLH1, MLH3, MSH2, MSH3, MSH6, PMS1, PMS2, POLE, EPCAM)] and others [BRAF, human epidermal growth factor receptor 2 (HER2)]. It is necessary to establish specialized team which focuses on precision treatments in pancreatic cancer for the reasons that only limited proportion of patients have therapeutic targets which are widely distributed. The overall survival of patients with pancreatic cancer is poor. It is hard to acquire tumor specimens from advanced pancreatic cancer. As great importance has been attached, we believe that there will be a bright future for the precision treatment in pancreatic cancer.关键词：Pancreatic cancer;Targeted therapy;Immunotherapy;KRAS;Fusion gene19|3502|0更新时间：2025-12-31
Specialists' Commentary
- 摘要：Background and purpose: Breast cancer has overtaken lung cancer as the most common malignant tumor in women. Early breast cancer patient can achieve a long survival time after comprehensive treatment, however the cardiotoxicity caused by radiotherapy may affect its long-term prognosis. Therefore, early monitoring of radiation-induced heart disease is important for improving the survival of breast cancer patients. Speckle-tracking echocardiography (STE) is a new technique to study myocardial deformation. Global longitudinal strain (GLS) is a good parameter for evaluating early cardiotoxicity caused by radiotherapy. The purpose of this study was to evaluate the value of GLS in evaluating radiotherapy-induced early cardiotoxicity in breast cancer. Methods: PubMed, EMBASE, Web of Science, Cochrane Library, Wanfang and China National Knowledge Infrastructure (CNKI) databases were searched by computer from January 2010 to March 2022. According to the pre-set inclusion and exclusion criteria, screening studies was performed using GLS and left ventricular ejection fraction (LVEF) to evaluate myocardial function changes during and after radiotherapy for breast cancer. Two researchers independently conducted literature screening and data extraction. Review Manager5.4 analysis software was used for data analysis. Results: Finally, 9 studies were included, involving a total of 543 patients. Meta-analysis results showed that LVEF of patients with left breast cancer decreased slightly immediately after radiotherapy, and WMD was -0.98. LVEF of those patients increased at 6 months after radiotherapy, and the WMD was -0.83, which was still lower than baseline. LVEF was almost unchangeable after radiotherapy for right breast cancer. GLS of left-sided breast cancer patients decreased significantly immediately after radiotherapy, at 6 weeks, 6 months and 12 months after radiotherapy, and WMD was 1.57, 1.84, 1.04 and 1.69, respectively. The differences were statistically significant. There was no significant heterogeneity among the studies. However, there was no significant change in GLS after radiotherapy for right breast cancer. There was no significant difference in GLSr between breast cancers of different sides. Conclusion: GLS may be a good predictor of radiation-induced heart disease in patients with left-sided breast cancer.关键词：Breast cancer;Speckle-tracking echocardiography;Radiotherapy;Cardiotoxicity19|2379|0更新时间：2025-12-31
- 摘要：Background and purpose: Breast cancer is the most common malignancy in women, and it is also the cancer with the highest number of new cases worldwide in 2020. Human epidermal growth factor receptor 2 (HER2)-positive breast cancer accounts for approximately 20% of all breast cancers, which indicates higher rate of recurrence and metastasis and a poor prognosis. Therefore, it is of great significance to explore the biomarkers related to HER2-positive breast cancer. This study aimed to investigate the expression of circ-0003910 in HER2-positive breast cancer tissues and cells, and to clarify the effect of circ-0003910 on the migration and invasion of breast cancer cells. Methods: Circular RNA (circRNA) microarray was used to screen circRNA differentially expressed in HER2-positive breast cancer cells, and significantly overexpressed circRNA was selected as the research target. Fluorescence in situ hybridization (FISH) assay was used to detect the subcellular localization of circ-0003910. BaseScope assay was used to analyze the expression and clinical significance of circ-0003910 in breast cancer tissues. Circ-0003910 overexpressed and knockdown breast cancer cells were constructed by transfection of cloned plasmid and siRNA in vitro. The effect of circ-0003910 on the migration and invasion ability of breast cancer cells was detected by transwell assay. The molecular mechanism of circ-0003910 promoting the migration and invasion of breast cancer cells was preliminarily explored by TMT quantitative proteomics techniques. Results: CircRNA microarray analysis showed that a total of 1 843 differentially expressed circRNAs were screened in HER2-positive breast cancer cells (fold change≥2, P<0.05), including 845 upregulated circRNAs and 998 downregulated circRNAs. Compared with normal breast epithelial cells, the differential expression ratio of circ-0003910 in HER2-positive breast cancer cells was 24.39. Real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) results showed that the expression of circ-0003910 was higher in HER2-positive breast cancer cells than in other molecular types of breast cancer cells, and BaseScope assay verified that circ-0003910 was mainly located in the cytoplasm of HER2-positive breast cancer tissue cells. Overexpression of circ-0003910 promoted the migration and invasion of breast cancer cells, while circ-0003910 knockdown produced the opposite effects. Proteomics identification showed that 197 proteins were changed after overexpression of circ-0003910, of which 104 proteins were upregulated and 93 proteins were downregulated. GO and KEGG enrichment analysis suggested that circ-0003910 may be involved in biological processes such as cell adhesion molecule synthesis, transcriptional dysregulation in cancer, and protein digestion and absorption. Conclusion: Circ-0003910 is upregulated in breast cancer cells and can promote the migration and invasion of breast cancer cells, which may be a new biomarker and target for the treatment of metastatic breast cancer.关键词：Breast cancer;Circ-0003910;Migration and invasion;Functional enrichment analysis10|2528|0更新时间：2025-12-31
- 摘要：Background and purpose: Hepatocellular carcinoma (HCC) is one of the most common tumors in the world. Long non-coding RNA (lncRNA) is determined to be involved in the occurrence and development of HCC. Recent reports suggest that a novel lncRNA-LINC00671 may be a new tumor suppressor, however, its role and molecular mechanism in HCC remain uncertain. Current research aimed to discover the role of LINC00671 in HCC and its potential molecular mechanism. Methods: The expression and prognosis of LINC000671 in hepatocellular carcinoma tissues were analyzed by GEPIA and starBase database. The expression of LINC00671 in normal and hepatoma cell lines was detected by real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR). The subcellular localization of LINC00671 was observed by RNA fluorescence in situ hybridization (FISH). After knockdown or overexpression of LINC00671 in vitro, the effects of LINC00671 on the proliferation, apoptosis, migration and invasion of hepatoma cells were investigated by cell counting kit-8 (CCK-8), flow cytometry, wound healing and transwell assays. Subsequently, online bioinformatics prediction was conducted to identify the target gene of LINC00671. The correlation between LINC00671 and target molecule c-myc was analyzed by starBase and GEPIA database. And the regulation of LINC00671 on c-myc was verified by RTFQ-PCR and Western blot. The effect of LINC00671 on the methylation level of target gene promoter was tested by methylated DNA immunoprecipitation-PCR (MeDIP-PCR). Results: The results of online database analysis showed that LINC00671 was significantly downregulated in hepatocellular carcinoma, and its high expression predicted a better prognosis (P<0.05). LINC00671 was down regulated and differentially expressed in different hepatoma cell lines, and it was mainly located in the nucleus of hepatoma cells. The results of tumor behavior experiment in vitro indicated that LINC00671 could significantly inhibit the proliferation, migration and invasion of hepatoma cells (P<0.05), and remarkably enhanced the apoptotic rate (P<0.05). Bioinformatics results showed that LINC00671 might bind to c-myc promoter by Hoogsteen pairing in nucleus. The results from database revealed that LINC00671 was significantly negatively correlated with c-myc expression in HCC (P<0.05). LINC00671 could significantly suppress the expression of c-myc (P<0.05). The results of MeDIP-PCR suggested that LINC00671 could increase the methylation level of c-myc promoter (P<0.05). Conclusion: LINC00671 may downregulate the expression of c-myc by inducing the hypermethylation of c-myc promoter, so as to inhibit the progression of HCC.关键词：Hepatocellular carcinoma;LINC00671;c-Myc15|2452|0更新时间：2025-12-31
Article
- 摘要：Renal cell carcinoma is one of the most common malignancies in genitourinary cancers. In China, the incidence of renal cell carcinoma has been increasing year by year. Regulated cell death is a cell-independent and orderly death controlled by genes, which is ubiquitous in organisms and plays a crucial role in maintaining the cell homeostasis. Recently, cuproptosis was reported in Science, which further reinforced the importance of cell death in living organisms. With the increasing understanding of regulated cell death, more and more studies have shown that regulated cell death (such as ferroptosis, autophagy, pyroptosis) is closely related to the tumorigenesis and development of renal cell carcinoma. For example, induction of ferroptosis inhibits the invasion and metastasis of renal cell carcinoma and is closely related with better prognosis; pyroptosis not only induce renal cancer cell death and also activate the immune-response against renal cancer; autophagy plays a "bidirectional" role in renal cell carcinoma, which can inhibit the growth of renal cell carcinoma cells but may weaken the efficacy of combinational therapy; inhibition of apoptosis and necrotizing apoptosis can significantly promote the proliferation and invasion of renal cell carcinoma. This review has summarized the molecular mechanisms of ferroptosis, pyroptosis, autophagy, apoptosis and necrotizing apoptosis and the advances of different regulatory cell death in the tumorigenesis and development of renal cell carcinoma to provide a new perspective for exploring the mechanisms of tumorigenesis and potential targets of treatment.关键词：Renal cell carcinoma;Cuproptosis;Ferroptosis;Autophagy;Pyroptosis;Necroptosis;Apoptosis18|1205|0更新时间：2025-12-31
- 摘要：Gastric precancerous lesions (GPL) are a special histopathological stage before the occurrence of gastric cancer. Effective treatment of GPL is the key to preventing its progression to gastric cancer. GPL has a high level of inflammation in gastric mucosa, and a large number of inflammatory cells, inflammatory factors and inflammatory mediators are metabolized at a high level, which increases oxygen consumption and leads to the formation of a hypoxia microenvironment in gastric mucosa at the GPL stage, which is conducive to the initiation of mitochondrial autophagy and glucose metabolism reprogramming. As a conserved biological process, mitochondrial autophagy exists in various tissues and cells of the body. It can form autophagosome to wrap mitochondria with damaged functions and bind with lysosomes to digest and reuse target mitochondria. Appropriate autophagy level can prevent excessive proliferation of GPL heterotype cells and inhibit the progress of GPL. However, mitochondrial autophagy activity is inhibited during the course of GPL, and the activity of glycometabolic reprogramming into glycolysis is increased during GPL. Glycolysis is a way of energy metabolism in the hypoxia state of cells, which can accelerate the energy supply of cells and the proliferation of abnormal cells, and thus accelerate the deterioration of GPL. Some evidences suggest that there may be a mutually restricting relationship between mitochondrial autophagy and glycolysis reprogramming. The inhibition of autophagy in GPL can increase glycolysis activity on the one hand, while the increase of autophagy inhibits glycolysis activity on the other hand. At present, the specific relationship and mechanism of autophagy and glycolysis are not clear, however, the complex pathological environment of GPL gastric mucosa composed of hypoxia, bacterial infection, inflammation, oxidative stress, activation disorder of signal molecules and other factors may be the key to the low autophagy level and high glycolysis activity. Hypoxia-inducible factor 1α (HIF-1α), which is involved in hypoxia adaptation, is stably expressed in gastric mucosa at the GPL stage and acts as a switch to initiate autophagy and glycolysis. However, HIF-1α seems to be more involved in the regulation of glycolysis in the pathological process of GPL. The cause of this change may be related to the above-mentioned pathological factors. H. pylori infection, activation of phosphoinositide 3-kinase (PI3K)/protein kinase (AKT)/mammalian target of rapamycin (mTOR) pathway and other factors inhibit autophagy. However, the continuous accumulation of reactive oxygen species (ROS) after autophagy inhibition and the aggravation of inflammation caused by H. pylori infection can promote a series of signal interactions and synergies among nuclear factor kappa-B (NF-Κb), signal transducer and activator of transcription 3 (STAT3) and PI3K/AKT/mTOR signaling pathways, and thus indirectly affect HIF-1α to promote glycolysis or directly improve glycolysis level. HIF-1α may be more involved in the activation of glycolysis due to the regulation of GPL pathological microenvironment and its upstream complex signals, thus unable to fully activate BNIP-3 mediated hypoxia-initiated autophagy, leading to the down-regulation or inhibition of autophagy level, and the inhibition of autophagy indirectly promotes the improvement of glycolysis level, forming a vicious cycle, and ultimately leading to the deterioration of GPL. This article reviewed the research progress of hypoxia-induced mitochondrial autophagy and glucose metabolism reprogramming in gastric precancerous lesions.关键词：Gastric precancerous lesions;Mitochondrial autophagy;Glycolysis;Hypoxia13|2276|0更新时间：2025-12-31
Review
- 摘要：Recent advances in the medical oncological treatment options for cancer have led to a clear improvement in the survival rate worldwide; however, many of the recently developed new drugs are directly or indirectly associated with cardiovascular side effects. Cardiovascular diseases are already the most frequent non-cancerous cause of death in tumor patients. Prevention and early detection of these complications, correct management and timely initiation of specific cardiac medical treatment are the keys to improvement of the cardiovascular prognosis. At present, many developed countries have established oncology-cardiology specialist clinics, wards and related multidisciplinary teams (MDT). In our country, development of cardio-oncology has just on the way. With improvement of survival of breast cancer patients, it is reasonable to foresee that more and more breast cancer patients might suffer from cardiovascular disease, which indicates that it is necessary to focus on risk associated with antitumor therapy-related cardiotoxicity. Therefore, an elaborate guideline supported by solid medical evidence is strongly needed for clinicians major in oncology. This consensus provides an overview and comprehensive summary of the possible cardiotoxic side effects of important oncological therapies and offers possible practical strategies with respect to risk stratification, cardiological follow-up care and management approaches for chemotherapy-induced left ventricular dysfunction. We believe this consensus will provide a practical clinical procedures for treatment and prevention of cardio-oncology in breast cancer in China, and make contributions to improvement of outcome of cardiotoxicity in Chinese breast cancer patients.关键词：Breast cancer;Cardio-oncology;Prevention;Treatment37|9058|0更新时间：2025-12-31
Guideline and Consensus
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