scholarly journals CARDIOVASCULAR COMPLICATIONS OF ANTICANCER THERAPY: CLINICAL FEATURES, DIAGNOSIS, TREATMENT, PREVENTION (PART II)

2018 ◽  
Vol 23 (1) ◽  
pp. 43-49
Author(s):  
N. T Vatutin ◽  
E. V Sklyannaya ◽  
Mariam A. El-Khatib ◽  
G. G Taradin
Keyword(s):  
Clinical Features ◽  
Kinase Inhibitors ◽  
Alkylating Agents ◽  
Cardiovascular Complications ◽  
Chemotherapeutic Agents ◽  
Left Ventricular ◽  
Protein Kinase Inhibitors ◽  
Anthracycline Antibiotics ◽  
Treatment And Prevention ◽  
The Given

The given review is devoted to the problem of the cardiotoxicity of chemotherapeutic agents. Many of chemotherapeutic agents can cause cardiovascular complications such as left ventricular dysfunction and heart failure development, myocardial ischemia, arterial hypertension, thromboembolism, QT prolongation and arrhythmias. The toxic influence of the most often used chemotherapeutic agents on heart (such as antimetabolites, alkylating agents, platinum compounds, taxanes, vinca alkaloids, monoclonal antibodies, anthracycline antibiotics, topoisomerase and protein kinase inhibitors, immunomodulatory agents and cytokines) has been described. The results of recent studies on etiology, pathogenesis and clinical features of chemotherapy-induced cardiotoxicity were present in the first part of review. The clinical features, diagnosis, treatment and prevention of the cardiotoxicity of chemotherapeutic agents, are described in the second part of the review

scholarly journals CARDIOVASCULAR COMPLICATIONS OF ANTICANCER THERAPY: DEFINITION, ETIOLOGY, EPIDEMIOLOGY, PATHOGENESIS, CLASSIFICATION (PART I)

2017 ◽  
Vol 22 (6) ◽  
pp. 345-350
Author(s):  
N. T Vatutin ◽  
E. V Sklyannaya ◽  
Mariam A. El-Khatib ◽  
G. G Taradin
Keyword(s):  
Kinase Inhibitors ◽  
Alkylating Agents ◽  
Cardiovascular Complications ◽  
Chemotherapeutic Agents ◽  
Left Ventricular ◽  
Protein Kinase Inhibitors ◽  
Anthracycline Antibiotics ◽  
Oncological Patients ◽  
Clinically Significant ◽  
Myocardial Injuries

The given review is devoted to the problem of the cardiotoxicity of chemotherapeutic agents. Modern cytostatics cause clinically significant manifestations of cardiotoxicity - myocardial injuries, reducing both quality and life expectancy of oncological patients. Many of chemotherapeutic agents can cause cardiovascular complications such as the development of the left ventricular dysfunction and heart failure, myocardial ischemia, arterial hypertension, thromboembolism, QT prolongation and arrhythmias. The toxic influence of the most often used chemotherapeutic agents on heart (antimetabolites, alkylating agents, platinum compounds, taxanes, vinca alkaloids, monoclonal antibodies, anthracycline antibiotics, topoisomerase and protein kinase inhibitors, immunomodulatory agents and cytokines) has been described. The results of recent studies on etiology, epidemiology, classification and pathogenesis are presented in the first part of review. Most attention is paid to recent research in pathogenesis of chemotherapy induced cardiotoxicity. Given the numerous aspects of cardiotoxicity are not completely studied yet, obviously the further researches are needed in this field.

Hepatotoxicity of chemotherapeutic agents: current state of the problem

2016 ◽  
Vol 21 (6) ◽  
pp. 325-333
Author(s):  
M. T Vatutin ◽  
E. V Sklyannaya ◽  
Mariam A. El-Khatib ◽  
S. V Starchenko ◽  
M. V Makarova
Keyword(s):  
Kinase Inhibitors ◽  
Antitumor Agents ◽  
Opportunistic Infections ◽  
Alkylating Agents ◽  
Chemotherapeutic Agents ◽  
Protein Kinase Inhibitors ◽  
Drug Induced ◽  
Anthracycline Antibiotics ◽  
Current State ◽  
High Level

This review is devoted to the actual for the present day problem of the hepatotoxicity of chemotherapeutic agents. Liver is the most important organ essential for the maintaining of the body’s internal environment. For the present time there is observed the high level of the morbidity and mortality rate against the background of drug-induced liver lesions due to, in the first instance, the lack ofproper manner for the substitution of the liver function but transplantation. Liver deteriorations due to the administration of antitumor agents have no pathognomonic clinical or histological features that significantly embarrasses the execution of the differential diagnosis with liver disorders against the background of administration of other preparations, either associated with opportunistic infections or the progression of previously acquired pathology of the liver. In the article there is described the toxic influence on the liver of most often used in oncology chemotherapeutic agents - antimetabolites, alkylating agents, platinum compounds, epothilones, taxanes, vinca alkaloids, monoclonal antibodies, anthracycline antibiotics, topoisomerase and protein kinase inhibitors is described in this article. In the review there are summarized results of recent studies of etiology, pathogenesis, clinical features, diagnosis, prevention and treatment of chemotherapy induced hepatotoxicity. The special attention is given to recent discoveries in the area of pathogenesis of chemotherapy induced hepatotoxicity. However many moments remain to be still not studied completely, that offers perspectives for further research in this field.

scholarly journals The Evolving Role of Immune Checkpoint Inhibitors in Hepatocellular Carcinoma Treatment

Vaccines ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 532
Author(s):  
Patrizia Leone ◽  
Antonio Giovanni Solimando ◽  
Rossella Fasano ◽  
Antonella Argentiero ◽  
Eleonora Malerba ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Immune Checkpoint ◽  
Immune Checkpoint Inhibitors ◽  
Kinase Inhibitors ◽  
Immune Escape ◽  
Checkpoint Inhibitors ◽  
Chemotherapeutic Agents ◽  
Protein Kinase Inhibitors ◽  
Great Promise ◽  
Chronic Injury

Hepatocellular carcinoma (HCC) is one of most common cancers and the fourth leading cause of death worldwide. Commonly, HCC development occurs in a liver that is severely compromised by chronic injury or inflammation. Liver transplantation, hepatic resection, radiofrequency ablation (RFA), transcatheter arterial chemoembolization (TACE), and targeted therapies based on tyrosine protein kinase inhibitors are the most common treatments. The latter group have been used as the primary choice for a decade. However, tumor microenvironment in HCC is strongly immunosuppressive; thus, new treatment approaches for HCC remain necessary. The great expression of immune checkpoint molecules, such as programmed death-1 (PD-1), cytotoxic T-lymphocyte antigen 4 (CTLA-4), lymphocyte activating gene 3 protein (LAG-3), and mucin domain molecule 3 (TIM-3), on tumor and immune cells and the high levels of immunosuppressive cytokines induce T cell inhibition and represent one of the major mechanisms of HCC immune escape. Recently, immunotherapy based on the use of immune checkpoint inhibitors (ICIs), as single agents or in combination with kinase inhibitors, anti-angiogenic drugs, chemotherapeutic agents, and locoregional therapies, offers great promise in the treatment of HCC. This review summarizes the recent clinical studies, as well as ongoing and upcoming trials.

scholarly journals Protein kinase inhibitors--potential chemotherapeutic agents.

1995 ◽  
Vol 42 (4) ◽  
pp. 405-418 ◽  
Author(s):  
D Shugar
Keyword(s):  
Protein Kinase ◽  
Kinase Inhibitors ◽  
Chemotherapeutic Agents ◽  
Protein Kinase Inhibitors ◽  
Donor And Acceptor ◽  
Catalytic Sites ◽  
Competitive Inhibitors ◽  
Preclinical Trials ◽  
Antiviral Chemotherapy

Protein kinase inhibitors, widely exploited for elucidation of the biological functions of kinases, have more recently come under active consideration as potential chemotherapeutic agents for tumour and other diseases. A brief overview is presented of diverse approaches to the design and development of selective protein kinase inhibitors, and related problems such as donor and acceptor specificities, stereochemical aspects, emerging relationships between protein, sugar and nucleoside kinases. In particular, and contrary to popular belief that ATP-competitive inhibitors cannot be selective because of the close homology of the ATP catalytic sites, numerous examples are presented of such inhibitors which are both potent and selective for a given kinase or class of kinases. Some of these are undergoing preclinical trials. Attention is also directed to the role of cellular and viral protein kinases in the life cycle of viruses, and the potential of these enzymes, especially those encoded by, and essential for replication of, a given virus as targets for antiviral chemotherapy.

scholarly journals Mitochondria Death/Survival Signaling Pathways in Cardiotoxicity Induced by Anthracyclines and Anticancer-Targeted Therapies

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
David Montaigne ◽  
Christopher Hurt ◽  
Remi Neviere
Keyword(s):  
Cell Death ◽  
Cell Fate ◽  
Tyrosine Kinases ◽  
Cellular Response ◽  
Kinase Inhibitors ◽  
Biological Effects ◽  
Chemotherapeutic Agents ◽  
Left Ventricular ◽  
Transcriptional Factors ◽  
Mitochondrial Functions

Anthracyclines remain the cornerstone of treatment in many malignancies but these agents have a cumulative dose relationship with cardiotoxicity. Development of cardiomyopathy and congestive heart failure induced by anthracyclines are typically dose-dependent, irreversible, and cumulative. Although past studies of cardiotoxicity have focused on anthracyclines, more recently interest has turned to anticancer drugs that target many proteins kinases, such as tyrosine kinases. An attractive model to explain the mechanism of this cardiotoxicity could be myocyte loss through cell death pathways. Inhibition of mitochondrial transition permeability is a valuable tool to prevent doxorubicin-induced cardiotoxicity. In response to anthracycline treatment, activation of several protein kinases, neuregulin/ErbB2 signaling, and transcriptional factors modify mitochondrial functions that determine cell death or survival through the modulation of mitochondrial membrane permeability. Cellular response to anthracyclines is also modulated by a myriad of transcriptional factors that influence cell fate. Several novel targeted chemotherapeutic agents have been associated with a small but worrying risk of left ventricular dysfunction. Agents such as trastuzumab and tyrosine kinase inhibitors can lead to cardiotoxicity that is fundamentally different from that caused by anthracyclines, whereas biological effects converge to the mitochondria as a critical target.

Cardiovascular complications of novel kinase inhibitors

ESC CardioMed ◽  
2018 ◽  
pp. 1170-1176
Author(s):  
Mark Sweeney ◽  
Alexander Lyon
Keyword(s):  
High Risk ◽  
Kinase Inhibitors ◽  
Kinase Inhibitor ◽  
Blood Pressure Measurement ◽  
Cardiovascular Complications ◽  
Left Ventricular ◽  
Cancer Therapies ◽  
Serine Kinase ◽  
Include Blood Pressure ◽  
New Cancer Therapies

Tyrosine and serine kinase inhibitors are new cancer therapies which have revolutionized the field of modern oncology and have transformed previously fatal conditions such as chronic myeloid leukaemia into treatable chronic diseases. The cardiovascular complications related to kinase inhibitor treatments have emerged and the importance of effective cardiovascular management is becoming clear. Precise cardiovascular toxicity profiles vary among different classes of kinase inhibitors and between different specific agents. The most important cardiovascular complications of these kinase inhibitors include hypertension, heart failure, arterial thromboembolic disease, QT prolongation, and pulmonary hypertension. The aim of effective cardiovascular management in this setting should be to minimize the impact of toxicities to facilitate the continuation of these highly effective cancer treatments. It is key to perform a thorough baseline cardiovascular risk assessment prior to commencing treatment so that reversible risk factors are identified and addressed appropriately. Preliminary assessment should, at a minimum, include blood pressure measurement, serum creatinine, lipid profile and fasting glucose, and a resting electrocardiogram. Additionally, in selected high-risk patients or those starting high-risk kinase inhibitors, baseline assessment of left ventricular function can also be helpful. Effective risk stratification will allow appropriate, individualized surveillance to be arranged for each patient in order to identify complications early and manage them effectively. When significant cardiovascular complications occur, decisions regarding the need to suspend or discontinue potentially life-prolonging treatments are exceptionally challenging and the input of the multidisciplinary team in this setting and communication between the cardiologists and the oncologists or haemato-oncologists is invaluable.

Alkaloids as Anticancer Agents: A Review of Chinese Patents in Recent 5 Years

2020 ◽  
Vol 15 (1) ◽  
pp. 2-13 ◽  
Author(s):  
Hongyu Tao ◽  
Ling Zuo ◽  
Huanli Xu ◽  
Cong Li ◽  
Gan Qiao ◽  
...  
Keyword(s):  
Anticancer Activity ◽  
Anticancer Agents ◽  
Kinase Inhibitors ◽  
Protein Kinase Inhibitors ◽  
Cdk Inhibitors ◽  
Comprehensive Overview ◽  
P53 Expression ◽  
Study Results

Background: In recent years, many novel alkaloids with anticancer activity have been found in China, and some of them are promising for developing as anticancer agents. Objective: This review aims to provide a comprehensive overview of the information about alkaloid anticancer agents disclosed in Chinese patents, and discusses their potential to be developed as anticancer drugs used clinically. Methods: Anticancer alkaloids disclosed in Chinese patents in recent 5 years were presented according to their mode of actions. Their study results published on PubMed, and SciDirect databases were presented. Results: More than one hundred anticancer alkaloids were disclosed in Chinese patents and their mode of action referred to arresting cell cycle, inhibiting protein kinases, affecting DNA synthesis and p53 expression, etc. Conclusion: Many newly found alkaloids displayed potent anticancer activity both in vitro and in vivo, and some of the anticancer alkaloids acted as protein kinase inhibitors or CDK inhibitors possess the potential for developing as novel anticancer agents.

The polymorphism at the microRNA-155 binding site in AGTR1 gene is not significantly associated with rheumatic heart disease in Saudi Arabia population

MicroRNA ◽  
2020 ◽  
Vol 09 ◽  
Author(s):  
S. Justin Carlus ◽  
Fiona Hannah Carlus ◽  
Mazen Khalid Al-Harbi ◽  
Abdulhadi H Al-Mazroea ◽  
Khalid M Al- Harbi ◽  
...  
Keyword(s):  
Saudi Arabia ◽  
Heart Disease ◽  
Rheumatic Heart Disease ◽  
Clinical Features ◽  
Left Ventricular ◽  
Genotype Distribution ◽  
Allelic Discrimination ◽  
Children And Young Adults ◽  
And Control ◽  
Rheumatic Heart

Background: Rheumatic heart disease (RHD) remains a major cause of cardiovascular diseases and the most devastating effects are on children and young adults. RHD is caused due to the interaction between microbial, environmental, immunologic, and genetic factors. The renin-angiotensin aldosterone system (RAAS) has been strongly implicated as the susceptibility pathway in the pathogenesis of cardiovascular disease. Objective: The present study investigated the modulating effect of Angiotensin II type 1 receptor (AGTR1) 1166A>C polymorphism on the RHD and its clinical features in Saudi Arabia. Methods: AGTR1 1166A>C polymorphism was genotyped in 96 echocardiographically confirmed RHD patients and 142 ethnically matched controls by TaqMan allelic discrimination method. Results: Genotype distribution of the AGTR1 1166A>C polymorphism was not significantly different between RHD and control groups. Further, AGTR1 1166A>C genotypes are not associated with the clinical features of RHD. These data support that there was no evidence for an association between AGTR1 1166A>C polymorphism and RHD in Saudi Arabia. Conclusion: To our knowledge, this is the first study that has investigated the possible association between AGTR1 1166A>C polymorphism and susceptibility to RHD and its clinical features. Even though AGTR1 gene is 1166A>C (rs5186) was reported to be associated with hypertension, left ventricular hypertrophy and coronary heart disease. Present study did not find any association between AGTR1 1166A>C polymorphism and RHD in Saudi Arabia. Further studies are needed to confirm our findings.

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