Cardiovascular effects of targeted cancer therapeutics

Reji, Nidhi
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When a cell's genes are altered, it stops acting like a normal cell. Gene modifications in cancer cells, for example, can cause the cell to expand and divide rapidly. These modifications are what distinguishes it as a cancer cell. However, there are several forms of cancer, and not all cancer cells are alike. Colon cancer and breast cancer cells, for example, have various gene variations that aid their growth and/or spread. Even among people with the same general type of cancer (such as colon cancer), cancer cells may have different gene variations, causing one person's colon cancer to be different from another's. Researchers have also discovered that the ecosystem in which cancers begin, develop, and survive differs from one cancer to the next. Any tumor has proteins or enzymes that give signals to the cancer cell telling it to expand and copy itself. Knowing this information has contributed to the discovery of medicines that can "target" these proteins or enzymes and prevent them from sending messages. Targeted therapy is a cancer treatment in which medications are used to target certain genes and proteins implicated in cancer cell development and survival. Targeted therapy can alter the tissue ecosystem that aids a cancer's development and survival, or it can target cancer-related cells such as blood vessel cells. Targeted drugs can either suppress or turn off the signals that cause cancer cells to rise, or they can signal cancer cells to die. These medications influence cancer cells but mostly leave normal, healthy cells alone due to their selective action while traditional chemotherapy is cytotoxic to most cells, i.e., it can damage normal, healthy cells as well as cancer cells. Targeted medications frequently act by preventing cancer cells from replicating. They will prevent a cancer cell from dividing and producing new cancer cells in this way. Traditional chemotherapy, on the other hand, destroys cancer cells that have already formed. Targeted therapies can identify and block those types of signals received within a cancer cell that tell it to spread or can locate and attack certain areas or substances in cancer cells. Some of the properties found in cancer cells that become "targets" for selective therapies are too much of a particular antigen on a cancer cell or a protein that is not seen in human cells, modified protein, genetic DNA modifications that do not occur in a healthy cell or new and extra growth of blood vessels to provide nourishment to cancer cells. Targeted drugs can be used to block or switch off chemical signals that tell cancer cells to divide and expand. Certain selective therapy medications, such as monoclonal antibodies, regulate cancer cells in many ways and can also qualify as immunotherapy because they improve the immune system. ‘Precision medicine’ or ‘personalized medicine’ are terms used to describe targeted therapy. This is due to the fact that they are designed to precisely target certain differences or substances in cancer cells, and these targets may vary even among individuals of the same cancer form. Following a biopsy or surgery, certain kinds of tumors are screened for various targets, which may aid in determining the most appropriate therapy. Finding a particular goal allows for more accurate or customized care matching. However, despite the precision and selectivity, targeted chemotherapy has also been found to cause various side effects in patients such as rashes, dry skin, high blood pressure or digestive problems. Cardiotoxicity of targeted chemotherapy has been seen to be a consequence of the direct effects of the drugs or because of underlying comorbidities or genetic predisposition of the patient. These side effects can be managed and treated appropriately after understanding the mechanism of the drug action, drug interaction with the cardiovascular system and also with early and regular screening of patients who have underlying risks and preventive treatment. In order to improve the overall survival of the cardiac consequences of targeted cancer chemotherapy, the monitoring and management should focus on not just the ejection fractions which remains the gold standard, but also the direct effects on the structure of the heart (such as fibrosis), cardiac function, diastolic dysfunction, cardiac conduction and arrhythmias, systemic and pulmonary vascular function and hemodynamics, hemostasis and thrombosis, as well as cardiac response to injury and stress. Observing the myocardial strain and precise biomarkers (e.g., troponin I and natriuretic peptides) amid oncological treatment can exhibit faint or profound disruptions in the cardiovascular system that are warning signs for the progression of HF before a fall in the LVEF. Therefore, cardiotoxicity is a wide name that should define changes in cardiac measures and also changing operative estimates of the cardiovascular systems (coronary blood flow reserve, stroke work, maximal functional capacity). Cancer patients and survivors have reduced exercise ability which can severely affect their life which is why regular and thorough cardiac monitoring and assessing are imperative so we can initiate pharmacologic or non-pharmacologic therapies to treat and minimize the damage caused to the cardiac system during targeted chemotherapy. Continued collaboration between the cardiology and oncology communities will enable the clinical studies necessary to answer these important questions and further optimize the long-term outcomes of cancer patients.
Oncology, Cardiology, Pharmacology