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Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Combination Therapies and Personalized Medicine02:50

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Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
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Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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Receptor tyrosine kinase inhibitors (TKIs) and calcium channel blockers (CCBs) are two critical categories of drugs employed in the treatment of pulmonary artery hypertension (PAH). PAH is a disease that causes high blood pressure in the pulmonary arteries, resulting in chest pain, fatigue, and shortness of breath.
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Inhibition of Cdk Activity02:34

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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Risk Stratification, Screening and Treatment of BRAF/MEK Inhibitors-Associated Cardiotoxicity.

Isabelle Senechal1,2, Maria Sol Andres3, Jieli Tong3

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BRAF and MEK inhibitors improve cancer prognosis but can cause cardiovascular adverse events like left ventricular dysfunction and hypertension. Early surveillance and management are key for patient safety and effective treatment.

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Area of Science:

  • Oncology
  • Cardiology
  • Pharmacology

Background:

  • BRAF and MEK inhibitors are standard treatments for BRAF-mutant cancers, notably melanoma.
  • These targeted therapies have significantly improved outcomes for previously intractable cancers.

Purpose of the Study:

  • To review cardiovascular adverse events associated with BRAF and MEK inhibitors.
  • To describe their pathophysiologic mechanisms.
  • To provide guidance on surveillance and management of cardiotoxicity.

Main Methods:

  • Literature review of cardiovascular adverse events and mechanisms.
  • Synthesis of current evidence for risk stratification and management.

Main Results:

  • BRAF/MEK inhibitors are linked to cardiotoxicities including left ventricular systolic dysfunction, hypertension, and QTc prolongation.
  • These toxicities are largely reversible and manageable with medical therapy.
  • Cardiotoxicity can limit the efficacy of these important anti-cancer agents.

Conclusions:

  • Cardiovascular surveillance is crucial for patients receiving BRAF and MEK inhibitors.
  • Prompt recognition and management of cardiotoxicity are essential for optimal patient outcomes.
  • Further research into mitigating cardiotoxicity is warranted.