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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
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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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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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Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

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Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates...
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M-Cdk Drives Transition Into Mitosis02:15

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Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
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MAPK blockade, toxicities, pathogenesis and management.

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BRAF/MEK inhibitors improve survival in advanced melanoma. Managing side effects is key for adherence, with combination therapies generally reversible and manageable.

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Area of Science:

  • Oncology
  • Pharmacology
  • Dermatology

Background:

  • BRAF/MEK inhibitors have transformed advanced and metastatic melanoma treatment.
  • Prolonged overall survival and progression-free survival are observed.
  • Therapy choices often depend on side effect profiles due to similar efficacy of available combinations.

Purpose of the Study:

  • To review the side effect profiles of BRAF/MEK inhibitor combinations in melanoma.
  • To discuss management strategies for on-target and class effects.
  • To evaluate the impact of combination therapy on treatment adherence.

Main Methods:

  • Review of current literature on BRAF/MEK inhibitor combination therapies.
  • Analysis of reported side effects and their management.
  • Evaluation of treatment discontinuation rates and reasons.

Main Results:

  • Sequential BRAF/MEK inhibition and immunotherapy may increase toxicity, presenting as sepsis-like syndrome.
  • Triple therapy with BRAF/MEK inhibitors and anti-PD1/PD-L1 antibodies induces severe side effects in most patients.
  • Toxicity from BRAF/MEK inhibitor combination therapy is typically manageable and reversible, rarely leading to discontinuation.

Conclusions:

  • BRAF/MEK inhibitor combination therapies offer significant survival benefits in melanoma.
  • Effective management of side effects is crucial for maintaining treatment adherence.
  • Switching to alternative combination therapies can resolve persistent off-target effects.