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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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The Ras Gene02:38

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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
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mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
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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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M cyclin...
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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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Targeting KRAS in cancer.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Discovery

Background:

  • RAS family variants, particularly KRAS, are common cancer-driving mutations linked to poor prognosis.
  • KRAS has historically been considered undruggable due to its structure.
  • Recent scientific advancements enable direct targeting of KRAS.

Purpose of the Study:

  • To review RAS pathobiology with a focus on KRAS.
  • To illustrate therapeutic approaches for KRAS-targeted therapies.
  • To summarize resistance mechanisms and future directions in KRAS therapeutics.

Main Methods:

  • Review of scientific literature on RAS pathobiology and KRAS inhibitors.
  • Analysis of therapeutic strategies including allele-specific and pan-RAS inhibitors.
  • Examination of combination therapies, immunotherapeutics, and resistance mechanisms.

Main Results:

  • Successful allele-specific targeting of KRAS G12C in non-small cell lung cancer with approved agents (sotorasib, adagrasib).
  • Emerging inhibitors show activity against other KRAS variants in refractory cancers like pancreatic cancer.
  • Understanding of resistance mechanisms and development of combination strategies are advancing.

Conclusions:

  • Direct KRAS targeting is now a reality, with initial successes in specific mutations.
  • Diverse therapeutic strategies, including combination approaches, are being developed for broader KRAS targeting.
  • Future KRAS therapeutics hold significant clinical potential for cancer treatment.