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Related Concept Videos

The Ras Gene02:38

The Ras Gene

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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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Treatment Resistant Cancers

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Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
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mTOR Signaling and Cancer Progression03:03

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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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Small GTPases - Ras and Rho01:24

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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.
Three regulatory proteins control their activity:
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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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Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

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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.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
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Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down
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Response and Resistance to RAS Inhibition in Cancer.

Richard Y Ebright1,2,3, Julien Dilly1,2,3, Alice T Shaw1,2

  • 1Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts.

Cancer Discovery
|April 28, 2025
PubMed
Summary
This summary is machine-generated.

RAS inhibitors show promise in treating various cancers, but resistance limits their effectiveness. Future strategies require developing superior inhibitors and combination therapies to overcome resistance and enhance patient outcomes.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Discovery

Background:

  • RAS pathway mutations are prevalent in many human cancers.
  • RAS inhibitors have demonstrated initial efficacy across diverse cancer types.
  • Acquired resistance mechanisms significantly impede the long-term clinical benefit of RAS-targeted therapies.

Purpose of the Study:

  • To review the current landscape of RAS inhibitors in cancer therapy.
  • To identify key challenges and opportunities in overcoming acquired resistance.
  • To outline strategies for developing next-generation RAS-targeted treatments and combinations.

Main Methods:

  • Literature review of preclinical and clinical studies on RAS inhibitors.
  • Analysis of resistance mechanisms associated with RAS-targeted therapy.
  • Evaluation of emerging drug development and combination therapy approaches.

Main Results:

  • Early clinical trials confirm the activity of RAS inhibitors in various malignancies.
  • Acquired resistance is a major cause of treatment failure.
  • Development of inhibitors with improved potency, selectivity, and pharmacokinetics is crucial.

Conclusions:

  • Overcoming acquired resistance is essential for maximizing the clinical impact of RAS-targeted therapy.
  • Next-generation inhibitors and rational combination strategies are necessary for durable responses.
  • Further research into resistance mechanisms will guide the development of more effective cancer treatments.