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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.
There are several types of targeted therapies against...
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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.
Ras is a...
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Abnormal Proliferation02:23

Abnormal Proliferation

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

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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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Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

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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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Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

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Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include:
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Related Experiment Video

Updated: Dec 2, 2025

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
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Therapeutics Targeting Mutant KRAS.

Kyaw Z Thein1, Amadeo B Biter2, David S Hong2

  • 1Division of Hematology and Medical Oncology, Oregon Health and Science University/Knight Cancer Institute, Portland, Oregon 97239, USA;

Annual Review of Medicine
|November 3, 2020
PubMed
Summary
This summary is machine-generated.

Genetic aberrations in rat sarcoma (RAS) viral oncogene, particularly KRAS mutations, drive cancer. New covalent inhibitors targeting KRASG12C show promise, but combination strategies are vital for overcoming resistance.

Keywords:
AMG 510KRAS mutationsKRASG12C inhibitorsMRTX849RASrat sarcoma viral oncogenesynthetic lethality

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Rat sarcoma (RAS) viral oncogene aberrations are prevalent in human cancers.
  • RAS signaling pathways, including MAPK and PI3K, are critical for tumorigenesis.
  • KRAS is the most frequently mutated RAS isoform, with codon 12 mutations common in malignancies.

Purpose of the Study:

  • To review the role of RAS mutations in cancer.
  • To discuss novel therapeutic strategies targeting KRAS, especially KRASG12C.
  • To highlight the importance of combination therapies for KRAS-mutant tumors.

Main Methods:

  • Review of existing literature on RAS oncogenes and targeted therapies.
  • Analysis of recent developments in covalent allosteric inhibitors.
  • Discussion of resistance mechanisms and combination strategies.

Main Results:

  • KRAS mutations, particularly at codon 12, are key drivers of many cancers.
  • Covalent allosteric inhibitors (e.g., AMG 510, MRTX849) targeting KRASG12C demonstrate early therapeutic potential.
  • Resistance to KRAS-targeted therapies necessitates combination approaches.

Conclusions:

  • Targeting KRAS mutations represents a significant area of cancer research.
  • Novel covalent inhibitors offer a promising avenue for treating KRAS-mutant cancers.
  • Overcoming therapeutic resistance through combination strategies is crucial for effective cancer treatment.