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Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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 specific...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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 specific...
The Ras Gene02:38

The Ras Gene

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 superfamily...
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

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.
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mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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.
The mTOR pathway or the...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

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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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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Targeting KRAS for cancer therapy.

Jianlong Jia1,2, Ruonan Liu3,4, Tonia A Adamide5

  • 1Institute of Lung Health and Immunity (LHI), Comprehensive Pneumology Center (CPC), Helmholtz Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.

British Journal of Pharmacology
|July 1, 2026
PubMed
Summary

Targeting KRAS-mutant cancers shows promise. New strategies for KRAS G12C and other mutations, including resistance mechanisms and novel dosing frameworks, aim to improve patient outcomes.

Keywords:
KRASKRAS inhibitorsKRAS mutationscombination therapytherapeutic resistance

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Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • KRAS proto-oncogene GTPase (KRAS)-mutant cancers are a significant therapeutic challenge.
  • Recent advancements have led to targeted therapies for KRAS-mutant cancers, particularly KRAS G12C.
  • Understanding KRAS alterations, resistance mechanisms, and adaptive pathways is crucial for improving treatment efficacy.

Purpose of the Study:

  • To review the biology and epidemiology of KRAS alterations.
  • To summarize clinical evidence for KRAS G12C inhibitors and explore strategies for non-KRAS G12C mutations.
  • To propose a novel framework for optimizing therapeutic interventions and patient survival.

Main Methods:

  • Literature review of KRAS biology, epidemiology, and clinical trial data.
  • Analysis of resistance mechanisms, including secondary mutations and adaptive circuits.
  • Development of a 'three-clock, two-window' framework for dosing optimization.
  • Proposal of a closed-loop system integrating biomarker dynamics (ctDNA, pERK) and imaging for treatment monitoring.

Main Results:

  • KRAS G12C inhibitors like sotorasib and adagrasib demonstrate clinical efficacy.
  • Non-KRAS G12C strategies, including RAS (ON)- and KRAS G12D-selective approaches, show early promise.
  • Identification of resistance mechanisms and adaptive cellular reprogramming.
  • A proposed framework and closed-loop system for enhanced therapeutic control.

Conclusions:

  • Targeted KRAS inhibition has revolutionized cancer therapy.
  • Addressing resistance and exploring non-G12C mutations are key future directions.
  • Optimized dosing strategies and integrated biomarker monitoring can improve durable inhibition and survival in KRAS-mutant cancers.