Related Experiment Video

Updated: Dec 6, 2025

Detection of Targetable Alterations in Non-small Cell Lung Cancer using Next-generation Sequencing
05:17

Detection of Targetable Alterations in Non-small Cell Lung Cancer using Next-generation Sequencing

Published on: October 10, 2025

173

KRAS oncogene may be another target conquered in non-small cell lung cancer (NSCLC)

Hanxiao Chen1, Jun Zhao1

  • 1Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Departments of Thoracic Medical Oncology, Peking University Cancer Hospital and Institute, Beijing, China.

Thoracic Cancer
|October 6, 2020
PubMed

Insights

KRAS mutations are common in non-small cell lung cancer, lowering survival. New KRAS G12C inhibitors and combination strategies offer hope for treating this challenging target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations are prevalent in non-small cell lung cancer (NSCLC).
  • Patients with KRAS mutations often exhibit poorer survival rates compared to those without these mutations.
  • KRAS's complex structure and biological properties present significant challenges for developing targeted therapies.

Purpose of the Study:

  • To review current therapeutic strategies targeting KRAS in NSCLC.
  • To highlight the potential of novel KRAS G12C inhibitors and combination therapies.
  • To discuss the importance of understanding downstream signaling pathways and resistance mechanisms for personalized treatment.

Main Methods:

  • Review of current medical research and clinical trial data.
  • Analysis of emerging therapeutic strategies, including direct KRAS inhibition and immunotherapy.
  • Exploration of combination approaches targeting KRAS downstream pathways.

Main Results:

  • KRAS G12C inhibitors represent a significant advancement in targeting specific KRAS mutations.
  • Combination strategies, including immunotherapy and downstream pathway inhibition, show promise.
  • Understanding resistance mechanisms is crucial for optimizing treatment efficacy.

Conclusions:

  • Targeted therapies, particularly KRAS G12C inhibitors, are transforming NSCLC treatment.
  • Combination strategies are essential for overcoming therapeutic challenges and improving patient outcomes.
  • Personalized treatment approaches considering individual KRAS mutation status and resistance profiles are key for future success.
Keywords:
KRAS mutationnon-small cell lung cancertargettherapy

More Related Videos

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer06:51

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

Published on: July 21, 2018

18.3K
Author Spotlight: Advancements in Molecular Biomarker Testing for Non-Squamous Non-Small Cell Lung Cancer07:59

Author Spotlight: Advancements in Molecular Biomarker Testing for Non-Squamous Non-Small Cell Lung Cancer

Published on: September 8, 2023

1.5K

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...
8.3K
Abnormal Proliferation02:23

Abnormal Proliferation

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...
5.0K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
10.6K
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...
6.8K
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
5.9K
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
4.5K