Related Experiment Video

Updated: Apr 16, 2026

Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib
09:38

Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib

Published on: June 26, 2019

8.5K

Crizotinib in the management of advanced-stage non-small-cell lung cancer

Herbert H Loong1, Kevin Mok, Linda K S Leung

  • 1Department of Clinical Oncology, State Key Laboratory in Oncology in South China, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong.

Future Oncology (London, England)
|March 12, 2015
PubMed

Insights

Crizotinib effectively treats ALK-rearranged non-small-cell lung cancer (NSCLC). Research is exploring its effects on ROS1 and c-Met, and strategies to overcome acquired resistance to this targeted therapy.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Anaplastic Lymphoma Kinase (ALK) gene rearrangements are key drivers in a subset of non-small-cell lung cancer (NSCLC).
  • Crizotinib is an oral targeted therapy inhibiting ALK, ROS1, and c-Met receptor tyrosine kinases.
  • The clinical efficacy of crizotinib in ALK-positive NSCLC is well-established.

Purpose of the Study:

  • To review the pharmacological profile of crizotinib.
  • To summarize preclinical and clinical data supporting crizotinib's approval for ALK-positive NSCLC.
  • To discuss emerging resistance mechanisms and ongoing research to overcome them.

Main Methods:

  • Literature review of pharmacological properties.
  • Analysis of preclinical studies.
  • Evaluation of clinical trial data and ongoing research.

Main Results:

  • Crizotinib demonstrates significant efficacy in ALK-rearranged NSCLC.
  • Mechanisms of acquired resistance, including secondary mutations in ALK, have been identified.
  • The role of crizotinib in targeting ROS1 and c-Met in NSCLC is under investigation.

Conclusions:

  • Crizotinib is a validated treatment for ALK-positive NSCLC.
  • Understanding and overcoming resistance mechanisms are critical for long-term patient benefit.
  • Further clinical research is focused on combination therapies and novel agents to address resistance.
Keywords:
EML4–ALK fusionROS1acquired resistancebrain metastasesc-Metcrizotinibnon-small-cell lung cancer

More Related Videos

Endobronchial Ultrasound-guided Intratumoral Injection of Cisplatin for the Treatment of Isolated Mediastinal Recurrence of Lung Cancer04:04

Endobronchial Ultrasound-guided Intratumoral Injection of Cisplatin for the Treatment of Isolated Mediastinal Recurrence of Lung Cancer

Published on: February 12, 2017

11.1K
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

18.9K

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...
9.2K
Treatment Resistent Cancers02:56

Treatment Resistent Cancers

1.5K
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.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
6.4K
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

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...
3.9K
Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers01:26

Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers

Receptor tyrosine kinase inhibitors (TKIs) and calcium channel blockers (CCBs) are two critical categories of drugs employed in the treatment of pulmonary artery hypertension (PAH). PAH is a disease that causes high blood pressure in the pulmonary arteries, resulting in chest pain, fatigue, and shortness of breath.
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
667
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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...
6.3K