Lung cancer is a leading cause of cancer-related mortality worldwide and in the People's Republic of China. Recently, the pathological proportions of the various forms of lung cancer have changed. A shift to a preponderance of adenocarcinoma at the expense of squamous cell carcinoma is observable. Treatment decisions have historically been based on tumor histology, and evolution of our molecular understanding of cancer has led to development of targeted therapeutic agents. It is essential to further understand mutations that drive cancer development (driver mutations) in relevant genes and their effects on cancer cell proliferation and survival. The epidemiology of lung cancer in the People's Republic of China has been extensively reviewed elsewhere. However, molecular epidemiological data from mainland China are scarce. Consequently, we herein review the prevalence of driver mutations in Chinese patients.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5217505PMC
http://dx.doi.org/10.2147/LCTT.S40817DOI Listing

Publication Analysis

Top Keywords

driver mutations
12
people's republic
12
republic china
12
lung cancer
12
prevalence driver
8
cancer
6
mutations
4
mutations non-small-cell
4
lung
4
non-small-cell lung
4

Similar Publications

Cancer genomics consortia have identified somatic drivers of breast cancer subtypes. However, these studies have predominantly included older, non-Black women, and the related socioeconomic status (SES) data is limited. Increased representation and depth of social data are crucial for understanding how health inequity is intertwined with somatic landscapes.

View Article and Find Full Text PDF

Several decades have passed since the description of the first patient with primary aldosteronism (PA). PA was initially classified in two main forms: aldosterone-producing adenoma (APA) and idiopathic hyperaldosteronism (IHA). However, the pathogenesis of PA has now been shown to be far more complex.

View Article and Find Full Text PDF

Inhibition of NLRP3 enhances pro-apoptotic effects of FLT3 inhibition in AML.

Cell Commun Signal

January 2025

Department of Biosciences and Medical Biology, Paris-Lodron University Salzburg, Hellbrunner Strasse 34, Salzburg, 5020, Austria.

FLT3 mutations occur in approximately 25% of all acute myeloid leukemia (AML) patients. While several FLT3 inhibitors have received FDA approval, their use is currently limited to combination therapies with chemotherapy, as resistance occurs, and efficacy decreases when the inhibitors are used alone. Given the highly heterogeneous nature of AML, there is an urgent need for novel targeted therapies that address the disease from multiple angles.

View Article and Find Full Text PDF

Objectives: Immune checkpoint inhibitor (ICI)-containing treatment is currently prescribed as first-line treatment for all patients with advanced non-small cell lung cancer (NSCLC) without targetable driver mutations. However, only 30-45% of patients show no progression within 12 months after treatment start. Various biomarkers are being studied to save costly and potentially harmful treatment in non-responders.

View Article and Find Full Text PDF

Tumour hypoxia in driving genomic instability and tumour evolution.

Nat Rev Cancer

January 2025

Translational Oncogenomics Laboratory, Cancer Research UK Manchester Institute, University of Manchester, Manchester, UK.

Intratumour hypoxia is a feature of all heterogenous solid tumours. Increased levels or subregions of tumour hypoxia are associated with an adverse clinical prognosis, particularly when this co-occurs with genomic instability. Experimental evidence points to the acquisition of DNA and chromosomal alterations in proliferating hypoxic cells secondary to inhibition of DNA repair pathways such as homologous recombination, base excision repair and mismatch repair.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!