Lung cancer is one of the most common leading causes of global mortality with a 5-year survival rate of less than 18%. There are approximately 1.6-1.8 million new cases of lung cancer on an annual basis followed by 1.4 million deaths each year. Up to 80% of lung cancer cases are due to non-small cell lung cancers (NSCLC) which have subtypes including squamous cell carcinoma, large cell carcinoma and adenocarcinoma, the most common subtype. The remaining cases of lung cancer are due to small cell lung cancer. Patients with NSCLC have poor survival outcomes primarily due to the challenges of early detection, high risk of metastasis and the development of resistance to multiple therapies. This has led to poor prognosis and therefore, a deeper understanding of the molecular mechanisms to improve therapies is essential to improve the survival rate and prognosis of this disease.
Over the years, there has been a continuous development in emerging therapies for the treatment of lung cancer, specifically using tyrosine kinase inhibitors. Epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) is currently understood to be the most significant treatment for NSCLC with EGFR mutations. There are currently three generations of approved EGFR TKIs known as first generation (gefitinib and erlotinib), second generation (afatinib), and third generation (osimertinib). However, these therapies may be associated with the development of drug resistance. Therefore, it is essential to better understand the genetic and nongenetic mechanisms associated with EGFR-TKI resistance in NSCLC and to use alternative therapies for an adequate treatment. Beyond EGFR mutations, it has been recommended the analysis of at least BRAF mutations, ALK and ROS1 gene fusions. Even in this setting of patients, the adoption of specific TKIs is associated with a significant improvement in clinical outcome. However, patients were later found to experience NSCLC progression due to drug resistance. Indeed, besides a diversity of genetic alterations associated with the (non) response to targeted therapies in NSCLC, it is increasingly recognized that tumor microenvironment may also shape specific tumor cell phenotypes prone to support long-term clinical relapse.
Treatment and therapies for lung cancer remain an emerging field which requires extensive research to develop effective therapies for lung cancer patients. The aim of this Research Topic is to explore the effects of anti-cancer drug therapies for lung cancer. Topics of interest include:
-Tyrosine kinase inhibitors for lung cancer and NSCLC
-Emerging drug therapies for lung cancer and NSCLC
-Effects of Sophoridine in the progression of lung tumors
-The effects of mutation on drug therapies
-Impact of drug resistance on lung cancer
-Molecular mechanisms supporting therapy resistance in lung cancer
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Lung cancer is one of the most common leading causes of global mortality with a 5-year survival rate of less than 18%. There are approximately 1.6-1.8 million new cases of lung cancer on an annual basis followed by 1.4 million deaths each year. Up to 80% of lung cancer cases are due to non-small cell lung cancers (NSCLC) which have subtypes including squamous cell carcinoma, large cell carcinoma and adenocarcinoma, the most common subtype. The remaining cases of lung cancer are due to small cell lung cancer. Patients with NSCLC have poor survival outcomes primarily due to the challenges of early detection, high risk of metastasis and the development of resistance to multiple therapies. This has led to poor prognosis and therefore, a deeper understanding of the molecular mechanisms to improve therapies is essential to improve the survival rate and prognosis of this disease.
Over the years, there has been a continuous development in emerging therapies for the treatment of lung cancer, specifically using tyrosine kinase inhibitors. Epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) is currently understood to be the most significant treatment for NSCLC with EGFR mutations. There are currently three generations of approved EGFR TKIs known as first generation (gefitinib and erlotinib), second generation (afatinib), and third generation (osimertinib). However, these therapies may be associated with the development of drug resistance. Therefore, it is essential to better understand the genetic and nongenetic mechanisms associated with EGFR-TKI resistance in NSCLC and to use alternative therapies for an adequate treatment. Beyond EGFR mutations, it has been recommended the analysis of at least BRAF mutations, ALK and ROS1 gene fusions. Even in this setting of patients, the adoption of specific TKIs is associated with a significant improvement in clinical outcome. However, patients were later found to experience NSCLC progression due to drug resistance. Indeed, besides a diversity of genetic alterations associated with the (non) response to targeted therapies in NSCLC, it is increasingly recognized that tumor microenvironment may also shape specific tumor cell phenotypes prone to support long-term clinical relapse.
Treatment and therapies for lung cancer remain an emerging field which requires extensive research to develop effective therapies for lung cancer patients. The aim of this Research Topic is to explore the effects of anti-cancer drug therapies for lung cancer. Topics of interest include:
-Tyrosine kinase inhibitors for lung cancer and NSCLC
-Emerging drug therapies for lung cancer and NSCLC
-Effects of Sophoridine in the progression of lung tumors
-The effects of mutation on drug therapies
-Impact of drug resistance on lung cancer
-Molecular mechanisms supporting therapy resistance in lung cancer
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.