Treatment strategies for lung cancer based on a patient's specific genetic makeup
A groundbreaking 2020 study revealed a significant decrease in mortality rates among people with NSCLC, corresponding with the approval of targeted therapies [1]. These treatments, which have revolutionized the landscape of NSCLC treatment, hone in on specific genetic mutations that drive tumor growth.
Targeted therapies work by blocking the signals that encourage the growth and division of cancer cells, preventing cancer growth [2]. Monoclonal antibodies are a common form of targeted therapies that block specific targets on the outside of cancer cells. Angiogenesis inhibitors, another type of targeted therapy, block the growth of new blood vessels surrounding tumors, starving the tumors of nutrients.
The rate of treatment success for medications targeting the EGFR, ALK, ROS1, and BRAF gene mutations is within a promising range [1]. The use of such medications can almost double median overall survival. Drugs targeting BRAF gene mutations include dabrafenib (Tafinlar) and trametinib (Mekinist), while those targeting ALK gene mutations can shrink tumors in people with advanced lung cancer with an ALK genetic mutation.
Newly targetable therapies for KRAS G12C mutations, which occur in approximately 30% of adenocarcinomas, are an important emerging target with novel therapies now available in clinical trials, such as AMG 510 [1][5]. Additionally, drugs targeting ROS1 rearrangements, NTRK, MET, RET, and other less common alterations may also be targeted with specific inhibitors.
Researchers have identified several gene mutations associated with NSCLC, including TP53, EGFR, KRAS, ALK, ROS1, BRAF, MET, RET, and NTRK. Common genotype-targeted drug therapies for NSCLC include EGFR tyrosine kinase inhibitors (TKIs) such as gefitinib, erlotinib, afatinib, and osimertinib for EGFR mutations; ALK inhibitors like crizotinib, alectinib, ceritinib, and lorlatinib for ALK rearrangements; AMG 510 (sotorasib) for KRAS G12C mutations; crizotinib and entrectinib for ROS1 rearrangements; capmatinib (Tabrecta) and tepotinib (Tepmetko) for MET gene mutations; selpercatinib (Retevmo) and pralsetinib (Gavreto) for RET genetic mutations; and larotrectinib (Vitrakvi) and Rozlytrek for NTRK gene mutations.
Comprehensive genomic profiling (CGP) of NSCLC tumors increases the chances of identifying actionable mutations, thereby improving the likelihood of receiving genotype-targeted treatments during first-line therapy, without significantly increasing overall healthcare costs [3].
In clinical trials, doctors continue target therapy for participants until either their cancer progresses or the side effects from the medications become too great. As scientists continue to identify new targets and create new therapies in the rapidly growing field of targeted therapy for lung cancer, the future of personalized medicine for NSCLC looks promising.
References:
- Society for Immunotherapy of Cancer (SITC), American Association for Cancer Research (AACR), and American Society of Clinical Oncology (ASCO)
- American Cancer Society
- National Comprehensive Cancer Network
- Cancer Research UK
- FDA Approves First Drug for Rare Form of Lung Cancer
- FDA Approves First Treatment for ROS1-Positive Metastatic Non-Small Cell Lung Cancer
- FDA Approves First Targeted Therapy for KRAS G12C-Mutated Non-Small Cell Lung Cancer
- A groundbreaking study in 2020 revealed a decrease in mortality rates among people diagnosed with NSCLC, corresponding with the approval of targeted therapies, such as AMG 510 for KRAS G12C mutations.
- Researchers have identified several gene mutations associated with NSCLC, including EGFR, KRAS, ALK, ROS1, BRAF, MET, RET, and NTRK, for which targeted drug therapies are available, such as EGFR tyrosine kinase inhibitors (TKIs) and ALK inhibitors.
- Science has led to the development of numerous therapies and treatments for medical conditions like health-and-wellness, including angiogenesis inhibitors, monoclonal antibodies, and targeted therapies that hone in on specific genetic mutations driving tumor growth, such as BRAF or ROS1 gene mutations.
- In lung cancer, targeted therapies, like dabrafenib (Tafinlar) and trametinib (Mekinist) for BRAF gene mutations, work by blocking the signals that encourage the growth and division of cancer cells, preventing cancer growth.
- The use of targeted therapies has revolutionized the landscape of treatments for cancer, particularly NSCLC, as these therapies can almost double the median overall survival of patients.
