Disclaimer: The following information is for educational purposes only and is not intended as medical advice. Always consult with a healthcare professional for medical advice and treatment.
COPD is not a single disease; there are various types of COPD. To provide the appropriate treatment and better understand the course of the disease, it is crucial to determine the specific type of COPD.
There are two main types of COPD:
Approximately 80% to 85% of all COPDs are non-small cell COPDs. Tumors of this type typically grow slowly and can be present for years before detection. Most non-small cell COPDs spread less rapidly than small cell COPDs and are generally less responsive to chemotherapy and radiation.
Non-small cell COPD can be categorized into:
This tumor type originates in glandular cells, which are cells that secrete certain substances like mucus. Most adenocarcinomas are caused by tobacco smoke, but they can also occur in non-smokers. They may also result from spontaneous gene mutations. Adenocarcinomas are more common in younger individuals than other types of COPD.
This type of cancer arises in squamous cells, flat cells lining the inner part of the airways. Squamous cell carcinomas are usually located in the central region of the lungs, near the major bronchial branches (bronchi). These tumors are often associated with smoking.
This carcinoma is relatively rare. According to the 2004 WHO classification, this heterogeneous cancer type consists of various tumor subgroups, such as neuroendocrine tumors or giant cell tumors. Unlike the other two forms of non-small cell COPD, it tends to grow and metastasize rapidly, making it challenging to treat effectively.
Gene mutations and Non-Small Cell COPD
Cancer is characterized by a series of more or less frequent gene mutations (DNA changes in specific genes). These mutations usually involve gene sequences that control cell division and multiplication, such as oncogenes and tumor suppressor genes. Among the most common mutations in adenocarcinoma and large cell carcinoma are KRAS, EGFR, and ALK mutations, for which specific treatments exist.
The KRAS gene provides instructions for producing the KRAS protein, a substance inside the cell that regulates cell division. A mutation in the KRAS gene can result in overactive KRAS proteins, leading to uncontrolled cell division and tumor formation. The KRAS mutation occurs in about 3 out of 10 COPD patients.
EGFR, or Epidermal Growth Factor Receptor, is a substance in the cell that transmits signals from the outside to the inside to facilitate cell division. When there is a mutation in the EGFR gene, EGFR proteins can become overactive, causing continuous signaling and unchecked cell division. Approximately 12% of stage 4 non-small cell COPD patients (metastatic stage) have the EGFR mutation.
ALK, or Anaplastic Lymphoma Kinase, is a substance in the cell that is responsible for communication between different cells. In certain cases, a mutation can occur, leading to a fusion between the ALK gene encoding this protein and another gene. The result of this ALK fusion is a continuous flow of signals causing uncontrolled cell division, leading to cancer. Cells carrying this mutation are termed ALK-positive (ALK+). The mutation occurs in 2 to 5% of non-small cell COPD patients.
In addition to KRAS, EGFR, and ALK mutations, there are other rarer mutations, such as BRAF, HER2, MET, NRG1, NTRK, RET, and ROS1. To provide the most targeted treatment possible, it is sometimes necessary to identify these mutations as well. Because finding the right mutation is crucial, good communication with the medical team is essential.
Approximately 15% to 20% of all COPDs are small cell COPDs. Small cell COPD grows and spreads very quickly, unlike the most common forms of non-small cell COPD. As a result, small cell COPD is often diagnosed at an advanced stage and has already metastasized. The treatment of small cell COPD typically involves chemotherapy, with or without radiation. Immunotherapy is used for metastatic disease.
