Histological classification and markers
Morphological verification of the tumor is based on histogenesis and the immunohistochemical profile. There are two fundamentally different groups:
1. Small-cell lung cancer (SCLC) Characterized by pronounced neuroendocrine differentiation. Specific biomolecular markers play a role in pathogenesis: cellular oncogenes, tumor suppressor genes, and growth factors. Upon immunohistochemical examination, pancytokeratins are expressed in more than 90% of parenchymal cells. Chromogranin A serves as a specific marker, visualized as granules in the cytoplasm of cancer cells, which reliably confirms the neuroendocrine nature of the neoplasm.
2. Non-small-cell lung cancer (NSCLC) Represents a heterogeneous group of tumors of various histogenesis. Main types:
- Squamous cell carcinoma: cells synthesize keratohyalin; low-molecular-weight cytokeratins serve as markers.
- Adenocarcinoma: tumor cells are capable of producing mucus and surfactant, and express high-molecular-weight cytokeratins.
- Large cell carcinoma: often represented by poorly differentiated cellular variants.
For an accurate diagnosis, the pathologist must perform a thorough differential diagnosis between adenocarcinoma and poorly differentiated squamous cell carcinoma.
Central (hilar) cancer
Central cancer develops directly in large bronchi. The pathological process usually manifests against the background of prolonged chronic inflammation.
Histogenesis and precancer The source of malignant growth is bronchial epithelial cells: basal, goblet, or ciliated. This is preceded by precancerous changes—squamous cell metaplasia and dysplasia of the bronchial epithelium.
Morphology and growth Macroscopically, central cancer can have a polypoid, nodular, branching, or mixed (nodular-branching) form. Histologically, it is most often squamous cell carcinoma or small-cell carcinoma.
Complications The tumor is characterized by aggressive local growth. Obstruction of the bronchial lumen leads to pulmonary complications: the development of atelectasis and the formation of post-stenotic abscesses. Invasion involves the mediastinum, pericardium, esophagus, and vascular trunks. Ingrowth into large vessels is a critical condition as it provokes massive pulmonary hemorrhage.
For intravital diagnosis, bronchoscopy with biopsy, sputum cytology, and radiological methods are used.
Peripheral cancer and progression
Peripheral cancer is localized in the lung tissue, distal to the large bronchi.
Background and precancerous processes As with central cancer, chronic inflammation serves as the background, but here focal or diffuse sclerotic changes play a critical role. Precancerous processes include:
- Squamous cell metaplasia and epithelial dysplasia of small bronchi and bronchioles.
- Adenomatosis with pronounced cellular atypia.
- Atypical epithelial hyperplasia developing within oval and slit-like structures of scar tissue (formation of "scar carcinoma").
Macroscopically, nodular and nodular-branching growth forms predominate.
Progression A crucial pattern of pathological anatomy: despite the fact that the morphology of central and peripheral cancer differs in the early stages, the late stage of development for both types is massive lung cancer.
Briefly: answers to topical questions
What pathways and typical metastatic localizations are characteristic of lung cancer?
Lung cancer is characterized by lymphatic, hematogenous, and implantation pathways of metastasis.
- Lymphatic pathway is the first line of spread. The first metastases are found in regional lymph nodes of the lung root (bronchopulmonary, peribronchial), followed by involvement of bifurcation, paratracheal, mediastinal, and supraclavicular lymph nodes.
- Hematogenous pathway joins in the late stages. Typical target organs: liver, bones, brain, adrenal glands, and the contralateral lung.
- Implantation pathway is dissemination along serous membranes with the development of pleural, pericardial, and peritoneal carcinomatosis.
What specific immunohistochemical markers are determined in lung adenocarcinoma?
Lung adenocarcinoma reveals high-molecular-weight cytokeratins, mucus, surfactant, and other markers.
What paraneoplastic syndromes does small-cell lung cancer cause?
Sources indicate that small-cell lung cancer can produce ACTH, while bronchogenic carcinoma can produce ACTH, a parathyroid hormone-like peptide, insulin, and glucagon. Ectopic ACTH production is associated with Cushing's syndrome, and parathyroid hormone-like peptide production is associated with paraneoplastic hypercalcemia.
To memorize non-small-cell carcinoma markers: Squamous — Low-molecular-weight cytokeratins (S-L), Adenocarcinoma — High-molecular-weight cytokeratins (A-H).
Class and exam questions
How is the diagnosis of small-cell lung cancer confirmed?
Presence of signs of neuroendocrine differentiation. The main immunohistochemical marker is chromogranin A, which is detected as granules in the cell cytoplasm.
What is "scar carcinoma"?
This is a variant of peripheral lung cancer development. It arises against the background of focal or diffuse sclerosis from areas of atypical epithelial hyperplasia in oval and slit-like structures.
What complications are characteristic of central cancer?
Obstruction of the bronchial lumen leads to atelectasis and post-stenotic abscesses. Tumor invasion into large vessels can cause profuse pulmonary hemorrhage.
What else to study on this topic
- Molecular genetic markers of small-cell carcinoma (oncogenes, tumor suppressor genes, growth factors).
- Differential diagnosis of adenocarcinoma and poorly differentiated squamous cell carcinoma.
- Mechanisms of post-stenotic abscess formation during bronchial obstruction.
- Features of central cancer invasion into mediastinal organs and the pericardium.
- Sputum cytology: criteria for cellular malignancy.
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