Lung Cancer
Malignant transformation of bronchial or alveolar epithelial cells, overwhelmingly driven by cumulative carcinogen exposure (chiefly smoking), produces a locally growing mass that can obstruct airways, invade neighbouring structures or spread distantly, so the clinical picture is dictated by exactly where the tumour sits and what it presses on.
First principles
Cancer arises from accumulated genetic damage in exposed epithelium
Repeated exposure to inhaled carcinogens, above all tobacco smoke, causes cumulative DNA damage in the bronchial epithelium lining the airways it constantly contacts. Over years, mutations accumulate in genes controlling cell division and apoptosis until a clone of cells escapes normal growth control. Because the epithelium exposed is the airway lining, most lung cancers arise centrally in or near a bronchus (particularly squamous and small cell types, strongly smoking-linked), while adenocarcinoma more often arises peripherally and is now the most common subtype even in never-smokers, reflecting a somewhat different, less exposure-dependent pathway.
Educational content pending clinical review. Not medical advice.