Bronchial asthma and cancer, particularly lung cancer, are global public health challenges. Although chronic inflammation in asthma is considered a potential procarcinogenic factor, epidemiological data on the association between these diseases remain contradictory. This review aims to systematize current data on the pathogenetic and epidemiological association of bronchial asthma with cancer. We critically analyzed data from modern prospective cohort studies, meta-analyses, and molecular biology research on the relationship between bronchial asthma and cancer risk. We paid special attention to methodological approaches, control for confounding factors, and the role of asthma phenotypes and disease control level. The review demonstrates the dual role of bronchial asthma in oncogenesis. On one hand, persistent uncontrolled inflammation, especially in the non-allergic (non-Th2) phenotype, is associated with an increased risk of lung cancer, most pronounced in patients with partially controlled asthma. On the other hand, the allergic (Th2) phenotype may exert a protective effect against several extrapulmonary tumors. A key modifiable risk factor is the level of asthma symptom control. Evidence indicates that baseline anti-inflammatory therapy (inhaled corticosteroids, leukotriene receptor antagonists) possesses potential anticarcinogenic properties. A pathogenetic link between bronchial asthma and cancer exists and is complex, determined by the type of inflammation and the degree of disease control. These findings justify the need for oncological vigilance in patients with uncontrolled asthma, especially those with asthma-COPD overlap syndrome, and for individualizing lung cancer screening approaches. Achieving complete asthma control is an important strategy not only for managing the respiratory disease but also for potentially preventing lung cancer.