Chronic hepatitis B virus (HBV) infection remains a major challenge in oncology because systemic anticancer treatment may trigger HBV reactivation (HBVr). This narrative review summarizes current knowledge on the incidence, mechanisms, risk factors and prevention of HBVr in patients receiving chemotherapy or other immunosuppressive regimens. HBVr occurs in approximately 20-50% of HBV-infected patients treated with cytostatics, with the highest risk in hematological malignancies and during anti-CD20 antibody therapy or allogeneic hematopoietic stem cell transplantation. Clinically, HBVr ranges from asymptomatic alanine aminotransferase flares to fulminant liver failure, causes treatment disruption in up to two-thirds of affected patients, and is associated with mortality of about 5%, rising to nearly 30% in hepatocellular carcinoma. The pathophysiology of HBVr involves persistence of intranuclear cccDNA, loss of T- and B-cell immune surveillance and direct pro-replicative effects of selected drugs, including strong glucocorticosteroids, TNF-α antagonists, anthracyclines, tyrosine kinase inhibitors and CAR-T-cell therapies. We compare key recommendations from European guidance (EASL) and Polish national recommendations regarding screening strategies, HBVr risk stratification, and indications for nucleos(t)ide analogue prophylaxis. Effective prevention of HBV reactivation starts with pre-treatment screening, followed by antiviral prophylaxis with high resistance barrier agents or structured virological surveillance in carefully selected clinical scenarios with feasible, reliable monitoring.