Since stroke is often associated with cancer, acute stroke patients with cancer undergoing endovascular therapy (EVT) are not uncommon. Reportedly, the proportion of such cases is approximately 6%–7% of all stroke EVT cases. Ischemic stroke in patients with active cancer (cancer-associated stroke) includes not only strokes caused by cancer-related hypercoagulability but also coincident strokes due to common etiologies, strokes associated with tumor emboli, direct tumor invasion of blood vessels, and strokes associated with cancer therapy. Stroke caused by cancer-related hypercoagulability itself encompasses various entities, including paradoxical embolism, stroke due to nonbacterial thrombotic endocarditis, and in situ arterial occlusion due to disseminated intravascular coagulation or thrombotic microangiopathy. Thus, diverse mechanisms contribute to cancer-associated stroke, emphasizing the need to consider individualized treatment strategies for acute cases involving large vessel occlusion. Observational studies have shown that EVT for cancer-associated stroke results in poorer clinical outcomes, but with comparable rates of successful reperfusion and symptomatic intracranial hemorrhage when compared with stroke patients without cancer. This suggests that denying patients EVT solely on the basis of comorbid active cancer is inappropriate, and decision-making should be shared with the patients and their families, preferably through a multidisciplinary team approach. Thrombi retrieved from patients with stroke caused by cancer-related hypercoagulability have unique characteristics, being predominantly platelet rich and difficult to retrieve. Preprocedural imaging and serum biomarkers, including the hyperdense vessel sign on non-contrast CT, susceptibility vessel sign on T2* or susceptibility-weighted MRI, three-territory sign on MRI, and D-dimer levels, are valuable in evaluating the stroke subtype and thrombus features. Thrombectomy techniques, such as contact aspiration and stent retriever monotherapy, have shown varying degrees of effectiveness for stroke caused by cancer-related hypercoagulability, warranting further study. After reperfusion therapy, appropriate treatment for the prevention of stroke recurrence should be initiated, considering the specific stroke subtypes. In conclusion, cancer-associated stroke encompasses diverse subtypes, and thrombi associated with stroke caused by cancer-related hypercoagulability present various challenges for thrombectomy. Individualized treatment approaches based on underlying mechanisms are essential for improving outcomes in acute stroke patients with active cancer. Optimization of preprocedural diagnosis, EVT techniques, and secondary prevention of stroke caused by cancer-related hypercoagulability will lead to better management of these patients and enhance their quality of life.