Sequential therapy with sorafenib and sunitinib in renal cell carcinoma.

BACKGROUND: Sunitinib and sorafenib are small-molecule tyrosine kinase inhibitors (TKI) with antitumor activity in advanced renal cell carcinoma. A retrospective study was conducted to assess the response of renal cell carcinoma to sequential treatment with these two agents. METHODS: Tumor response was evaluated by using Response Evaluation Criteria In Solid Tumors (RECIST) criteria in patients failing first-line therapy with either sunitinib or sorafenib and subsequently receiving second-line therapy with the other TKI agent. RESULTS: Twenty-nine patients received sorafenib followed by sunitinib (Group A), and 20 patients received sunitinib followed by sorafenib (Group B). TKI drugs were terminated in 6 (12%) patients in Group A and 4 (8%) in Group B because of toxicity. Median duration of stable disease for Groups A and B was 20 and 9.5 weeks, respectively. Median time from starting first TKI to disease progression after second TKI (time to progression) in Groups A and B was 78 and 37 weeks, respectively. Multivariate analysis revealed that Group B had a shorter time to progression than Group A (risk ratio [RR] 3.0; P=.016). Median overall survival was 102 and 45 weeks in Groups A and B, respectively (P=.061). CONCLUSIONS: The longer duration of disease control in patients who received sorafenib followed by sunitinib warrants further investigation.

Thymic carcinoid responds to neoadjuvant therapy with sunitinib and octreotide: a case report.

Carcinoids are malignant neuroendocrine tumors consisting of a spectrum of neoplasms from low-grade typical carcinoid to high-grade small cell carcinoma. We report a case of atypical thymic carcinoid that responded to neoadjuvant therapy with octreotide and sunitinib, an oral multikinase inhibitor. After 3 weeks of treatment, tumor size significantly decreased to allow for a safe surgical resection with clear margins. We believe that further study of sunitinib and octreotide with the neoadjuvant intent of preparing tumors for resection is warranted as a strategy to improve curative management of neuroendocrine tumors.

Castleman disease.

PURPOSE OF REVIEW: Castleman disease was initially described over 50 years ago as a benign localized mass of lymph nodes found primarily in the mediastinum of asymptomatic patients. Subsequently, additional types were recognized that extend the spectrum of this heterogeneous group of diseases. Optimal standard therapies have not been established. Currently, most patients receive treatments derived from past experience with non-Hodgkin lymphoma that are not altogether satisfactory. RECENT FINDINGS: Advances in understanding the biological basis of Castleman disease have provided new targets for therapeutic exploitation. Recognition of the role of interleukin-6 in disease perpetuation has led to the use of an antihuman interleukin-6 receptor monoclonal antibody, tocilizumab. Rituximab, an anti-CD20 monoclonal antibody, targets CD20-positive B lymphocytes, a prominent component of this disorder. Human herpes virus-8 and angiogenesis, both involved in the pathogenesis of Castleman disease, may provide additional unique therapeutic opportunities. SUMMARY: Rational approaches to the treatment of Castleman disease have begun to have an impact on disease management; however, the role of these new agents remains to be established. As the complexity of Castleman disease is more fully understood, additional targets for new innovative therapies undoubtedly will be identified.