%0 Journal Article
%T Metastatic Renal Cell Carcinoma Change Vascularity
%A Takeshi Azuma
%A Yukihide Matayoshi
%A Yohsuke Sato
%A Yujiro Sato
%A Yasushi Nagase
%J Case Reports in Urology
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/654617
%X Several molecular targeted agents have been approved for clinical use for metastatic renal cell carcinoma (mRCC). A case of a 32-year-old woman with mRCC is presented. These tumors could change vascularity by administration of molecular agents. We could select a drug timely based on findings of computed tomography. To our knowledge, this is the first report that tumor¡¯s character change induced by molecular targeted agents can be detected and the efficacy of molecular targeted agents can be predicted. 1. Introduction Recently new molecular targeted agents were approved for metastatic renal cell carcinoma (mRCC) [1]. These agents are largely divided into two types. One is multitargeted tyrosine kinase inhibitor (TKI) that inhibits vascular endothelial growth factor receptor [2]. Another is an inhibitor of the mammalian target of rapamycin (mTOR) [3]. However, optimum use of these agents has not been defined for the maximum benefit yet. We report a case of mRCC, who received sequential therapy of sunitinib and temsirolimus as well as rechallenge of these drugs. We discuss the efficacy and the vascularity change of tumors. 2. Case Report A 32-year-old woman presented with acute abdominal pain and fever. She had undergone a right radical nephrectomy for pT2N0M0, Fuhrman¡¯s grade 2, clear cell renal cell carcinoma 4 months ago. Enhanced abdominal computed tomography (CT) revealed multiple hypovascular tumors in the liver. Laboratory findings were increased white blood cells count, as well as elevations of serum C-reactive protein and lactic dehydrogenase (LDH), which was consisted of subtype 1 and 2 (Figure 1). Because these laboratory data were similar to those at the diagnosis of primary RCC, we diagnosed multiple liver metastases of RCC. We started 50£¿mg sunitinib per day for 4 weeks followed by a 2-week rest period as a first line. Sunitinib is an oral TKI. Serum LDH level was 2500£¿U/L before sunitinib treatment, then transiently decreased to 694. However, it increased up to 8350£¿U/L again and CT confirmed progression after 3 months (Figure 2(a)). Sunitinib was stopped, and temsirolimus was administered at a dose of 25£¿mg per week as a second line. Temsirolimus is an inhibitor of mTOR. Two months after temsirolimus administration, serum LDH level decreased to 233£¿U/L and CT showed the shrinkage of tumor (Figure 2(b)). Five months after temsirolimus administration, serum LDH level increased to 2290£¿U/L again and strongly enhanced tumor¡¯s progression was confirmed (Figure 2(c)). We thought the tumor was switched from hypovascular to hypervascular tumor and
%U http://www.hindawi.com/journals/criu/2012/654617/