This treatment was complicated by acute renal failure and ifosfamide induced CNS toxicity. Adjuvant chemotherapy was therefore inhibitor Idelalisib altered for the third cycle to actinomycin D, cyclophosphamide, and etoposide. Inhibitors,Modulators,Libraries A CT abdomen and pelvis showed no evidence for recurrent disease. He was followed closely Inhibitors,Modulators,Libraries with serial CT scans along with serum tumor markers. In 2010 a new pulmonary nodule and rising serum tumor markers were de tected. He was then enrolled on the clinical study with su nitinib for chemotherapy refractory germ cell tumors in June 2010. He received sunitinib 50 mg orally for 4 weeks on and 2 weeks off cycle. By 09 20010 a decline in serum tumor markers was observed. His most significant response was in serum beta hCG with Inhibitors,Modulators,Libraries a more mild and fluctuating AFP response.

He developed hypothyroidism while on treatment with sunitinib, Inhibitors,Modulators,Libraries a documented side effect and began levothyroxine therapy with an appropriate response. He otherwise suffered no other treatment related G3 or 4 toxicity related to the sunitinib. Subsequent CT scans show a continued response to the treatment and has not revealed any new disease sites. He continued to be followed up with clinical and biochemical response with a very good performance status. Unfortunately, in November 2011, he experienced progressive weakness of his legs accompanied by saddle anesthesia, and urinary incontinence. MRI spines showed progressive disease involving the cauda equina and biopsy was consistent with metastatic GCT immunostain re sults were positive for cytokeratin, CD30, SALL4, and fo cally positive for Oct3 4.

He was taken off the study at that time, 17 months after starting sunitinib. Because of worsening performance status he elected to receive sup portive care and was referred to hospice care. This patient was enrolled on the unusual responder program at our institution, a program that applies ap propriate next generation Inhibitors,Modulators,Libraries sequencing and other genomic and proteomic technologies to tumor and germline sam ples from patients with exceptional responses to chemo therapies and targeted regimens in an attempt to identify potential genetic explanations for the outlier response. Next generation sequencing of unusual responder patient with testicular cancer indicated tumor harboring multiple copy number aberrations. Several genetic alter ations were identified in this patients tumor.

Of these, some of the variants identified represented potential can didates for further exploration to understand this patients response to sunitinib. The only alterations were found to have reported relevant information in tumors cells treated with sunitinib were RET amplification, PTEN loss, EGFR and KRAS amplification. We carried out an ex tensive literature search in National kinase inhibitor Imatinib Library of Medicines MEDLINE database on the five alterations and tabulated the levels of evidence significance of genes relevant to su nitinib based therapy.