CMTTdb

An integrated database for cancer molecular targeted thearpies

Entry Detail


General information
Database:DB00375
Objective:Vascular endothelial growth factor (VEGF) and ckit are highly expressed in adenoid cystic carcinoma (ACC) and associated with biologic aggressiveness. This study aimed to assess the antitumor activity of sunitinib, a multitargeted inhibitor of vascular endothelial growth factor receptor, ckit, plateletderived growth factor receptor, ret protooncogene (RET) and FMSlike tyrosine kinase 3 (FLT3), in ACC of the salivary gland.
Authors:Chau NG, et al
Title:a phase II study of sunitinib in recurrent and/or metastatic adenoid cystic carcinoma (ACC) of the salivary glands: current progress and challenges in evaluating molecularly targeted agents in ACC.
Journal:Ann Oncol.
Year:2012
PMID:22080184
Trial Design
Clinical Trial Id:NCT00886132
Agent:sunitinib
Target:FL cytokine receptor
Mast/stem cell growth factor receptor
Vascular endothelial growth factor receptor 2
Plateletderived growth factor receptor
Cancer Type:advanced solid tumors
Cancer Subtype:ACC of major or minor salivary glands and recurrent and/ormetastatic disease deemed progressive and not amenable to surgery orcurative radiotherapy. recurrent and/ormetastatic adenoid cystic carcinoma (ACC) of thesalivary glands:
Therapy Type:mono
Therapeutic Combination Type:NA
Therapeutic Combination Content:NA
Study Type: singlearm, twostagephase II trial
Key Patients Feature:ligible patients were aged 18 years with histologically or cytologicallyconfirmed ACC of major or minor salivary glands and recurrent and/ormetastatic disease deemed progressive and not amenable to surgery orcurative radiotherapy. Progressive disease was defined as one of thefollowing occurring within 6 months of study entry: (i) at least a 20%increase in radiologically or clinically measurable disease, (ii) appearance ofnew lesions or (iii) deterioration in clinical status. Any number of priortherapies were allowed; however, patients must have completedchemotherapy, radiotherapy and major surgery at least 4 weeks beforeenrollment. Other key eligibility criteria included unidimensionallymeasurable disease according to RECIST [19], life expectancy over12 weeks, Eastern Cooperative Oncology Group performance status of zeroto two, cardiac ejection fraction within institutional range of normal, QTc<500 ms, leukocytes 3000/ml, absolute neutrophil count 1500/ml, platelets 100 000/ml, total bilirubin within normal institutional limits, aspartate aminotransferase and alanine aminotransferase ¡ê2.5 .institutional upper limit of normal, amylase and lipase within normalinstitutional limits, and serum creatinine within normal institutional limitsor creatinine clearance 60 ml/min/1.73 m2 for patients with creatininelevels above institutional normal.
Biomarker:NA
Biomark Analysis:NA
Control Group Info:single arm
Treatment Info:Patients with progressive, recurrent and/or metastatic ACC were treated with sunitinib 37.5 mg daily in this singlearm, twostagephase II trial. Response was assessed every 8 weeks.
Primary End Point:the objective response rate (complete and partial responses);
Secondary End Point:the duration of objective response; duration and rate of SD; PFS, median survival and OS rates; and safety and tolerability
Patients Number:14
Trial Results
DLT_MTD:NA
Objective Response Rate: Among 13 assessable patients, there were no objective responses, 11 patients had stable disease (SD), 8 patients had SD more than and equal to 6 months and 2 patients had progressive disease as best response.
Disease Control Rate:NA
Median Time to Progression:7.2 months(95% CI 2.2-9.0)
Median PFS A vs. C:NA
Median OS A vs. C:18.7months [95% confidence interval (CI) 9.8-28.3].
Adverse Event(agent arm):Toxic effectsoccurring in at least 50% of patients included fatigue, oral mucositis and hypophosphatemia usually of mild to moderate severity.
Conclusions:Although no responses were observed, sunitinib was well tolerated, with prolonged tumor stabilization of more than and equal to 6 months in 62% of assessable patients. The lack of responses is comparable with other trials of molecularly targeted agents in ACC and highlights the need for novel strategies inphase II clinical trial design.