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Manoharan, S.,Palanimuthu, D.,Baskaran, N.,Silvan, S. Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.11
Apoptosis, also known as cell suicide or programmed cell death, removes unwanted and genetically damaged cells from the body. Evasion of apoptosis is one of the major characteristic features of rapidly proliferating tumor cells. Chemopreventive agents inhibit or suppress tumor formation through apoptotic induction in target tissues. The aim of the present study was to investigate the pro-apoptotic potential of lupeol during 7,12-dimethylbenz(a) anthracene (DMBA) induced hamster buccal pouch carcinogenesis. Topical application of 0.5% DMBA three times a week for 14 weeks in the buccal pouches of golden Syrian hamsters resulted in oral squamous cell carcinoma. The expression pattern of apoptotic markers was analyzed using immunohistochemistry (p53, Bcl-2, Bax) and ELISA reader (caspase 3 and 9). In the present study, 100% tumor formation with defects in apoptotic markerexpression pattern was noticed in hamsters treated with DMBA alone. Oral administration of lupeol at a dose of 50mg/kg bw completely prevented the formation oral tumors as well as decreased the expression p53 and Bcl-2, while increasing the expression of Bax and the activities of caspase 3 and 9. The present study thus indicated that lupeol might inhibit DMBA-induced oral tumor formation through its pro-apoptotic potential in golden Syrian hamsters.
Prabhakar, M. Manoj,Vasudevan, K.,Karthikeyan, S.,Baskaran, N.,Silvan, S.,Manoharan, S. Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.10
The present study was designed to explore the anti-cell proliferative efficacy of ferulic acid by analysing the expression pattern of cell proliferative markers, proliferating cellular nuclear antigen (PCNA) and cyclin D1, in the buccal mucosa of golden Syrian hamsters treated with 7,12-dimethylbenz(a)anthracene (DMBA). Oral squamous cell carcinomas developed in the buccal pouch of hamsters using topical application of 0.5% DMBA three times a week for 14 weeks. Immunohistochemical (PCNA) and RT-PCR (Cyclin D1) analysis revealed over expression of PCNA and cyclin D1 in the buccal mucosa of hamsters treated with DMBA alone (tumor bearing hamsters). Oral administration of ferulic acid at a dose of 40 mg/kg bw to hamsters treated with DMBA not only completely prevented the tumor formation but also down regulated the expression of PCNA and cyclin D1. The results of the present study thus suggests that ferulic acid might have inhibited tumor formation in the buccal mucosa of hamsters treated with DMBA through its anti-cell proliferative potential as evidenced by decreased expression of PCNA and cyclin D1.
Cheng, Ann-Lii,Kang, Yoon-Koo,Lin, Deng-Yn,Park, Joong-Won,Kudo, Masatoshi,Qin, Shukui,Chung, Hyun-Cheol,Song, Xiangqun,Xu, Jianming,Poggi, Guido,Omata, Masao,Pitman Lowenthal, Susan,Lanzalone, Silvan American Society for Clinical Oncology 2013 Journal of clinical oncology Vol.31 No.32
<P><B>Purpose</B></P><P>Open-label, phase III trial evaluating whether sunitinib was superior or equivalent to sorafenib in hepatocellular cancer.</P><P><B>Patients and Methods</B></P><P>Patients were stratified and randomly assigned to receive sunitinib 37.5 mg once per day or sorafenib 400 mg twice per day. Primary end point was overall survival (OS).</P><P><B>Results</B></P><P>Early trial termination occurred for futility and safety reasons. A total of 1,074 patients were randomly assigned to the study (sunitinib arm, n = 530; sorafenib arm, n = 544). For sunitinib and sorafenib, respectively, median OS was 7.9 versus 10.2 months (hazard ratio [HR], 1.30; one-sided <I>P</I> = .9990; two-sided <I>P</I> = .0014); median progression-free survival (PFS; 3.6 <I>v</I> 3.0 months; HR, 1.13; one-sided <I>P</I> = .8785; two-sided <I>P</I> = .2286) and time to progression (TTP; 4.1 <I>v</I> 3.8 months; HR, 1.13; one-sided <I>P</I> = .8312; two-sided <I>P</I> = .3082) were comparable. Median OS was similar among Asian (7.7 <I>v</I> 8.8 months; HR, 1.21; one-sided <I>P</I> = .9829) and hepatitis B–infected patients (7.6 <I>v</I> 8.0 months; HR, 1.10; one-sided <I>P</I> = .8286), but was shorter with sunitinib in hepatitis C–infected patients (9.2 <I>v</I> 17.6 months; HR, 1.52; one-sided <I>P</I> = .9835). Sunitinib was associated with more frequent and severe adverse events (AEs) than sorafenib. Common grade 3/4 AEs were thrombocytopenia (29.7%) and neutropenia (25.7%) for sunitinib; hand-foot syndrome (21.2%) for sorafenib. Discontinuations owing to AEs were similar (sunitinib, 13.3%; sorafenib, 12.7%).</P><P><B>Conclusion</B></P><P>OS with sunitinib was not superior or equivalent but was significantly inferior to sorafenib. OS was comparable in Asian and hepatitis B–infected patients. OS was superior in hepatitis C–infected patients who received sorafenib. Sunitinib-treated patients reported more frequent and severe toxicity.</P>