Supplementary Figures 1 - 4, Table 1 from Real-Time Immune Monitoring to Guide Plasmid DNA Vaccination Schedule Targeting Prostatic Acid Phosphatase in Patients with Castration-Resistant Prostate Cancer

PDF file - 729KB, Supplementary Table 1: Adverse events. Supplementary Figure 1: Patient allocation. Supplementary Figure 2: DNA immunization elicits PAP-specific cellular immune responses. Supplementary Figure 3: Immune responses to PSA and tetanus evaluated by intracellular cytokine staining. Supplementary Figure 4: Immune responses to PAP, PSA and tetanus evaluated by cytokine secretion.</p

Supplemental Figure 2 from Clinical Trial Characteristics and Barriers to Participant Accrual: The MD Anderson Cancer Center Experience over 30 years, a Historical Foundation for Trial Improvement

Slow accruing national cooperative group trials with respect to submission year</p

Supplemental Figure Legend from Clinical Trial Characteristics and Barriers to Participant Accrual: The MD Anderson Cancer Center Experience over 30 years, a Historical Foundation for Trial Improvement

Figure legend for supplemental figures</p

Supplemental Figure 1 from Clinical Trial Characteristics and Barriers to Participant Accrual: The MD Anderson Cancer Center Experience over 30 years, a Historical Foundation for Trial Improvement

Trial Inclusion Diagram</p

Supplemental Table 1-2 from Clinical Trial Characteristics and Barriers to Participant Accrual: The MD Anderson Cancer Center Experience over 30 years, a Historical Foundation for Trial Improvement

Supplemental Tables 1-2</p

Supplementary Figure Legends, Table Legend from Real-Time Immune Monitoring to Guide Plasmid DNA Vaccination Schedule Targeting Prostatic Acid Phosphatase in Patients with Castration-Resistant Prostate Cancer

PDF file - 26KB</p

Supplementary Figure from Effects of Adjuvant Sorafenib and Sunitinib on Cardiac Function in Renal Cell Carcinoma Patients without Overt Metastases: Results from ASSURE, ECOG 2805

Supplementary Figure: Consort diagram of patients participating in cardiac sub study</p

Cyclopropane-Containing Polyamine Analogues Are Efficient Growth Inhibitors of a Human Prostate Tumor Xenograft in Nude Mice

Polyamine analogues 7, 10, 18, 27, and 32 containing cyclopropane rings were obtained by chemical synthesis. Their antineoplastic activities were assessed against the cultured human prostate tumor cell lines DU-145, DuPro, and PC-3. Decamines 32 and 27 exhibited variable levels of cytotoxicity against all three cell lines, while 7, 10, and 18 were efficacious against DU-145 and DuPro. Maximum tolerated doses (MTD) for all five compounds in a NCr-nu mouse model were determined at dosing schedules of q1d × 5 (ip) in two cycles with a break of 10 days between cycles. Their antitumor efficacies were then tested against DU-145 tumor xenografts in mice treated with all five agents at their respective MTDs. In addition, the efficacies of 7 and 10 against the same tumor xenograft were assessed at doses below their respective MTDs. In all experiments, administration began two weeks after tumor implantation. All compounds efficiently inhibited tumor growth for up to 50 days postimplantation, with negligible animal body weight loss. Tetramine 10 and hexamine 18 were the most efficient among the five analogues in arresting tumor growth. Tetramine 10 containing two cyclopropane rings had the lowest systemic toxicity as reflected in animal body weight loss. It was further assessed at a weekly administration regimen of (q1w × 4) in two cycles with a four-week break between the cycles. At this dosing schedule, 10 again efficiently arrested tumor growth with negligible effect on animal body weight. Tetramine 10 also arrested the growth of large tumors (ca. 2000 mm3) treated 66 days postimplantation. Studies on the metabolism of 10 showed that it accumulates in tumor within 6 h after the end of administration and reached a maximum level 72 h after cessation of dosing. Intracellular concentrations of 10 in liver and kidney were much smaller when compared to those in the tumor when measured 72 h after cessation of dosing. In liver and kidney, the deethyl metabolites of 10 accumulated over a 96 h period after cessation of dosing

Supplementary Tables 1-5, Figures 1-3 from Effects of Adjuvant Sorafenib and Sunitinib on Cardiac Function in Renal Cell Carcinoma Patients without Overt Metastases: Results from ASSURE, ECOG 2805

Supplementary Tables 1-5, Figures 1-3. Supplemental Table 1: Events per person-year of follow-up Supplemental Table 2: Event rates among patients randomized to sorafenib or sunitinib who started at reduced vs. full dose Supplemental Table 3a. Event rates among patients who did or did not discontinue treatment due to adverse events, and among patients with ECOG PS 0 vs. 1 Supplemental Table 3b: Baseline LVEF and change in LVEF among patients who did or did not discontinue treatment due to adverse events Supplemental Table 4: Relationship among treatment duration, baseline LVEF by MUGA, and probability of an event by any definition Supplemental Table 5: Relationship among treatment duration, baseline LVEF by MUGA, and probability of an event by the definition "Per Protocol Including Other" Supplemental Figure 1: Relationship among baseline LVEF by MUGA, treatment duration, and event status, where event is defined by any of the criteria Supplemental Figure 2: Relationship among baseline LVEF by MUGA, treatment duration, and event status, where event is defined as a decline in LVEF of 16% or more to below the lower limit of normal, or a grade 3 or higher cardiac adverse event Supplemental Figure 3: Algorithm for management of study drug-induced hypertension</p