Covariate analysis of minimal mean hepatic tolerance dose 6 weeks after BT (per protocol, n = 22).

<p>*Two-way ANOVA for categorical factors, ANCOVA for metric covariables.</p><p>Covariate analysis of minimal mean hepatic tolerance dose 6 weeks after BT (per protocol, n = 22).</p

Minimal mean hepatic tolerance dose (Gy) and evidence of detectable focal radiation-induced liver injury (fRILI) after BT, group comparison.

<p>Per protocol analysis (n = 22); Intention-to-treat analysis (n = 26) in square brackets.</p><p>Minimal mean hepatic tolerance dose (Gy) and evidence of detectable focal radiation-induced liver injury (fRILI) after BT, group comparison.</p

Patient characteristics (per protocol analysis).

<p>Continuous data: mean ± standard deviation, frequencies: counts or percent.</p><p>*Group comparison, continuous data compared by Mann-Whitney U test, frequency data compared by Pearson’s chi square test.</p><p>Patient characteristics (per protocol analysis).</p

Laboratory parameters at baseline and follow-up (per protocol analysis).

<p>*Between group comparison, Mann-Whitney U test;</p><p>**Comparison versus baseline (in brackets p-value of control group), Wilcoxon test.</p><p>Laboratory parameters at baseline and follow-up (per protocol analysis).</p

T1w-axial THRIVE 20 min after application of Gd-EOB-DTPA (A, C–E and G, H) and BT planning CT with dosimetry (B and F).

<p>A–D, control group. A: pre-treatment MRI displaying a metastasis scheduled for BT treatment (black arrow). B: Planning-CT after introduction of the brachytherapy catheters (black arrows). Clinical target volume (CTV) represented by bold red circle and dosimetry by coloured lines (red: 20 Gy-, blue: 12 Gy-isodose). C: MRI at 6 weeks showing substantial reduction in Gd-EOB-DTPA uptake by liver parenchyma adjacent to treated metastases (i.e. focal radiation-induced liver injury, fRILI). Note: The area of fRILI matches the geometry of the dosimetry (B). Determined threshold dose: 9.75 Gy. D: MRI at 3 months showing shrinkage of the fRILI. Determined threshold dose: 11.9 Gy. E–H, treatment group. E: pre-treatment MRI displaying two metastases (black arrow); two more treated lesions are not displayed in the plane. F: Planning-CT (annotations: see B). G: MRI at 6 weeks showing no fRILI. H: MRI at 3 months after radiotherapy (and 1 month after finishing study treatment) showing a substantial region of fRILI. Determined threshold dose: 15.8 Gy.</p

CONSORT-diagram.

<p>*Exclusion criterion age was initially disregarded by error in this patient (aged 82). **Exclusion criterion prior radiotherapy was initially disregarded by error in this patient (prior radiotherapy was performed 2 years earlier with location in the contralateral liver lobe).</p

Summary of published studies on drug treatments for the prevention of VOD/RILD.

<p>*Group comparison; LMWH: Low molecular weight heparin; BMT: Bone marrow transplantation; Max: Maximum; NS: Not significant; VOD: Veno-occlusive disease; RCT: Randomized controlled trial; UDCA: ursodeoxycholic acid (ursodiol); aPTT: activated Partial Thromboplastin Time.</p><p>Summary of published studies on drug treatments for the prevention of VOD/RILD.</p

Comparison of port duration between interventionally and surgically implanted devices

<p><b>Copyright information:</b></p><p>Taken from "Interventionally implanted port catheter systems for hepatic arterial infusion of chemotherapy in patients with colorectal liver metastases: A phase II-study and historical comparison with the surgical approach"</p><p>http://www.biomedcentral.com/1471-2407/7/69</p><p>BMC Cancer 2007;7():69-69.</p><p>Published online 24 Apr 2007</p><p>PMCID:PMC1871598.</p><p></p

DataSheet1_Sorafenib increases cytochrome P450 lipid metabolites in patient with hepatocellular carcinoma.PDF

Hepatocellular carcinoma (HCC) is a leading cause of cancer death, and medical treatment options are limited. The multikinase inhibitor sorafenib was the first approved drug widely used for systemic therapy in advanced HCC. Sorafenib might affect polyunsaturated fatty acids (PUFA)-derived epoxygenated metabolite levels, as it is also a potent inhibitor of the soluble epoxide hydrolase (sEH), which catalyzes the conversion of cytochrome-P450 (CYP)-derived epoxide metabolites derived from PUFA, such as omega-6 arachidonic acid (AA) and omega-3 docosahexaenoic acid (DHA), into their corresponding dihydroxy metabolites. Experimental studies with AA-derived epoxyeicosatrienoic acids (EETs) have shown that they can promote tumor growth and metastasis, while DHA-derived 19,20-epoxydocosapentaenoic acid (19,20-EDP) was shown to have anti-tumor activity in mice. In this study, we found a significant increase in EET levels in 43 HCC patients treated with sorafenib and a trend towards increased levels of DHA-derived 19,20-EDP. We demonstrate that the effect of sorafenib on CYP- metabolites led to an increase of 19,20-EDP and its dihydroxy metabolite, whereas DHA plasma levels decreased under sorafenib treatment. These data indicate that specific supplementation with DHA could be used to increase levels of the epoxy compound 19,20-EDP with potential anti-tumor activity in HCC patients receiving sorafenib therapy.</p