Summary Induction of haem oxygenase-1 (HO-1) as well as nitric oxide (NO) biosynthesis during tumour growth was investigated in an experimental solid tumour model (AH136B hepatoma) in rats. An immunohistochemical study showed that the inducible isoform of NO synthase (iNOS) was localized in monocyte-derived macrophages, which infiltrated interstitial spaces of solid tumour, but not in the tumour cells. Excessive production of NO in the tumour tissue was unequivocally verified by electron spin resonance spectroscopy. Tumour growth was moderately suppressed by treatment with either N ω -nitro-L-arginine methyl ester (L-NAME) or S-methylisothiourea sulphate (SMT). In contrast, HO-1 was found only in tumour cells, not in macrophages, by in situ hybridization for HO-1 mRNA. HO-1 expression in AH136B cells in culture was strongly enhanced by an NO (NO + ) donor S-nitroso-N-acetyl penicillamine. HO-1 mRNA expression in the solid tumour in vivo decreased significantly after treatment with low doses of NOS inhibitors such as L-NAME and SMT (6-20 mg kg -1 ). However, the level of HO-1 mRNA in the solid tumour treated with higher doses of NOS inhibitor was similar to that of the solid tumour without NOS inhibitor treatment. Strong induction of HO-1 was also observed in solid tumours after occlusion or embolization of the tumour-feeding artery, indicating that ischaemic stress which may involve oxidative stress triggers HO-1 induction in the solid tumour. Lastly, it is of great importance that an HO inhibitor, zinc protoporphyrin IX injected intra-arterially to the solid tumour suppressed the tumour growth to a great extent. In conclusion, HO-1 expression in the solid tumour may confer resistance of tumour cells to hypoxic stress as well as to NO-mediated cytotoxicity.

Background We developed a new combined 99m Tcgalactosyl human serum albumin (GSA) scintigraphy single-photon emission computed tomography (SPECT)/CT system to evaluate the changes in functional liver volume with portal vein embolization (PVE). Methods We performed a prospective analysis of 25 patients treated with right PVE, and evaluated their functional liver volume perioperatively with a 99m Tc-GSA scintigraphy SPECT-CT fusion system. The percentage of the non-tumorous remnant liver volume (%LV) and the percentage of functional remnant liver volume (%FLV) were estimated by using the following calculations: (future remnant volume -tumor volume)/(total liver volumetumor volume) and functional future remnant liver volume/ functional total liver volume, respectively. Results Before PVE, the correlation was strongly significant between %LV and %FLV of the non-embolized liver, and the data were nearly equal (the regression coefficient was 1.005, P \ 0.0001). In contrast, after PVE, there was a significant correlation between %LV and %FLV (P \ 0.0001), but the regression coefficient was 1.192. The % LV increased significantly, from 38.1 to 52.0%, and the increment was 13.9% (P \ 0.0005). The %FLV was also increased significantly, from 36.6 to 58.0%, and the increment was 21.4% (P \ 0.0001). The increment was 7.5% greater for the %FLV compared to that of the %LV (P \ 0.001).Conclusions The 99m Tc-GSA scintigraphy SPECT-CT fusion system can estimate the correct functional liver volume and is useful in comparison with conventional CT volumetry.

LAT for HCCs (even those less than 3 cm in diameter) adjacent less than 5 mm to the main or sectional portal vein possibly promotes intrahepatic dissemination.

HR is proposed as the first-line treatment for patients with solitary small-sized HCC rather than RFA, especially for those with tumors in the range 2-3 cm.

Combined measurements of the serum bile acid level and splenic volume may be useful to noninvasively assess the PVP prior to further invasive procedures.

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Undifferentiated embryonal sarcoma of the liver (UESL) in adults, especially over 30 years old, is quite rare. We report two adult UESL patients that one of them survived 62 months and one is now surviving more than 65 months treated with repeated hepatic resections and radio-frequency ablations. Although UESL is an entirely unusual and aggressive tumor, multidisciplinary treatments including repeated hepatic resections and radio-frequency ablations may provide a longer survival.