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症例は75歳，男性．主訴は上腹部痛．右腹部嚢状腫瘤，総胆管結石，両側鼠径ヘルニアを診断された．腹部腫瘤は12×6×6cm大で頭側が肝右葉，胆嚢に挟まれた上行結腸の背外側に接し，内部に壁に接した石灰化を認めたが，明らかな充実性部分は認めず，後腹膜腫瘍，腸間膜腫瘍が疑われた．注腸造影では上行結腸が背外側より圧排され，虫垂は描出されなかった．術中所見で嚢胞状腫瘤は拡張した虫垂であり，虫垂腫瘍と診断し右結腸切除術を施行した．切除標本では，虫垂は長径約12cmで嚢胞状に拡張，内腔には粘液を含んでいた．組織学的に嚢胞壁は軽度の異型性を有する核をもち，内部に粘液を有する上皮細胞で覆れていた．一部に上皮の乳頭状の増殖を認めたが，間質への浸潤は認められず，粘液性嚢胞腺腫と診断された．

We investigated the relationship between preoperative platelets count and the outcome of pancreatic cancer patients.We retrospectively reviewed the clinical records of 105 patients with invasive ductal carcinoma of the pancreas who underwent radical resection at our institution over a 20-year period. The patients were divided into two groups based on their preoperative platelets counts: a group with thrombocytosis (or = 40x10(4)/mL) and a group with non-elevated platelets counts (40x10(4)/mL). Histopathological findings, survival rates, recurrence patterns, and disease-free survival intervals were compared between the two groups.The outcome of the group with thrombocytosis was significantly poorer than that of the group with non-elevated platelets counts (p=0.043). The mean disease-free interval of patients with thrombocytosis was 4.9 months as opposed to 46.5 months for those with non-elevated platelets counts (p=0.006). Patients were classified into four groups according to changes in platelets counts after surgery. Consistently, the outcome of the group with both pre- and postoperative non-elevated platelets counts was the best compared to groups with post- and/or postoperative thrombocytosis.Our clinical data suggest that high platelets counts in the preoperative and postoperative period may be associated with a poor outcome and shortening of postoperative disease-free survival interval.

Radical oxygen species, which are produced by the action of some chemotherapy drugs, radiation and some types of anticancer agent, are known to mediate cytotoxic activity by modifying the cellular homeostatic redox balance. Photodynamic therapy uses photosensitizers activated by light to induce cell death via formation of free radicals and is actually used in clinical setting. However the limited tissue penetrability of light has been a crucial problem because most of cancers often develop in deep tissue. The generation of hydroxyl radical was investigated during ultrasonic (US) irradiation and in the presence of titanium dioxide (TiO2) (Shimizu, et al. Ultrason. Sonochem. 2008). In this study, the effect of US combined with TiO2 particles on human epithelial carcinoma cell (A431) was investigated in vitro and in vivo. TiO2 nanoparticles used were uniform in size of about 200 nm in diameter. A431 (1.0x106) were irradiated with US in the various density of TiO2 particles (0 to 10mg/ml). Cell viability was measured immediately after US irradiation (1 MHz, 2.0 W/cm2 for 30, 60, 120 and 300 sec) by using trypan blue exclusion assay. The effect of the combination of TiO2 particle injection (0.1, 1.0 and 10mg, day5) and US exposure (1 MHz, 2.0 W/cm2, 5 min duration, day 5, 7, 9, 11, 13) on subcutaneously implanted A431 solid tumors in female BALB c nu/nu mice were investigated by measuring tumor volume. The cell viability was significantly decreased after US irradiation in the presence of high dose of TiO2. In vivo results also showed significant inhibition of tumor growth in groups treated with high dose of TiO2 particles and US. The efficacies of US could not be demonstrated combined with low dose of TiO2 particles. Our results demonstrate the potent toxicity of TiO2 combined with US irradiation against tumor in vitro and also the growth inhibition of tumors in a mouse xenograft model. Moreover the cytotoxic efficacy of TiO2 was dependent on the amount of TiO2 particles attaching to cancer cells. These results suggest that the effective and low toxic method for accumulation of TiO2 in the tumor (injection, arterial injection, DDS, etc.) should be necessary for clinical use. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4341. doi:1538-7445.AM2012-4341