Transcriptional inhibition of feline immunodeficiency virus by alpha-amanitin.

Alpha-amanitin, one of the amatoxins in egg amanita, has a cyclic peptide structure, and was reported as having antiviral activity against several viruses. We investigated whether α-amanitin has antiviral activity against feline immunodeficiency virus (FIV). FL-4 cells persistently infected with FIV Petaluma were cultured with α-amanitin.

Photodynamic hyperthermal chemotherapy with indocyanine green in feline vaccine-associated sarcoma.

The anticancer effects of photodynamic hyperthermal chemotherapy (PHCT), which consists of a combination of indocyanine green photodynamic hyperthermal therapy and local chemotherapy, have previously been reported. The present study investigated the effect of PHCT in six cases of feline vaccine-associated sarcoma (FVAS) following conservative surgical resection. No recurrence was observed in three out of six (50%) cases, while recurrence was observed in the remaining three cases.

Photodynamic hyperthermal chemotherapy with indocyanine green: a novel cancer therapy for 16 cases of malignant soft tissue sarcoma.

Sixteen cases of malignant soft tissue sarcoma (STS; 10 canines and six felines) were treated with a novel triple therapy that combined photodynamic therapy, hyperthermia using indocyanine green with a broadband light source, and local chemotherapy after surgical tumor resection. This triple therapy was called photodynamic hyperthermal chemotherapy (PHCT). In all cases, the surgical margin was insufficient.

Retrospective evaluation of sequential outpatient chemotherapy for advanced gastric cancer.

Background/aim: Due to the recent development of several promising chemotherapeutic agents, such as S-1, irinotecan (CPT-11) and paclitaxel, response rates for advanced gastric cancer to chemotherapy have improved. Thus far, however, the efficacy and survival benefits of sequential chemotherapy using these agents have not been evaluated. An additional benefit of outpatient sequential chemotherapy, that is, without hospitalization, would be its contribution to the maintenance of patients' social activities.

SIAH1 causes growth arrest and apoptosis in hepatoma cells through beta-catenin degradation-dependent and -independent mechanisms.

We have previously shown that expression of SIAH1 is frequently down-regulated in HCCs and associated with their advanced stages. It has been shown that SIAH1 functions in the phosphorylation-independent degradation of beta-catenin and induces apoptosis and growth arrest. To examine if the effects of SIAH1 overexpression depend on the altered beta-catenin signaling pathway, we transferred the SIAH1 gene into three hepatoma cell lines with different genetic backgrounds: HepG2 (mutant beta-catenin), SNU475 (mutant AXIN1), and Huh7 cells (wild type beta-catenin and AXIN1).

[Combined chemotherapy with oral leucovorin (LV) + tegafur/uracil (UFT) and hepatic arterial infusion (HAI) therapy for liver metastasis of colorectal cancer].

The liver is the most frequent metastatic site from colorectal cancer, and the control of liver metastasis is an important issue in the treatment of progressive colorectal cancer. Hepatic arterial infusion (HAI) therapy can achieve a high drug concentration in the liver and relatively low level in the systemic circulation because of the first pass effect of the drug metabolism. With the high response rate, several reports have failed to show a significant survival benefit of HAI monotherapy, partially due to its inability to control extrahepatic metastasis.

Suppression of VEGFR-3 signaling inhibits lymph node metastasis in gastric cancer.

In gastric cancer, lymph node metastasis is one of the major prognostic factors and forms the basis for surgical removal of local lymph nodes. Recently, several studies have demonstrated that overexpression of lymphangiogenic growth factor VEGF-C or VEGF-D induces tumor lymphangiogenesis and promotes lymphatic metastasis in mouse tumor models. We examined whether these processes could be inhibited in naturally metastatic tumors by blocking of their cognate receptor VEGFR-3 signaling pathway.