Biomedical subjects

Yen-Hao Su

Publications and source records attributed to Yen-Hao Su.

5 recordsLinked to original sources

PubMed2006

Clinicopathological features and prognosis in resectable synchronous and metachronous colorectal liver metastasis.

INTRODUCTION: Hepatic resection may offer long-term survival for patients with colorectal metastases. However, controversies exist regarding the prognostic factors. Herein, the impact of synchronicity of liver metastasis on patient clinicopathological features and prognosis was evaluated. METHODS: One hundred and fifty-five patients who underwent hepatectomy for colon cancer metastasis, from 1995 to 2004, were enrolled in this study. Patients were divided into two groups: synchronous and metachronous colorectal liver metastasis. Patient demographics, the nature of the primary and metastatic tumors, surgery-related complications, and long-term outcome were analyzed. RESULTS: Patients included in the synchronous group tended to be younger than those in the metachronous group. Compared to the metachronous group, patients in the synchronous group showed more metastases (P = 0.008) and bilobarly distributed metastases (P = 0.016). Bile leakage was the most common surgical complication. The estimated 5-year disease-free and overall survival rates were 16.8 and 41.1%, respectively. Univariate analysis indicated that synchronous metastases, advanced stage of the primary tumor, bilobar distribution of the metastases, more than three metastases, and colonic versus rectal location of the primary tumor were prognostic factors of shorter disease-free survival, but not overall survival. Multivariate analysis revealed that synchronous metastases and the advanced stage of the primary tumor were indicators for a worse disease-free survival. CONCLUSION: The synchronous presence of primary colon cancer and liver metastasis may indicate a more disseminated disease status and is associated with a shorter disease-free survival than metachronous metastasis. These patients may need more careful monitoring and aggressive chemotherapy following curative resection.

Colorectal Neoplasms↗

PubMed2006

Pituitary abscess.

Pituitary abscess is a rare disease, but one with potentially high mortality and morbidity. We present a 46-year-old man with progressive visual disturbance and general malaise for 1 year. Endocrine studies revealed hypopituitarism, and magnetic resonance imaging revealed a pituitary lesion with suprasellar extension. We attempted to excise the lesion using a transsphenoidal approach, but pus in the pituitary fossa was found at operation, and no tumour was identified. The culture yielded coagulase-negative Staphylococcus. Antibiotics were administered for 3 weeks, and the patient made a good postoperative recovery. He required life-long hormone replacement therapy. After one and a half years of follow-up, he was well and had no evidence of focal or systemic infection. We review the literature regarding pituitary abscess and discuss the appropriate treatment and possible pathological mechanism.

Anti-Bacterial Agents↗

PubMed2005

Effects of irradiated tumor vaccine and infusion of granulocyte-macrophage colony-stimulating factor and interleukin-12 on established gliomas in rats.

PURPOSE: We investigated granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-12 (IL-12) infused into the injection site of irradiated tumor vaccine (TV) as therapy for gliomas. METHODS: Rats with subcutaneous RT-2 gliomas were treated with irradiated TV and/or subcutaneous infusion of GM-CSF and/or IL-12 via osmotic minipump 5 days after tumor-cell inoculation. Cytotoxic T lymphocyte (CTL) and natural killer (NK) cell activity were analyzed to investigate immune responses. Rats with intracerebral gliomas were treated with irradiated TV and infused GM-CSF/IL-12 3 days after tumor-cell inoculation. Tumor growth rates and animal survival were followed. Survivors were re-challenged with wild-type RT-2 cells subcutaneously or intracerebrally to study long-term anti-tumor immunity. RESULTS: Rats with subcutaneous gliomas treated with GM-CSF and IL-12 or TV plus GM-CSF or IL-12 did not have increased survival rate (P>0.2), but did have prolonged survival time (P<0.05); in contrast, rats treated with TV plus GM-CSF/IL-12 had increased survival rate (P<0.05) and prolonged survival time (P<0.05) compared with controls. These treatment strategies showed enhanced CTL and NK cell activities. Rats with intra-cerebral gliomas treated with TV plus GM-CSF/IL-12 did not have increased survival rate (P=0.11), but did have prolonged survival time (P<0.0001). Survivors in each group were re-challenged with wild-type RT-2 cells, and all had long-term survival. CONCLUSIONS: Irradiated TV plus continuous localized infusion of GM-CSF/IL-12 may induce a tumor-specific anti-tumor immune response on established subcutaneous or intra-cerebral gliomas, and such a treatment strategy deserves consideration as adjuvant treatment for glioma.

Animals↗

PubMed2004

Resveratrol suppresses the angiogenesis and tumor growth of gliomas in rats.

PURPOSE: We wanted to investigate the antitumor effects and effect on angiogenesis of resveratrol in rat RT-2 gliomas. EXPERIMENTAL DESIGN: RT-2 glioma cells were treated with resveratrol, and then cytotoxicity was assayed, apoptosis was measured by flow-activated cell sorter flow cytometry, and expression of vascular endothelial growth factor was measured by reverse transcription-PCR. Tumor size, animal survival time, and survival rate were followed in resveratrol-treated rats with s.c. or intracerebral gliomas. Furthermore, in vitro proliferation was assayed to explore the effect of resveratrol on the proliferation of ECV304 human umbilical vein endothelial cells. Expression of CD31 in resveratrol-treated gliomas was followed immunohistochemically to study the effect of resveratrol on the glioma-induced angiogenesis. RESULTS: Resveratrol was demonstrated to exert cytotoxic effects and induce glioma cell apoptosis in a concentration- and time-dependent manner (P < 0.05). Resveratrol (40 mg/kg/day) exerted significant antitumor effects on s.c. tumors, including slower tumor growth rate, longer animal survival time, and higher animal survival rate (P < 0.05). In contrast, resveratrol affected intracerebral tumors at only an increased dose (100 mg/kg/day), prolonging animal survival (P < 0.05) without affecting survival rate. The expression of vascular endothelial growth factor in the glioma cells and the proliferation of ECV304 cells were inhibited by resveratrol in a concentration-dependent manner. Immunohistochemical analyses showed that the s.c. gliomas from resveratrol-treated rats had fewer microvessel densities than did control rats (P < 0.01). CONCLUSIONS: Resveratrol caused significant glioma cell cytotoxicity and apoptosis, exerted antitumor effects on the s.c. and intracerebral gliomas, and inhibited angiogenesis in s.c. gliomas. Thus, resveratrol might be considered a possible treatment strategy for gliomas.

Angiogenesis Inhibitors↗

PubMedDate not supplied

Induction of apoptosis and cell cycle arrest in glioma cells by GL331 (a topoisomerase II inhibitor).

BACKGROUND: GL331 is a topoisomerase II inhibitor and, in this study, the effects of GL331 upon rat C6 glioma cells were investigated. MATERIALS AND METHODS: The glioma cells were treated with GL331, then a cytotoxicity assay was done to evaluate the cytotoxic effects of GL331 and flow-activated cell sorter analysis was performed to analyze the cellular apoptosis and cell cycle distribution of the glioma cells. The expressions of p53, p21 and 14-3-3sigma in glioma cells treated with GL331 were investigated by Western blot analysis. RESULTS: GL331 was demonstrated to exert cytotoxic effects upon and induce apoptosis of the C6 glioma cells in a concentration- and time-dependent manner (p < 0.05). GL331 also caused the glioma cells to accumulate in the G2/M-phase of the cell cycle and increased the expressions of p53, p21 and 14-3-3sigma. CONCLUSION: GL331 exerts cytotoxic effects and induces apoptosis in C6 glioma cells, accompanied by cell accumulation in the G2/M-phase and activation of p53, p21 and 14-3-3sigma.

14-3-3 Proteins↗