Biomedical subjects

Toshiaki Watanabe

Publications and source records attributed to Toshiaki Watanabe.

129 records · Page 8Linked to original sources

PubMedDate not supplied

Exogenous expression of hRFI induces multidrug resistance through escape from apoptosis in colorectal cancer cells.

BACKGROUND: hRFI is a newly discovered gene encoding a Ring Finger domain highly homologous to that of the X-chromosome-linked inhibitor of apoptosis protein, which is among the most potent inhibitors of apoptosis. The hRFI protein is preferentially expressed in colorectal cancers, although its actual function is unknown. The aim of this study was to determine whether hRFI possesses an anti-apoptotic function in colorectal cancer cells against chemotherapeutic agents. MATERIALS AND METHODS: HCT116 colorectal cancer cells were exogenously transfected with hRFI or LacZ as a control. After exposure to either cisplatin, irinotecan or 5-fluorouracil, apoptosis and caspase-3 activity were evaluated by flow cytometry analysis. RESULTS: The hRFI transfectant exhibited significant resistance to apoptosis induced by each of the three agents, along with inactivation of caspase-3. Growth in the normal medium was not altered. CONCLUSION: hRFI plays an important role in the resistance to chemotherapeutic agent-induced apoptosis in colorectal cancer cells.

Apoptosis↗

PubMedDate not supplied

Absence of pretreatment markers that predict the emergence of YMDD mutants during lamivudine treatment--the results of a prospective multi-center study.

BACKGROUND/AIMS: The emergence of YMDD mutants in patients who are treated with lamivudine may determine the clinical prognosis. However, currently there are no clinical or virological factors that predict specifically the emergence of the mutants. METHODOLOGY: To define these factors, we analyzed 69 patients with chronic hepatitis B infection who were treated with lamivudine (LAM) and followed prospectively for at least 12 months. RESULTS: Of the 69 patients, 12 (17.4%) developed YMDD mutants up to 12 months after the start of LAM. The incidence of YMDD mutants was slightly higher in those who were younger, had higher HBV DNA titers, lower ALT levels, genotype C, and mutations in the core promoter before treatment. However, we could not find any significant factors that correlated with the appearance of the mutants. CONCLUSIONS: Currently, using conventional virological assays, it is difficult to predict the development of mutants before LAM treatment. Management of flare-ups of hepatitis, due to the appearance of mutants, should always be envisaged when LAM treatment is started.

Adult↗

PubMedDate not supplied

Telomerase subunit immunoreactivity and recurrence in colorectal cancer.

BACKGROUND/AIMS: Telomerase is expressed in human germ tissues and in the majority of primary human tumors. The catalytic subunit of telomerase, hTERT is one of the most important components of telomerase. In this study we attempted to show by means of immunohistochemistry the association between hTERT expression and recurrence in 128 colorectal cancer patients surgically treated in the University of Tokyo Hospital. METHODOLOGY: Immunostaining was performed in a conventional manner using a commercial monoclonal antibody. RESULTS: In our results, negative TERT immunoreactivity in the primary lesion was significantly associated with advanced tumor stage (p=0.0007), the presence of lymph node metastasis (p=0.00018) and recurrence (p<0.0001). Recurrence-free survival rate was significantly lower in patients with negative TERT immunoreactivity (p=0.0002). In the same way, if limited in patients without metastatic lymph nodes at surgery or in patients with T3 or T4 tumor, the recurrence-free survival rate was significantly lower in those with negative TERT immunoreactivity (p=0.019, p=0.016). CONCLUSIONS: Negative TERT immunoreactivity may be a novel indicator for poor prognosis of colorectal cancer patients and additional studies with a larger number of patients may lead to identifying patients at high risk for recurrence more accurately.

Adenocarcinoma↗