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K Suto

Publications and source records attributed to K Suto.

At least 37 records · Page 2Linked to original sources
PubMed1998

Results of surgical treatments and prognostic factors for hepatic hilar bile duct cancer.

Results of surgical treatments for 57 patients who underwent resection for hepatic hilar bile duct cancer between 1984 and 1997 were studied. Bile duct resection was performed in eight patients, and combined resection of bile duct and liver was performed in 49 patients, of whom vascular reconstruction was added in 15 patients and pancreatoduodenectomy (PD) in six patients. All the operations of bile duct resection that were not combined with hepatectomy were non-curative. In the patients who underwent combined resection of the bile duct with liver, outcomes of the patients with well-differentiated adenocarcinoma were better than those with other lower-grade tumors. The factors related to the degree of tumor extension, such as serosal invasion, lymph node metastasis, lymphatic vessel invasion, perineural invasion, venous vessel invasion, and vascular involvement, were other factors which significantly influenced the survival. Curative resection yielded significantly better results than non-curative resection. Of all these variables, good tumor differentiation and vascular involvement were recognized as important prognostic factors by multivariate analysis. Most of the postoperative deaths were encountered in patients who underwent additional operations to hepatectomy, such as vascular reconstruction or PD. Improvement of surgical techniques and perioperative care has yielded better outcomes of vascular reconstruction. However, the application of hepatopancreatoduodenectomy should be limited due to poor outcomes of widespread bile duct cancer of which the histological grade is usually low. Whereas prognosis of bile duct cancer involving the hepatic hilus is mainly determined by the biologic characteristics of the tumor, surgeons should consider the fact that most patients die of local recurrence regardless of the biologic character of the tumor when curative resection is not performed.

Adenocarcinoma↗
PubMed1997

The effect of YNK-01 (an oral prodrug of cytarabine) on hepatocellular carcinoma.

Thirty-two patients with hepatocellular carcinoma (HCC) were treated with YNK-01, a prodrug of cytarabine for oral administration. A dose of 200 mg/d of YNK-01 was administered to 17 cases and 300 mg/d to 15 cases. One course was 2 weeks in duration, and this was repeated every 4 weeks for as long as the patients were able to tolerate it. There were five partial responses (15%) and 13 patients with no change (41%). A higher partial response rate was observed in the 300 mg/d group (27%) compared with the 200 mg/d group (6%). The average durations of partial response and no change were approximately 4 and 3 months, respectively. The main side effects of YNK-01 were anemia, leukopenia, thrombocytopenia, and symptoms of the alimentary tract (nausea, anorexia, diarrhea, etc). These results suggest that YNK-01 is a potentially useful oral agent for chemotherapy of hepatocellular carcinoma.

Administration, Oral↗
PubMed1994

Cdc25A is a novel phosphatase functioning early in the cell cycle.

The cdc25+ tyrosine phosphatase is a key mitotic inducer of the fission yeast Schizosaccharomyces pombe, controlling the timing of the initiation of mitosis. Mammals contain at least three cdc25+ homologues called cdc25A, cdc25B and cdc25C. In this study we investigate the biological function of cdc25A. Although very potent in rescuing the S.pombe cdc25 mutant, cdc25A is less structurally related to the S.pombe enzyme. Northern and Western blotting detection reveals that unlike cdc25B, cdc25C and cdc2, cdc25A is predominantly expressed in late G1. Moreover, immunodepletion of cdc25A in rat cells by microinjection of a specific antibody effectively blocks their cell cycle progression from G1 into the S phase, as determined by laser scanning single cell cytometry. These results indicate that cdc25A is not a mitotic regulator but a novel phosphatase that plays a crucial role in the start of the cell cycle. In view of its strong ability to activate cdc2 kinase and its specific expression in late G1, cdc2-related kinases functioning early in the cell cycle may be targets for this phosphatase.

Amino Acid Sequence↗
PubMed1991

Wee1(+)-like gene in human cells.

The wee1+ gene is a mitotic inhibitor controlling the G2 to M transition of the fission yeast Schizosaccharomyces pombe and encodes a protein kinase with both serine- and tyrosine-phosphorylating activities. We have cloned a human gene (WEE1Hu) similar to wee1+ by transcomplementation of a yeast mutant. WEE1Hu encodes a protein homologous to the S. pombe wee1+ and mik1+ (a functionally redundant sibling of wee1+) kinases and effectively rescues a wee1 mutation. We report here that overexpression of WEE1Hu in fission yeast generates very elongated cells as a result of inhibition of the G2-M transition in the cell cycle. In addition, we detected a 3-kilobase-long WEE1Hu messenger RNA in all the human cell lines we examined. We conclude that a wee1(+)-like gene exists and is expressed in human cells.

Amino Acid Sequence↗
PubMed1991

An additional homolog of the fission yeast cdc25+ gene occurs in humans and is highly expressed in some cancer cells.

The gene cdc25+ is a mitotic inducer controlling transition from the G2 to the M phase of the cell cycle in the fission yeast, Schizosaccharomyces pombe. Using phenotypic complementation of a mutant of S. pombe, we have cloned a human homolog (CDC25Hu2) of the cdc25+ gene that differs markedly in structure from CDC25 (referred to here as CDC25Hu1), the first such homolog to be isolated. The carboxyl-terminal region of p63CDC25Hu2 shares significant sequence similarity with cdc25 protein homologs from other eukaryotes and possesses full complementation activity. CDC25Hu2 is expressed in human cell lines 10 to 100 times more than CDC25Hu1, and its expression is particularly high in some cancers, including SV40-transformed fibroblasts. Whereas CDC25Hu1 is predominantly expressed in G2, CDC25Hu2 is expressed throughout the cell cycle with a moderate increase in G2. Thus, at least two homologs of the cdc25 gene exist and are both expressed in human cells. The implications of CDC25Hu2 overexpression in some cancer cells are discussed.

Amino Acid Sequence↗
PubMed1991

Mammalian G2 regulatory genes and their possible involvement in genetic instability in cancer cells.

In the fission yeast Schizosaccharomyces pombe, mitosis is initiated following the activation of the cdc2+/cyclin B kinase. The cdc2+/cyclin B kinase is positively regulated by cdc25+ tyrosine phosphatase and negatively regulated by wee1+/mik1+ tyrosine kinases. This regulatory system is evolutionarily conserved throughout higher eukaryotes. Drosophila and humans contain a cdc25+ gene homolog called String and CDC25Hs (hereafter referred to as CDC25Hul), respectively. We recently cloned a wee1+ homolog (WEE1Hu) and two additional cdc25+ homologs (CDC25Hu2 and CDC25Hu3) from human cells. Consequently, human cells contain at least one wee1+ and three cdc25+ homologs. Both CDC25Hu1 and CDC25Hu2 resemble the cdc25+ gene not only in structure and function but also in the mode of expression. They are expressed mostly in G2. On the other hand, CDC25Hu3 is expressed mostly in early S, indicating that it has some novel function in the early phase of the cell cycle. In all the cell lines examined, CDC25Hu2 is expressed to a greater extent than CDC25Hu1 or CDC25Hu3. The expression of CDC25Hu2 is particularly high in various cancer cells including those transformed by SV40 or human papilloma virus type 16 E6, E7, both of which are well known for their ability to induce genomic instability. In addition, there is a noticeable correlation between the extent of aneuploidy and the level of CDC25Hu2 expression in the cancer cells examined. In view of the fact that overexpression of cdc25+ under certain conditions induces genomic instability in the fission yeast, overexpression of CDC25Hu2 associated with many cancer cells might play at least a role in the induction of their chromosomal abnormalities.

Amino Acid Sequence↗