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Biomedical subjects

S Yazumi

Publications and source records attributed to S Yazumi.

15 recordsLinked to original sources
PubMed2005

Ischemic duodenitis.

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Arteriosclerosis Obliterans↗
PubMed2002

The possible involvement of micro-organisms other than Helicobacter pylori in the development of rectal MALT lymphoma in H. pylori-negative patients.

It remains unclear whether lymphoma of the mucosa-associated lymphoid tissue (MALT) in the extragastric organs is related to Helicobacter pylori infection or not. This report describes three patients with rectal MALT lymphoma negative for H. pylori infection, all of whom showed disease regression after being treated with antibiotics. One patient had MALT lymphoma in both the descending colon and the rectum; the other two patients had rectal disease only. None of the patients had chronic gastritis which was detectable either endoscopically or histologically and H. pylori infection was completely ruled out by various methods, including a urease breath test. These patients received antibiotic therapy. In all the patients, regression of MALT lymphoma was observed endoscopically and histologically, and polymerase chain reaction revealed that a previously observed rearranged band of immunoglobulin heavy chain had also disappeared after antibiotic treatment. These cases therefore suggest involvement of micro-organisms other than H. pylori in the development of rectal MALT lymphoma.

Adult↗
PubMed2002

Regression of fundic gland polyps following acquisition of Helicobacter pylori.

The prevalence of Helicobacter pylori infection is very low in patients with fundic gland polyps (FGPs) of the stomach. We report here two cases with multiple FGPs that regressed following new H pylori acquisition. Patient Nos I and II had multiple FGPs in normal fundic mucosa without inflammatory changes or atrophy. Both were not infected with H pylori. Following acquisition of H pylori infection however, all FGPs in both patients completely disappeared except for one FGP in patient No I. Although the size of the remaining polyp in patient No I was greatly reduced after H pylori acquisition, it became enlarged again after eradication. Interestingly, in the remaining polyp, we found an activating beta-catenin gene mutation whereas no such mutations were detected in FGPs of patient No II. Thus H pylori infection may have an inhibitory effect on the development of FGPs.

Adult↗
PubMed2000

Migration and differentiation of autoreactive B-1 cells induced by activated gamma/delta T cells in antierythrocyte immunoglobulin transgenic mice.

Using normal and transgenic (Tg) mice, we have shown that peritoneal B-1 cells are activated by administration of cytokines or lipopolysaccharide and migrate to other lymphoid organs where they differentiate into antibody-secreting cells. However, little is known about the process of B-1 cell migration and differentiation in vivo. We developed a mouse line by crossing the antierythrocyte antibody Tg mice (HL mice) with TCR-gamma/delta Tg mice specific for a self-thymus leukemia (TL) antigen in the recombination activating gene (RAG)2(-/-) background. In the presence of the self-antigen, Tg gamma/delta T cells increased in number and manifested activated phenotypes. Peritoneal B-1 cells in these mice migrated into mesenteric lymph nodes and differentiated into autoantibody-secreting cells, resulting in strong autoimmune hemolytic anemia. Furthermore, transfer of RAG2(-/-) x HL bone marrow or peritoneal cells into the peritoneal cavity of RAG2(-/-) x TCR-gamma/delta Tg mice gave rise to donor-derived B-1 cells in mesenteric lymph nodes, and these cells produced the autoantibody. Thus, this study demonstrates that the migration of B-1 cells and differentiation into the antibody-secreting cells can be induced by noncognate T cell help and implies the possibility that gamma/delta T cells may induce B-1 cell differentiation in vivo.

Anemia↗
PubMed2000

Abnormal expression of BRCA1 and BRCA1-interactive DNA-repair proteins in breast carcinomas.

Breast cancer is one of the most common malignancies among women. The molecular mechanisms involved in breast carcinogenesis, however, remain to be elucidated. Although somatic mutation of BRCA1 is rare, BRCA1 protein expression is reduced in about 30% of sporadic breast carcinomas (Yoshikawa et al., Clin. Cancer Res., 5:1249-1261, 1999), indicating its possible involvement even in sporadic breast carcinogenesis. Among the BRCA1-interactive proteins are hRAD51 (a human homologue of Escherichia coli rec A protein), BARD1 (BRCA1-associated RING domain 1) and p53, all of which are involved in DNA repair. We have analyzed the expression patterns of the hRAD51, BARD1 and p53 proteins in five breast cancer cell lines, including a BRCA1-deficient cell line, and in 179 breast cancer tissue samples from Japanese women, including 113 sporadic, 47 hereditary (i.e., BRCA1 status unknown), and 19 BRCA1-associated cases. Of the 179 breast carcinomas, fifty-four (30%) exhibited reduced hRAD51 expression, and sixty-two (35%) exhibited p53 overexpression. On the other hand, reduced expression level of BARD1, and of hMSH2 and hMLH1, which are components of DNA mismatch-repair pathway and are involved in colorectal carcinogenesis, was observed respectively in only 10 (6%), 8 (5%) and 3 (2%) cases. The overall frequency of sporadic breast carcinomas with abnormal expression of either BRCA1 or the BRCA1-interactive proteins was 67% (76/113). These results indicate that there may be an important role for the BRCA1-associated DNA-repair pathway, not only in BRCA1-associated breast carcinomas, but also in sporadic breast carcinomas.

Adaptor Proteins, Signal Transducing↗
PubMed2000

Activation of fibroblast-derived matrix metalloproteinase-2 by colon-cancer cells in non-contact Co-cultures.

Stromal fibroblasts interact with invading cancer cells by secreting and activating matrix metalloproteinases (MMPs). To elucidate the mechanisms involved in the expression and activation patterns of MMPs, human colon-cancer cell lines Caco-2 and LoVo and colon-fibroblast cell line CCD18-Co were co-cultivated in non-contact and contact conditions which mimic in vivo interaction between cancer cells and fibroblasts before and after cancer invasion respectively. Gelatin zymography disclosed that MMP-2 was secreted from the fibroblasts but not from the cancer cells. The quantity of fibroblast-derived MMP-2 in conditioned medium was not significantly changed in either the contact or the non-contact co-cultures when compared with that of individual cultures of CCD18-Co fibroblasts. Cancer cells in non-contact co-cultures, however, enhanced the activation of fibroblast-derived MMP-2. Transcripts of membrane-type matrix metalloproteinase-1 (MT1-MMP), which is thought to be present on the cell surface and to work as a candidate activator of MMP-2, were detected in both cancer cell lines. Plasma membrane extracts of cancer cells also activated MMP-2 in conditioned media in cell-free conditions. This activation of MMP-2 may be caused by MT1-MMP of the cancer cells, since it was inhibited by a series of MMP inhibitors, including ethylenediaminetetraacetic acid (EDTA), the tissue inhibitor of metalloproteinase-2 (TIMP-2), and the MMP inhibitor CGS 27023A, but not by TIMP-1. Our data demonstrate that in non-contact co-cultures colon-cancer cells activate fibroblast-derived MMP-2 on their plasma membranes. These findings should help to elucidate the mechanism involved in the initial destruction of basement membrane by cancer cells.

Basement Membrane↗
PubMed2000

Disrupted transforming growth factor-beta signaling and deregulated growth in human biliary tract cancer cells.

Biliary tract carcinoma is a common neoplasm in Japan, and its treatment is difficult because it tends to promote fibrosis and easily invades surrounding tissues. To better characterize the biological features of this carcinoma, we investigated abnormalities in the transforming growth factor-beta (TGF-beta) signaling pathway in five human biliary tract cancer cell lines: RBE, KMBC, SK-ChA-1, Mz-ChA-1, and Mz-ChA-2. We stably transfected into these cells the luciferase reporter plasmid carrying promoter of the plasminogen activator inhibitor-1 gene, the expression of which is stimulated by TGF-beta1. Treating the KMBC and Mz-ChA-1 cells with TGF-beta1 neither inhibited cell growth nor stimulated luciferase activity. In contrast, the RBE and Mz-ChA-2 cells responded well to TGF-beta1 treatment. TGF-beta1-treated SK-ChA-1 cells exhibited attenuated luciferase activity and their growth was not inhibited. Smad4 mRNA was not detected in SK-ChA-1 and Mz-ChA-1 cells by Northern blot analysis. Genetic analysis disclosed a nonsense mutation in the Mad homologue 2a domain of the Smad4 gene in the SK-ChA-1 cells and a heterozygous deletion in the TGF-beta type II receptor gene in the KMBC cells. Expression of the exogenous Smad4 gene in the Mz-ChA-1 cells by transient transfection restored their luciferase activity. When these TGF-beta1-insensitive and less-TGF-beta1-sensitive cell lines were xenografted into nude mice, they developed tumors that had more prominent, intervening fibrosis (desmoplasia) than the tumors caused by TGF-beta1-sensitive cells. Thus, a tight correlation between disruption of the TGF-beta signaling pathway and deregulated growth of cancer cells has been demonstrated in biliary tract carcinoma. This seems to be a critical event in this carcinoma and may also be correlated with stromal cell reaction in cancer invasion.

Animals↗
PubMed2000

Retinoblastoma protein-initiated cellular growth arrest overcomes the ability of cotransfected wild-type p53 to induce apoptosis.

The retinoblastoma gene, RB, participates in the regulation of the G1/S-phase transition and in p53-mediated apoptosis. We have previously reported that stably transfected RB functions as a growth and tumour suppressor in HTB9 human bladder carcinoma cells, which carry a mutation of the p53 gene at codon 280 and lack RB expression. To elucidate the potential role of RB in the regulation of p53-mediated apoptosis, we transfected a wt p53 expression plasmid under the control of the human cytomegalovirus promoter into parental and RB-transfected HTB9 cells. The p53(+)/RB(-)cells were susceptible to apoptosis under various experimental conditions: 1) incubation in serum-free culture for 72 h, 2) short-term (6 h) or long-term (48 h) exposure to etoposide, and 3) culturing in soft agar. In contrast, p53(+)/RB(+)cells were significantly resistant to apoptosis under similar conditions and exhibited efficient growth arrest, as measured by laser scanning cytometry. Tumorigenicity in nude mice of parental HTB9 cells was lost by exogenous expression of wt p53. Likewise, none of mice injected subcutaneously with either p53(-)/RB(+)or p53(+)/RB(+)cells developed tumours, indicating that RB allows suppression of tumorigenesis, regardless of p53 status. These results suggest that the growth-inhibitory function of RB may overcome the ability of wt p53 to induce apoptosis.

Animals↗
PubMed2000

A case of adenoma of the ampulla of Vater.

A case of adenoma of the ampulla of Vater is presented in a 48-year-old man who was admitted with epigastric pain. Gastroendoscopy revealed a sessile tumor about 3 cm in diameter at the ampulla of Vater, and the pathological diagnosis of a biopsy specimen was adenoma with moderate atypia. Because of the possibility of a malignant component, pylorus-preserving pancreatoduodenectomy was performed to avoid local recurrence. The final pathological diagnosis was adenoma with severe atypia.

Adenoma↗