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Biomedical subjects

Sakan Maeda

Publications and source records attributed to Sakan Maeda.

12 recordsLinked to original sources
PubMed2003

Adenocarcinoma arising in a tubular duplication of the jejunum.

To our knowledge, only five cases of malignant changes in small-bowel duplication have been reported previously in the English-language literature, and these were found only in ileal duplications. We describe a unique case of adenocarcinoma arising in a tubular duplication of the jejunum; this is the oldest patients in whom malignant tumor of alimentary tract duplication has been reported. A 73-year-old man was admitted to our hospital because of lower abdominal pain. Computed tomography (CT) and ultrasonography showed two abdominal masses; one, about 5 cm in size, was observed in the upper abdomen, the superior mesenteric artery (SMA) and the other, which was a well-demarcated heterogeneous mass, was revealed in the lower abdomen. Laparotomy revealed the mass in the upper abdomen involved the SMA and transverse colon, while the mass in the lower abdomen was of white globular form, ping-pong ball size, in the jejunal serosa approximately 40 cm on the anal side from Treiz's ligament. Transverse colostomy and a partial jejunectomy were performed, and the tumor was resected. Histologically, the diagnosis was adenocarcinoma arising in a tubular duplication of the jejunum. The patient died of necrosis and perforation of the intestine due to obstruction of the SMA 7 months after the surgery. Autopsy revealed that the upper abdominal mass consisted of metastatic foci associated with the lymph node of the SMA.

Adenocarcinoma↗
PubMed2003

MeCP2 and promoter methylation cooperatively regulate E-cadherin gene expression in colorectal carcinoma.

Reduced expression of E-cadherin (E-cad) owing to aberrant 5'CpG island hypermethylation has been regarded as one of the main molecular events involved in the dysfunction of the cell-cell adhesion system. The molecular mechanisms providing diversity and heterogeneity of E-cad expression in colorectal carcinoma were explored. In 29 cases of colorectal carcinoma in Indonesia, the expression of E-cad was analyzed by immunohistochemical staining, the methylation status of the E-cad promoter was determined by methylation-specific PCR, and the expression of methyl-CpG-binding protein (MeCP) 2 was studied by in situ hybridization. E-cad expression was strong, and no methylation was observed in normal colon mucosa and most of the well-differentiated adenocarcinoma. In contrast, both signet-ring cell carcinoma and mucinous adenocarcinoma showed fully methylated patterns and strong MeCP2 expression. In moderately- and poorly-differentiated adenocarcinomas, however, E-cad expression was rather heterogeneous, especially at the front of invasion and in the dissociated areas, where loss of MeCP2 expression correlated with E-cad reexpression even in the presence of E-cad promoter methylation. We conclude that both CpG methylation of the E-cad promoter and significant MeCP2 expression cooperatively and epigenetically regulate E-cad expression in colorectal cancer.

Adenocarcinoma↗
PubMed2003

Decrease in vitamin D receptor and calcium-sensing receptor in highly proliferative parathyroid adenomas.

OBJECTIVE: A significant decrease in vitamin D receptor (VDR) and calcium-sensing receptor (CaSR) protein expression has been demonstrated recently in parathyroid (PT) adenomas. In this study, we investigated the relationships between the proliferative activity of parathyroid glands (PTGs) and the expression of VDR as well as CaSR, and compared it with the clinical severity in patients with primary hyperparathyroidism (1 degrees HPT). DESIGN: Seven patients with 1 degrees HPT were included in this study. Four patients with thyroid carcinoma served as controls. METHODS: Immunohistochemical staining was performed on serial sections of PTGs with specific antibodies against CaSR, VDR, and Ki67. Areas examined in each section were selected at random in relation to the gland size. The number of Ki67-positive cells was expressed as a labeling index (LI; positive cells per 1000 PT cells). The expression of CaSR and VDR was semi-quantitatively analyzed based on the intensity of staining. After averages of the scores from all areas were calculated, CaSR and VDR scores, and Ki67 LI were assigned to each gland for use in statistical analyses. RESULTS: In PT adenomas, scores of VDR and CaSR were markedly lower than in normal PTGs (P<0.01), while the proportion of Ki67-positive cells in PT adenomas was significantly higher than in normal PTGs (P<0.01). Single regression analyses revealed that Ki67 LI was positively correlated with serum levels of intact parathyroid hormone and Ca, and PTG weight (R=0.70, P<0.05, R=0.78, P<0.01 and R=0.84, P<0.05 respectively). Ki67 LI was negatively correlated with CaSR and VDR scores (R=-0.78, P<0.01 and R=-0.72, P<0.05 respectively). Moreover, there was a strong positive relationship between CaSR and VDR expression (R=0.95, P<0.001). CONCLUSIONS: Marked decreases in VDR and CaSR expression could, at least in part, be responsible for the high proliferation of PT cells and the pathological progression of 1 degree HPT.

Adenoma↗
PubMed2002

RANK ligand, RANK, and OPG expression in type II collagen-induced arthritis mouse.

Rheumatoid arthritis (RA) is a systemic disorder characterized by synovial inflammation and subsequent destruction and deformity of synovial joints. The articular lesions start with synovitis, focal erosion of unmineralized cartilage, and then culminate in the destruction of subarticular bone by pannus tissue. Periarticular osteopenia and systemic osteoporosis follow as late complications of RA. Osteoclasts, specialized cells that resorb bone, play a central role in developing these osteolytic lesions. To elucidate the mechanism of osteoclastogenesis and bone destruction in autoimmune arthritis, we investigated the expression of RANK ligand (RANKL), RANK, and osteoprotegerin (OPG) mRNA in a mouse type II collagen-induced arthritis (CIA) model by in situ hybridization. The results indicated that most of the TRAP-positive mono- and multinucleated cells in the inflamed and proliferating synovium and in the pannus were RANK-positive authentic osteoclasts and their precursors. In the inflamed synovium and pannus of the mouse CIA model, synovial fibroblastic cells around these RANK-positive cells were strongly positive for RANKL. Moreover, RANKL-positive osteoblasts on the endosteal bone surface, at a distance from the affected synovial joints, increased significantly in the mouse CIA model prior to periarticular osteopenia and systemic osteoporosis. These data indicated that the RANKL-RANK system plays an important role for osteoclastogenesis in both local and systemic osteolytic lesions in autoimmune arthritis, and can therefore be a good target for therapeutic intervention.

Animals↗
PubMed2002

7,12-DMBA-induced rat leukemia: a review with insights into future research.

7,12-Dimethylbenz[a]anthracene (DMBA) elicits leukemia in Long-Evans rats (LE). This leukemia is mostly erythroblastic and 30% of leukemias have total and partial trisomy of #2 chromosome and the rest have diploid karyotype. The common duplication site is in 2q26-q34 and N-ras gene is located in 2q34. 7,8,12-Trimethylbenz[a]anthracene (TMBA) also induces similar leukemias. These leukemias reveal a highly specific mutation of N-ras gene as in human leukemias. N-ras mutation is induced 48h after DMBA treatment. Wild type N-ras allele is frequently lost in diploid leukemias but not in trisomy type. Therefore, a gene dosage problem related to the mutant N-ras gene is involved in development of leukemia. Some secondary genetic rearrangements involving abl and H-ras are also observed in cultured leukemia cells. DMBA-induced chromosome aberrations as well as leukemia are enhanced by erythropoietin and blocked by Sudan III given prior to DMBA treatment. This leukemia will provide an important tool for chemical carcinogenesis and leukemia studies.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2002

Expression of parathyroid hormone-related protein (PTHrP) in multiple myeloma.

Multiple myeloma is a plasma cell neoplasia often associated with multiple skeletal lesions and hypercalcemia. Several cytokines, including interleukin (IL)-1, IL-6 and tumor necrosis factor-beta (TNF-beta), derived from myeloma cells are thought to accelerate osteoclastic bone resorption and cause hypercalcemia through a paracrine mechanism. We report on a case of a 69-year-old man with multiple myeloma associated with hypercalcemia and advanced osteolytic lesions. After bisphosphonate treatment and MP (melphalan and prednisolone) therapy, the patient's serum calcium level was successfully but transiently recovered to the normal range. Biochemical analysis showed a remarkable increase in serum parathyroid hormone-related protein (PTHrP; 3.7 pmol/L) and IL-6 (22.0 pg/mL). On the other hand, parathyroid hormone and 1alpha,25(OH)2 vitamin D3 were suppressed. By immunohistochemistry and in situ hybridization on aspiration-biopsied bone marrow clot sections, PTHrP mRNA and protein were detected in the cytoplasm of myeloma cells. The rate of PTHrP-positive myeloma cells was estimated to be at least one-third. Since PTHrP can, as an endocrine factor, systemically act on bone and kidney, hypercalcemia in this case might have been caused through both local osteolytic hypercalcemia and humoral hypercalcemia of malignancy mechanisms.

Aged↗
PubMed2002

Prognostic significance of S100A4 expression in gallbladder cancer.

The calcium-binding protein S100A4 has been characterized as a metastasis-inducing molecule, and regulates cell motility and invasiveness of cancer cells. In order to clarify the significance of the expression of S100A4 as a prognostic factor in gallbladder cancer, S100A4 expression in resected gallbladder cancers were examined using an immunohistochemical staining technique. The relationship between S100A4 expression and clinicopathological factors including prognosis were evaluated. Twenty-five of 60 cases (42%) demonstrated positive staining for S100A4. There was no statistically significant association between S100A4 and histological grade, T, N, M factor, presence of stone, or stage. Kaplan-Meier method showed the 5-year survival rate of the group staining positive for S100A4 (31.5%) to be statistically poorer than that of the group staining negative for S100A4 (78.2%). Also in T2 cases, the 5-year survival rate of the group staining positive for S100A4 (57.1%) was statistically poorer than that of the group staining negative for S100A4 (83.3%). On univariate analysis, positive staining for S100A4 was a significant prognostic factor, and the hazard ratio was 4.05. On multivariate analysis, positive staining for S100A4 is also a significant predictor of prognosis second to T factor. These results indicate that positive staining for S100A4 is useful in assessing the prognosis of patients with gallbladder cancer as well as TNM factors.

Aged↗
PubMedDate not supplied

Double cancer, cholangiocellular and hepatocellular carcinomas, in the cirrhotic liver.

A 70-year-old male patient presented with cirrhotic liver caused by hepatitis C virus and complicated with hepatocellular carcinoma. The carcinoma was effectively treated by transarterial chemoembolization, but cholangiocellular carcinoma occurred in a different segment of the liver and rapidly grew and metastasized systemically. He died 13 months after the first admission. Double cancer of the liver is uncommon, but it must be considered in the differential diagnosis of cases of hepatocellular carcinoma associated with chronic hepatitis or cirrhosis. Failure to note the occurrence of cholangiocellular carcinoma is thought to be a diagnostic pitfall in the follow-up studies of patients with hepatocellular carcinoma.

Aged↗
PubMedDate not supplied

Genetic analysis of xanthogranulomatous cholecystitis: precancerous lesion of gallbladder cancer?

Xanthogranulomatous Cholecystitis is a chronic inflammatory disease of the gallbladder, a variant of the chronic cholecystitis. As xanthogranulomatous cholecystitis is occasionally seen with carcinoma of the gallbladder, the association with cancer is a controversial issue. A focal type of xanthogranulomatous cholecystitis is found simultaneously with gastric cancer diagnosed preoperatively. The resected specimen was genetically studied. Polymerase chain reaction amplification, single-strand conformational polymorphism analysis for mutation of p53 showed no abnormality indicating that less association with cancer in which the mutation of p53 is often seen. Etiopathologic factors of xanthogranulomatous cholecystitis might have relation with cancer, but xanthogranulomatous cholecystitis itself may not be the direct cause for cancer.

Adenocarcinoma↗