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Biomedical subjects

S Takeda

Publications and source records attributed to S Takeda.

At least 955 records · Page 53Linked to original sources
PubMedDate not supplied

Merosin and congenital muscular dystrophy.

Merosin (also called as Laminin-2) is an isoform of laminin comprised of the alpha2, beta1 and gamma1 chains. In European populations, half of the patients with classical congenital muscular dystrophy have mutations of the LAMA2 gene (6q22-23) and present reduced or absence of laminin alpha2 chain. This form is generally referred to as merosin-deficient CMD. Merosin-deficient CMD is characterized by involvement of not only skeletal muscle but also central and peripheral nervous systems: Extensive brain white matter abnormalities are found by magnetic resonance imaging (MRI). However, most patients show no mental retardation. Recent case studies reported that some patients have several structural abnormalities such as abnormal cerebral cortical gyration, hypoplasia of cerebellum and pons, and dilation of ventricles. At present, functions of merosin related to muscle degeneration have not been fully elucidated. In addition, the mechanisms responsible for pathogenesis of diffuse brain white matter abnormalities remain to be determined. As mouse models for merosin-deficient CMD, three spontaneous mutants(dy, dy(2J), dy(PAS1)) and two mutants named dy(W) and dy(3K) by targeted gene disruption have been reported. These mice will help to elucidate the pathogenesis of merosin-deficient CMD and serve to develop therapy.

Animals↗
PubMedDate not supplied

Pathogenesis of hepatocellular carcinoma: a review from the viewpoint of molecular analysis.

Chronic liver inflammation and hepatic regeneration by infection with hepatitis B (HBV) or C virus (HBC) seem to be important risk factors for hepatocellular carcinoma (HCC). Regarding the hepatocarcinogenesis of HBV DNA integration, it has been variously hypothesized that mechanisms such as the alteration of host chromosomal DNA and transcriptional trans-acting activity of the X gene are activated. On the other hand, integration of HCV virus into chromosomal DNA has not been reported. It is suggested that HCV could replicate more efficiently in noncancerous than in cancerous tissues. Therefore, it might affect some oncogenes or cause an inactivation of tumor suppressor genes in the early stage of HCC. Genetic alterations such as a point mutation and loss of heterozygosity are considered to be late events occurring after tumorigenesis. Regeneration of liver cells through chronic hepatitis increases the incidence of genetic alterations in hepatic cells and/or HCCs in both HBV- and HCV-infected patients.

Carcinoma, Hepatocellular↗
PubMedDate not supplied

Clinical usefulness of CA-19-9 in pancreatic carcinoma.

Preoperative and postoperative serum levels of carbohydrate antigen-(CA)19-9 in 148 patients with carcinoma of the pancreas were studied. All 18 patients with carcinoma of the pancreas of Stage I, II, and III were resectable, and their pre-operative serum levels of CA-19-9 were under 1,344 U/ml. Pre-operative serum levels of CA-19-9 in patients with Stage IV ranged widely between 5 and 32,240 U/ml. The postoperative survival rate was significantly superior in patients (n = 15) whose CA-19-9 pre-operative serum levels were less than 2,000 U/ml compare to those (n = 64) whose levels were over that level. Fifteen resectable patients who showed serum levels of CA-19-9 over 2,000 U/ml pre-operatively died within 2 years postoperatively due to recurrence, especially by liver metastasis in spite of aggressive surgery. Intraoperative quick immunostaining of CA-19-9 and carcinoembryonic antigen (CEA) was useful to diagnose intrapancreatic carcinoma development on frozen sections of cut margin of the pancreas and also useful in abdominal washing cytology combined with conventional staining.

Adenocarcinoma↗
PubMedDate not supplied

Clinical application of K-ras oncogene mutations in pancreatic carcinoma: detection of micrometastases.

Pancreatic adenocarcinomas are known to have a high incidence of K-ras gene mutation. We summarize our efforts to detect micrometastases through a search for mutated K-ras oncogene in liver tissues, peritoneal washings, para-aortic lymph nodes, and perioperative peripheral blood. Two-stage polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) analysis were used to detect K-ras oncogene mutations at codon 12. Our results suggest that PCR/RFLP analysis is potentially highly sensitive for the detection of micrometastases in various tissues and might be of value in the diagnosis, treatment and follow-up of metastases in other organs with pancreatic adenocarcinoma.

Adenocarcinoma↗
PubMedDate not supplied

Gene therapy for pancreatic cancer.

It has been approximately 7 years since the introduction of gene therapy. Since conventional procedures such as surgery, chemotherapy, and radiotherapy have had limited therapeutic value for cancer patients, the evolution of gene therapy seems a promising alternative to many researchers and clinicians. Indeed, about half of all gene therapy treatments are administered to patients with cancer. However, there are relatively few studies of using gene therapy with pancreatic cancer. We will review the general concept of gene therapy for cancer and its accomplishments to date.

Genes, MDR↗