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Biomedical subjects

M Monden

Publications and source records attributed to M Monden.

At least 289 records · Page 16Linked to original sources
PubMed1996

Establishment of anaplastic thyroid carcinoma cell lines useful for analysis of chemosensitivity and carcinogenesis.

Anaplastic thyroid carcinoma (ATC) is usually associated with a poor prognosis, with most patients dying within a few months. The mechanism of its carcinogenesis is unclear, and its rapid growth and spread often prevent effective surgical therapy. Thus, chemotherapy is necessary. However, ATC is often resistant to anticancer drugs. Therefore, prediction of chemosensitivity is important in selecting appropriate treatment. In this study, after the establishment of three cell lines (K119, KOA2, and IAA) from patients with ATC, we analyzed them for abnormalities in certain oncogenes (myc, ras, ret, and c-erbB2) and the p53 tumor suppressor gene. Only one of three cell lines (KOA2) had a N-ras mutation [codon 61 CAA(Gln)-->CGA(Arg)] and a p53 gene mutation [exon 6 codon 192 Caa(Gln)-->TAG(stop)]. We also investigated their in vitro drug sensitivity and compared it with clinical chemosensitivity, retrospectively. In vitro drug sensitivity was determined using an adhesive tumor cell culture system. Only the K119 cells were sensitive to adriamycin and cisplatin in vitro. The other two were resistant to them in vitro. These results paralleled the clinical responses. We also evaluated the in vitro drug sensitivity of a poorly differentiated thyroid carcinoma cell line (SMP) and papillary thyroid carcinoma cell lines (NPA). None of the five cell lines expressed the multidrug resistance gene (mdr-1). In conclusion, we established ATC cell lines that are suitable models for characterizing the nature of multidrug resistance and carcinogenesis.

Aged↗
PubMed1996

Beta-catenin expression in human cancers.

Cell-cell adhesion in tissue is mainly regulated by homotypic interaction of cadherin molecules, which are anchored to the cytoskeleton via cytoplasmic proteins, including alpha- and beta-catenin. Although we previously demonstrated that alpha-catenin is crucial for cadherin function in vivo, little is known about the role of beta-catenin. We examined the expression of beta-catenin in human carcinoma samples along with normal tissue (esophagus, stomach, and colon) by immunostaining using our antibody for beta-catenin. Normal epithelium strongly expressed beta-catenin. However, beta-catenin expression was frequently reduced in primary tumors of the esophagus (10 of 15, 67%), stomach (9 of 19, 47%), and colon (11 of 22, 50%). From an immunoprecipitation study, we found that beta-catenin forms a complex with E-cadherin not only in the normal epithelium but also in cancerous tissues. In coexpression patterns of E-cadherin and beta-catenin, 43 (77%) of the 56 tumors showed a similar expression of both molecules, whereas the other 13 tumors (23%) showed positive staining for E-cadherin and reduced expression of beta-catenin. These findings suggest that beta-catenin forms a complex with E-cadherin in vivo and down-regulation of beta-catenin expression is associated with malignant transformation.

Adenocarcinoma↗
PubMed1996

A new technique for exposing Calot's triangle during laparoscopic surgery: usefulness of extracorporeal lifting of the round ligament and gallbladder.

We developed a maneuver for holding and lifting the intraperitoneal organs from the extracorporeal side using a new instrument, the leading bar, by which we could guide the tape or the thread to the outside of the abdomen. In the case of cholecystolithiasis with a thickened wall or a stone stuck in the neck, we lifted the round ligament and gallbladder for better exposure of Calot's triangle, using the tape or thread through the abdominal wall to the extracorporeal side, and then clamped them with Kocher's forceps. With this technique, a good view of Calot's triangle was maintained so that the surgeon could expose the cystic duct easily and safely using both hands.

Cholangiography↗
PubMed1996

[Locoregional injection of OK-432/fibrinogen/thrombin for unresectable metastatic liver tumors].

We performed the locoregional injection of OK-432/fibrinogen/thrombin to unresectable hepatic tumors metastasized from colorectal cancers, which were hardly controlled by arterial infusion chemotherapy. CEA was markedly decreased following this treatment, although abdominal CT did not show a significant reduction of tumor mass. This immuno-injection therapy may be a choice of treatment for metastatic liver tumors, refractory to treatment by conventional chemotherapy.

Antineoplastic Agents↗
PubMed1996

[A patient with HCC successfully treated by ethanol injection therapy with etoposide].

A patient with hepatocellular carcinoma (HCC) who underwent successfully percutaneous ethanol injection therapy (PEIT) with etoposide was reported. A 72-year-old Japanese man with positive HCV-Ab developed multiple tumors of HCC. He underwent transcatheter arterial embolization (TAE) four times and PEIT three times, but the growth of tumors (particularly, S8) could not be controlled by these modalities. Then, the mixture of etoposide (20 mg), ethanol (8.5 ml) and lipiodol (1.5 ml) was injected into S6 tumors. Consistent with the normalization of serum AFP level, CT scan revealed the marked remaining lipiodol in these tumors. PEIT with etoposide is the treatment of choice in patients with HCC refractory to treatment by conventional TAE or PEIT.

Aged↗
PubMed1996

[A patient with hepatocellular carcinoma originating from the caudate lobe, who underwent hepatectomy following microwave coagulation therapy].

Hepatocellular carcinoma (HCC) originating from the caudate lobe is rare (about 2%), and prognosis is poor due to difficulties in early diagnosis, transarterial chemoembolization (TAE), and surgical resection. Distant metastasis is also likely to develop. To prevent metastasis during surgical manipulations, we performed microwave coagulation therapy before caudate lobectomy in one patient. Although the efficacy of this procedure remains to be elucidated, the multidisciplinary treatment described in this study is essential for the improvement of prognosis in patients with HCC developing from caudate lobe.

Carcinoma, Hepatocellular↗
PubMed1996

[A patient with pancreatic acinar cell carcinoma, effectively treated by the infusion chemotherapy through hepatic artery using 5-FU, CDDP and MMC].

Chemotherapy for pancreatic acinar cell carcinoma has not been well studied. We report herein one patient, in whom arterial chemotherapy with 5-FU, CDDP and MMC was extremely effective. He underwent distal pancreatectomy associated with partial resection of transverse colon. Hepatic recurrence was detected by MRI 8 months after the surgery. 5-FU (250 mg/day), CDDP (20 mg/day), and MMC (10 mg) was injected through a catheter introduced into the proper hepatic artery. His tumor became hardly detectable by MRI, and he was discharged about 1 month after admission. 5-FU (250 mg) and CDDP (20 mg) were injected every two weeks, and recurrence was not observed for 5 months.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1996

[A patient with unresectable cancer of pancreas head, effectively treated by a local injection of the mixture of OK-432, fibrinogen and thrombin].

The effective treatment of unresectable pancreatic cancer remains to be elucidated. We report herein a patient who underwent a local injection of a mixture of OK-432, fibrinogen and thrombin. Tumor size and tumor markers significantly decreased following this procedure. Local injection therapy with OK-432, fibrinogen and thrombin may be a promising treatment for unresectable pancreatic cancer.

Adenocarcinoma↗
PubMed1996

[RB gene expression in gastrointestinal tract].

pRB, the retinoblastoma tumor suppressor gene product, regulates the cell cycle at G1/S transition negatively. Many cell cycle regulators modulate pRB function through its phosphorylation status. G1 cyclins (cyclin D, E)/cyclin-dependent kinases (cdk2, 4) inactivates pRB through its phosphorylation, while p21 (WAF1) and p16 inhibit cdks. In several kinds of cancer, Rb gene alteration or functional inactivation of pRB has been reported. In esophageal cancer, loss of heterozygosity of Rb gene and cyclin D gene amplification were frequently detected. But in gastric and colorectal cancer, Rb gene loss or deletion has been shown to be rare. In this study we investigated the expression of pRB, G1 cyclins, cdks and cdk-inhibitors in adenoma-carcinoma sequence of colorectum. And we compared the phosphorylation status of pRB in colorectal normal mucosa and cancer tissue. In adenoma only cyclin D and E were overexpressed but not cdks. In cancer in adenoma pRB and cdk2 were overexpressed with high frequency, and cdk4 overexpression was detected in advanced cancer. p16 overexpression was detected in almost all cancers, but in contrast p21 overexpression was rare event. Comparative study showed that pRB-positive cancer cells also expressed both cdc2/cdk2 and cyclin E. Densitometric analysis revealed that in advanced cancer pRB was hyperphosphorylated compared with normal mucosa. These results indicate that overexpression of cyclin D/cdk4 and cyclin E/cdk2 would phosphorylate pRB, and insufficient expression of p21 may accelerate pRB inactivation.

Cell Cycle↗
PubMed1996

[Cyclin D, CDK4 and p16 expression in colorectal cancer].

G1/S transition of cell cycle is regulated by G1 cyclins/cyclin-dependent kinases (CDKs) and their inhibitors. Cyclin D/CDK4 complex phosphorylates retinoblastoma gene product and p16 inhibits CDK4 in competition with cyclin D. Aberrant expression of these proteins may deregulate cell proliferation and moreover may lead to tumor formation and progression. In this study we examined the expression of cyclin D, CDK4 and p16 in adenoma-carcinoma sequence of colorectum. Immunohistochemical staining revealed that cyclin D was overexpressed in 55 of 66 (83%) adenomas, 8 of 8 (100%) carcinomas in adenoma (CIAs), 26 of 45 (58%) advanced carcinomas and even in hyperplastic mucosa. CDK4 was overexpressed in 0 of 52 (0%) adenomas, 0 of 14 (0%) CIAs and 39 of 45 (87%) advanced carcinomas, but not in hyperplastic mucosa. p16 was overexpressed in only 5 of 52 (10%) adenomas, 10 of 14 (71%) CIA and 59 of 60 (98%) advanced carcinomas, but not in hyperplastic mucosa. And comparative study of CDK4 and p16 showed that CDK4-positive cancer cells also expressed p16. Western blot analysis also revealed that primary regions of advanced colorectal cancer tissues showed 4.61, 3.30, 1.65 and 8.03-fold overexpression on the average in cyclin D1, cyclin D2, CDK4 and p16 respectively. These results indicate that both cyclin D and CDK4 may contribute to phosphorylation of pRB. p16 overexpression would be induced as a brake at G1/S transition through pRB phosphorylation by CDK4 overexpression in advanced colorectal carcinomas.

Adenoma↗
PubMed1996

Ex vivo evidence of platelet activating factor on ischemic liver injury.

Recently, platelet activating factor has attracted a lot of research interest due to its involvement in ischemia-reperfusion injury including ischemic liver injury. However, due to its propagating effect to cause systemic hypotension, the direct effect of platelet activating factor on the liver could not be demonstrated easily. In order to avoid the interference of other factors in vivo, ex vivo isolated rat liver perfusion system was applied in this study. Administration of platelet activating factor as high as 10(-7)M, which caused shock and death through intravenous injection, did not exacerbate ischemic injury of 30 or 60 mins ischemia with the perfusion model. These results show that platelet activating factor, unlike it dose in vivo, neither hurts hepatocyte nor exacerbates ischemic liver injury directly. It is suggested that the effect of platelet activating factor on ischemic liver injury may be operated through other factors, which are present with intact circulatory system and blood components, to exacerbate the ischemia-reperfusion injury on liver.

Animals↗
PubMed1996

[Endoscopic mucosal resection for early esophageal cancer].

'xcently, a new method of endoscopic mucosal resection (EMR) for early esophageal cancer has been developed with the advance of the endoscopic equipment. There are three methods for EMR, one is 2 channel method, the second is EMR using over-tube and the third is EMR using cap-fitted panendoscope. Using a new type of over-tube (EEMR-tube) for EMR, which was designed by Makuuchi, esophageal mucosal lesions can be resected easily and certainly. It is thought that the indication of EMR for early esophageal cancer is the lesion limited to the muscularis mucosae. Large ulcers by endoscopic mucosal resection will disappear without any stenotic change within two months. We think that EMR is a useful technique for the treatment of early esophageal cancer because of keeping quality of life of patients and capability of histological findings.

Endoscopy↗
PubMed1995

Expression of autocrine motility factor receptor in human esophageal squamous cell carcinoma.

Autocrine motility factor and its receptor (gp78) have been shown to play an important role in tumor cell migration, invasion and metastasis. We have detected gp78 expression in buffered-formalin-fixed, paraffin-embedded sections of esophageal squamous cell carcinomas using an anti-gp78 monoclonal antibody (MAb), 3F3A, and examined the relationship between gp78 expression and clinicopathological and prognostic factors. In 55 of 101 (54%) patients, gp78 was detected in the tumor cells. The frequency of gp78-positive expression was significantly associated with tumor size, infiltrative growth, depth of invasion and lymph node metastasis. The cumulative survival rate of patients with gp78 was significantly lower than that of patients without gp78. Our results suggest that autocrine motility factor receptor (gp78) expression could be a useful biomarker for malignancy grading and prognosis in patients with esophageal squamous cell carcinoma.

Adult↗