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Hitoshi Funahashi

Publications and source records attributed to Hitoshi Funahashi.

At least 19 recordsLinked to original sources
PubMed2006

The stem cell factor/c-kit receptor pathway enhances proliferation and invasion of pancreatic cancer cells.

BACKGROUND: The transmembrane protein c-kit is a receptor tyrosine kinase (KIT) and KIT is expressed in solid tumors and hematological malignancies such as gastrointestinal stromal tumor (GIST), small-cell lung cancer and chronic myelogenous leukemia (CML). KIT plays a critical role in cell proliferation and differentiation and represents a logical therapeutic target in GIST and CML. In pancreatic cancer, c-kit expression has been observed by immunohistochemical techniques. In this study, we examined the influence of c-kit expression on proliferation and invasion using five pancreatic cancer cell lines. In addition, the inhibitory effect of imatinib mesylate on stem cell factor (SCF)-induced proliferation and invasion was evaluated. Finally, we also analyzed KIT and SCF expression in pancreatic cancer tissues using immunohistochemistry and correlated the results with clinical features. RESULTS: RT-PCR revealed that two pancreatic cancer cell lines, PANC-1 and SW1990, expressed c-kit mRNA. By Western blot analysis, c-kit protein was also present in those lines. In KIT-positive pancreatic cancer cell lines, proliferation and invasion were significantly enhanced by addition of SCF. In contrast, SCF did not enhance proliferation and invasion in the three KIT-negative lines (BxPC-3, Capan-2 and MIA PaCa-2). 5 muM imatinib mesylate significantly inhibited SCF-enhanced proliferation to the same extent compared with the control. Similarly, SCF-enhanced invasive ability was significantly inhibited by 5 muM imatinib mesylate. KIT was expressed in 16 of 42 clinical specimens by immunohistochemistry, and KIT expression was significantly related to venous system invasion. Furthermore, patients expressing both KIT and SCF had a somewhat lower survival. CONCLUSION: Our results demonstrated that the SCF-KIT pathway enhanced the proliferation and invasiveness in KIT-positive pancreatic cancer cell lines and that the enhanced proliferation and invasion were inhibited by imatinib mesylate. We propose that inhibitors of c-kit tyrosine kinase receptor have the potential to slow the progression of KIT-positive pancreatic cancers.

Aged↗
PubMed2006

Malignant solitary fibrous tumor originating from the peritoneum and review of the literature.

BACKGROUND: Solitary fibrous tumor (SFT) is a rare neoplasm frequently involving the pleura. Benign and malignant forms of the tumor occur, the benign variant being three to four times more common than the malignant. CASE REPORT: We present herein a rare case of large malignant solitary fibrous tumor (SFT) originating from the peritoneum. An abdominal computed tomography scan revealed a well-defined solid tumor with mixed density. An abdominal ultrasonography (US) revealed a well-circumscribed solid tumor containing a partially cystic lesion. T1-weighted abdominal magnetic resonance imaging demonstrated a hypo- to isointensity, which was a hypo- to hyperintensity on T2-weighted images. Liposarcoma originating from the retroperitoneum was suggested, and the patient underwent a complete resection of the tumor as well as the left kidney because tumor invasion of the upper left kidney was suspected. Immunohistochemically, the spindle-shaped cells were positive for CD34, and the diagnosis was SFT originating from the peritoneum. At the 14-month follow-up evaluation, no recurrence or metastasis was detected. CONCLUSIONS: This case gave us some difficulty, and the correct diagnosis of the peritoneal mass was valuable. To diagnose the malignant potential of this type of tumor accurately may have value to direct the appropriate therapeutic operations after surgery and postoperative progress observation.

Adult↗
PubMed2006

Reactive lymphoid hyperplasia of the liver in a patient with colon cancer: report of two cases.

BACKGROUND: Reactive lymphoid hyperplasia (RLH) of the liver is very rarely reported, and we encountered two cases of RLH of the liver in a patient with colon cancer. CASE PRESENTATION: In the first case, a 77-year-old woman was admitted for the surgical removal of a ascending colon cancer. A hepatic tumor in the left lobe was concurrently revealed by computed tomography (CT), and magnetic resonance imaging (MRI). The appearance suggested liver metastasis. Right hemicolectomy and partial hepatectomy were performed. On histopathological examination, lymphoid follicles with germinal centers were seen in the tumor-like lesion, and remarkable lymphoid infiltration with germinal centers was seen in the portal area around the nodule. Immunohistochemical studies revealed polyclonality of infiltrating lymphocyte. Consequently, this nodular lesion was diagnosed as RLH of the liver. In the second case, a 64-year-old woman who had a radical right hemicolectomy for stage II ascending colon cancer 10 years ago was admitted with dysuria. A hepatic tumor in the left lobe was concurrently revealed by CT and MRI, suggesting hepatocellular carcinoma. A left lateral segmentectomy was performed. Microscopically, this lesion revealed the almost same findings as the first case, so this nodular lesion was diagnosed as RLH of the liver. CONCLUSION: Our two cases were the first report of RLH of the liver accompanying colon cancer. Because there are a very few cases, so it is not clear whether the malignancies were involved in the onset of RLH. But we believe that new factors involved in the onset mechanism of RLH may be identified by carefully monitoring the clinical course of our two patients.

Adenocarcinoma↗
PubMed2006

A new method for constructing an ileal J pouch without an enterotomy.

The conventional methods of making an ileal J pouch require an enterotomy to introduce a linear stapler. We devised a new surgical technique that removes any need for this enterotomy by using both circular and linear staplers. We applied this method to two patients who underwent a total colectomy for ulcerative colitis and succeeded in making a J pouch without difficulty. This procedure may represent an improved method of making a J pouch.

Colectomy↗
PubMed2006

Interleukin-1alpha enhances the aggressive behavior of pancreatic cancer cells by regulating the alpha6beta1-integrin and urokinase plasminogen activator receptor expression.

BACKGROUND: In human pancreatic cancer progression, the alpha6beta1-integrin is expressed on cancer cell surface during invasion and metastasis formation. In this study, we investigated whether interleukin (IL)-1alpha induces the alterations of integrin subunits and urokinase plasminogen activator/urokinase plasminogen activator receptor (uPA/uPAR) expression in pancreatic cancer cells. We hypothesize that the alterations of integrin subunits and uPA/uPAR expression make an important role in signaling pathways responsible for biological behavior of pancreatic cancer cells. RESULTS: IL-1alpha upregulated the expression of alpha6 and beta1 integrins without any alterations of alpha5 and alphav integrins expression. IL-1alpha also induced enhancement in the expression of uPA/uPAR in pancreatic cancer cells. IL-1alpha enhanced the proliferation, adhesion, and migration in pancreatic cancer cells, and IL-1alpha-induced alterations of uPA/uPAR expression correlated with the increased the migration of pancreatic cancer cells. Upregulation of alpha6 integrin subunit and uPA/uPAR correlated with the activation of Ras and downstream extracellular signal-regulated kinase (ERK) pathways. IL-1alpha-induced activation of Ras and downstream ERK can be inhibited by using inhibitory antibodies against alpha6 and beta1 integrin and uPAR, consistent with the inhibition of proliferation, adhesion and migration of pancreatic cancer cells. Immunohistochemical analysis demonstrated a significant association between strong expressions of alpha6 integrin with uPAR in pancreatic cancer specimens. Furthermore, the strong expression of alpha6 integrin and uPAR was found to be independent prognosticator in pancreatic cancer patients. CONCLUSION: Based on these findings, we conclude that IL-1alpha can induce selective upregulation of alpha6beta1-integrin and uPA/uPAR in pancreatic cancer cells and these changes may modulate the aggressive functions of pancreatic cancer.

Aged↗
PubMed2006

Limiting vein puncture to three needle passes in subclavian vein catheterization by the infraclavicular approach.

PURPOSE: With central venous catheterization, each additional vein puncture raises the risk of complications. We assessed the rate of failure and complications using a limiting rule whereby the number of needle passes for subclavian vein catheterization was restricted to three. METHODS: A prospective clinical trial was conducted between September 2001 and December 2003 in a university hospital surgical department. Two hundred and thirty-two adult patients were enrolled to undergo subclavian vein catheterization under non-emergency conditions. The patients were subjected to right subclavian vein catheterization by the infraclavicular approach. Vein puncture failure was defined as such if venipuncture was not accomplished after three attempts. Any arterial puncture was judged to be a failure immediately. RESULTS: Vein puncture failure occurred in nine patients (3.9%), and included two arterial punctures (0.9%). No other complications, such as pneumothorax, hemothorax, plexus lesion, mediastinal hematoma or bleeding, or air embolism, were observed. In multivariate analyses, a close to average body mass index (weight in kilograms divided by the square of the height in meters, odds ratio 0.74; 95% confidence interval 0.56-0.97; P = 0.028) was associated with a low risk of failure. CONCLUSION: Limiting the number of needle passes to three may therefore prevent mechanical complications. A low body mass index was predictive of vein puncture failure.

Aged↗
PubMed2005

Activation of focal adhesion kinase enhances the adhesion and invasion of pancreatic cancer cells via extracellular signal-regulated kinase-1/2 signaling pathway activation.

BACKGROUND: Interaction with integrin and focal adhesion kinase (FAK) regulates the cancer cell adhesion and invasion into extracellular matrix (ECM). In addition, phosphorylation of FAK correlates with the increase of cell motility and invasion. Adhesion and spreading of cancer cells on a variety of ECM proteins, including collagen type IV (Coll IV), leads to an increase in tyrosine phosphorylation and activation of FAK. In this study, we investigated the mechanism of activation of FAK and its downstream extracellular signal-regulated kinase (ERK)-1/2 signaling following stimulation by interleukin (IL)-1alpha and adhesion to ECM with subsequent enhancement of pancreatic cancer cell adhesion and invasion. RESULTS: In immunoblotting analysis, all three pancreatic cancer cell lines (AsPC-1, BxPC-3, and Capan-2) expressed the protein of FAK and beta1 integrin. Enhancement of FAK protein association with beta1 integrin when cells were plated on Coll IV was more increased by stimulation with IL-1alpha. Preincubation with anti-beta1 integrin antibody and FAK siRNA transfection inhibited the association of FAK with beta1 integrin of pancreatic cancer cells. FAK phosphorylation was observed by adhesion to Coll IV, furthermore, stronger FAK phosphorylation was observed by stimulation with IL-1alpha of pancreatic cancer cells adhered to Coll IV in time-dependent manner. Genistein, a tyrosine kinase inhibitor, markedly inhibited the FAK phosphorylation. IL-1alpha stimulation and Coll IV adhesion enhanced the activation of Ras, as evidenced by the increased Ras-GTP levels in pancreatic cancer cells. Activation of Ras correlated with the phosphorylation of ERK. While not statistical affecting the apoptosis of pancreatic cancer cells, IL-1alpha-induced adhesion and invasion on Coll IV were inhibited with FAK gene silencing by siRNA, beta1 integrin blocking, and inhibition of FAK phosphorylation. PD98059, a MEK inhibitor, also inhibited IL-1alpha-induced enhancement of adhesion and invasion in pancreatic cancer cells. CONCLUSION: Our results demonstrated that activation of FAK is involved with the aggressive capability in pancreatic cancer through Ras/ERK signaling pathway. Based on our results, we suggest that the modification of IL-1, FAK, and integrins functions might be a novel therapeutic approach to aggressive spread of pancreatic cancer.

Apoptosis↗
PubMed2005

Interleukin-1alpha enhances IL-8 secretion through p38 mitogen-activated protein kinase and reactive oxygen species signaling in human pancreatic cancer cells.

BACKGROUND: Interleukin (IL)-1alpha plays an important role in modulating the expression of various growth factors and angiogenic factors in tumor cells. In here, we investigated effect of IL-1alpha on IL-8 secretion in human pancreatic cancer cells and underlying signal transduction pathways. MATERIAL/METHODS: IL-8 expression and secretion by pancreatic cancer cells was measured by Western blot and enzyme-linked immunosorbent assay (ELISA), respectively. Activation of extracellular signal regulated kinases-1/2 (ERK-1/2), p38 mitogen-activated protein kinase (MAPK), c-jun aminoterminal kinase, Akt, and nuclear factor-kappaB (NF-kappaB) was determined by Western blot. Involvement of reactive oxygen species (ROS) were examined by measuring the H2O2. Activity of activator factor-1 (AP-1) and NF-kappaB was examined by electrophoretic mobility sift assay (EMSA). Proliferation of human umbilical vein endothelial cells (HUVECs) was determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide dye reduction method and cell count. RESULTS: IL-1alpha modulated IL-8 secretion and induced activation of ERK-1/2 and p38 MAPK. Specific inhibitors for MEK-1 and p38 MAPK suppressed IL-8 secretion. IL-1alpha also induced production of ROS. Exogenous H2O2 enhanced IL-8 secretion and N-acetyl cysteine (NAC) prevented IL-1alpha-induced ROS production and IL-8 secretion. EMSA confirmed that IL-1alpha increased DNA-binding activity of AP-1 and NF-kappaB. Inhibitors and ROS scavenger studies revealed that upstream signalings for AP-1 and NF-kappaB were MAPK and ROS, respectively. Conditioned media from pancreatic cancer cells pretreated with IL-1alpha remarkably stimulated in vitro HUVECs growth. CONCLUSIONS: These results suggest that MAPK/AP-1 and ROS/NF-kappaB signaling pathways are involved in IL-1alpha-induced IL-8 secretion and that these paracrine signaling pathways enhance endothelial cell proliferation.

Blotting, Western↗
PubMed2005

The role of glial cell line-derived neurotrophic factor (GDNF) and integrins for invasion and metastasis in human pancreatic cancer cells.

BACKGROUND AND OBJECTIVES: It is generally accepted that the malignancy of pancreatic cancer is dependent upon the extent of invasion as well as metastasis. However, the factors and mechanisms are incompletely understood. We investigated whether glial cell lined-derived neurotrophic factor (GDNF) enhances the invasive and adhesive behaviors of pancreatic cancer cells by altering of the expression of integrins. METHODS: The expression of the GDNF receptor in pancreatic cancer cell lines (SW1990 and Capan-2) was confirmed by RT-PCR. Then we determined the expression of integrin subunits and the alteration of their expression by GDNF using flow-cytometric analysis and a cellular enzyme-linked immunosorbent assay (CELISA). Adhesion and invasion assay were performed to investigate whether increased integrin expression affected the interaction between cancer cells and ECM proteins. RESULTS: The GDNF receptor subunits were expressed in pancreatic cancer cells. GDNF enhanced the expression of some of the integrin subunits and increased their adhesive and invasive abilities. The enhanced expression and associated increase in adhesive and invasive abilities were inhibited by blocking the GDNF receptor or the integrin beta1 subunit. CONCLUSION: The enhancement of integrin expression by GDNF signaling through the GDNF receptor strongly influences invasion and adhesion to ECM proteins by pancreatic cancer cells.

Cell Adhesion↗
PubMed2005

An anti-stray stylet for subclavian catheterization by the infraclavicular approach.

OBJECTIVE: Misplacement of subclavian vein catheters has been reported. We assessed the rate of misplacement of a subclavian vein catheter with and without a novel stylet. METHODS: A prospective, randomized, controlled clinical trial was conducted between September 2001 and June 2003 in a university hospital. Two hundred sixteen adult patients were enrolled to receive subclavian vein catheterization under non-emergency conditions. Patients were randomly assigned to undergo right subclavian vein catheterization with the stylet (n = 109, stylet group) or without the stylet (n = 107, control group). The rate of subclavian vein catheter misplacement was determined and risk factors for failure and complications were analyzed. RESULTS: There was no incidence of catheter misplacement in the stylet group, but this occurred in 12 patients in the control group in whom the catheter was misplaced into the ipsilateral internal jugular vein (0% versus 11.2%, P = 0.0003). In multivariate analyses, use of the stylet (odds ratio = 0.062, 95% confidence interval = 0.008 to 0.495, P = 0.009) and a close to average body mass index (odds ratio = 0.73, 95% confidence interval = 0.54 to 0.98, P = 0.038) were associated with low risks of complications and failure, respectively. CONCLUSIONS: This stylet is useful for decreasing the incidence of misplacement of subclavian vein catheters. Body mass index is predictive of failed vein puncture.

Aged↗
PubMed2005

Expression of glial cell line-derived neurotrophic factor family members and their receptors in pancreatic cancers.

BACKGROUND: The glial cell line-derived neurotrophic factor (GDNF) is a member of neurotrophic polypeptide family, which promotes survival and rescue of various neural cells in the central and peripheral nerve systems. We previously reported that GDNF promotes tumor cell invasion in pancreatic cancer cell lines. The purpose of this study was to investigate GDNF family expression and the status of related receptors in actual cancer tissues, and assess correlations with clinicopathologic behavior. METHODS: Immunohistochemical assessment of GDNF, neurturin, persephin, artemin, GDNF family receptor alpha-1 and alpha-2, and RET was performed for 51 cases of surgically resected pancreatic cancer. RESULTS: In all intrapancreatic nerves, GDNF and artermin were expressed strongly. In pancreatic cancer tissues. The expression of RET was stronger than that seen in normal ductal cells and was significantly related to the survival rate after resection (P = .026) and lymphatic invasion (P = .014). Intrapancreatic neural invasion was significantly related to the expression of GDNF (P = .047). CONCLUSIONS: We conclude that the expression of RET in pancreatic cancer tissues may be a useful prognostic marker and GDNF may play an important role in neural invasion.

Adult↗
PubMed2005

Anaplastic carcinoma of the pancreas with squamous features: report of a case and immunohistochemical study.

BACKGROUND: Anaplastic carcinomas of the pancreas are rare aggressive tumors with survival measurable in weeks. Many terms have been applied used to describe these tumors, and anaplastic foci are identified in ductal adenocarcinomas and in ectopic pancreata, but are not the dominant pattern of growth. We herein present our experience with a case of anaplastic carcinoma of the pancreas with squamous features in order that allowed us to delineate the clinicopathologic and immunohistochemical features of this rare entity. CASE REPORT: According to imaging findings, the 77-year-old Japanese man was diagnosed as the malignant pancreatic tumor, and underwent a surgical resection. Histopathologically, anaplastic tumor cells showed focal ductal and squamous features infiltrated into pancreatic parenchyma, extrapancreatic fatty tissue, and stomach. The tumor cells showed strong reactivity for cytokeratin, alpha-SMA, vimentin, NSE, and S-100 protein. Although immunoreactivity against p53 was negative, strong positive immunostaining for proliferating cell nuclear antigen and interleukin-1 receptor type I (IL-1RI) was observed in a the majority of tumor cells, while the alpha6 integrin subunit was predominantly strong expressed in the adenocarcinomatous lesion. The patient's postoperative course was uneventful and he was treated with a chemotherapy consisting of gemcitabine. After discharging from the hospital, he had subsequently been observed as an outpatient and same chemotherapy was followed by weekly. However, the patient suffered from peritonitis carcinomatosa and re-increases of multiple liver metastases, and he died in the fourteenth month after surgery. CONCLUSIONS: Our immunohistochemical studies suggested that the prognosis of the case with anaplastic carcinoma presented here would be poor, due to the strong expression of integrins and IL-1RI.

Aged↗
PubMed2004

Expression of integrins in intraductal papillary-mucinous tumors of the pancreas as an indicator of malignancy.

INTRODUCTION AND AIMS: Intraductal papillary-mucinous tumors (IPMTs) of the pancreas are intraductal tumors with diffuse or segmental dilation of the pancreatic ducts and intraductal papillary growth with abundant mucous secretion. We examined clinicopathological features and immunohistochemical findings to investigate the malignancy of IPMTs. METHODOLOGY: Between April 1994 and December 2002, 23 patients with IPMT underwent pancreatic resections at Nagoya City University Hospital, Japan. We immunohistochemically analyzed the expression of p53 protein, proliferating cell nuclear antigen, alpha6-integrin subunit, alpha5beta1 integrin, and interleukin-1 receptor type I in tumor specimens from the 23 patients with IPMT. RESULTS: The tumors were classified as intraductal papillary adenoma (n = 16), intraductal papillary adenocarcinoma and moderate dysplasia (n = 7). At a median follow-up of 42.9 months, 2 patients had died of this disease. The actuarial 5-year disease-free survival rate was 80.7%. Expression of the alpha6-integrin subunit was significantly strong in adenocarcinoma and moderate dysplasia tissues of IPMTs (P = 0.038). CONCLUSIONS: Our current results indicate that alpha6-containing integrin expression can be a significant marker of malignancy in IPMTs. We emphasize that immunohistochemical investigation of resected specimens is indispensable in cases of IPMT, so that appropriate postoperative treatments for malignant IPMTs are initiated to improve prognosis.

Adenocarcinoma, Mucinous↗
PubMed2004

Enhanced angiogenesis due to inflammatory cytokines from pancreatic cancer cell lines and relation to metastatic potential.

OBJECTIVES: To investigate the mechanisms of metastasis formation in human pancreatic carcinoma, we examined the angiogenic capabilities of human pancreatic cancer cell lines with different metastatic potentials and the roles of inflammatory cytokines. METHODS: Interleukin (IL)-8 secretion by human pancreatic cancer cells stimulated with IL-1alpha or IL-1 receptor antagonist (IL-1ra) was measured by enzyme-linked immunosorbent assay (ELISA). We then examined how cancer cells with different metastatic potentials influenced the proliferation and tube formation of human umbilical vein endothelial cells (HUVECs) using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide dye reduction method (MTT assay) and an angiogenesis assay, respectively. We also examined the role of inflammatory cytokines in relation to tumor metastatic potential and angiogenesis. RESULTS: IL-8 secretion levels by pancreatic cancer cells were regulated by IL-1alpha and correlated with metastatic potential. Both HUVEC proliferation and tube formation were strongly enhanced by coculture with metastatic pancreatic cancer cells and were enhanced to a similar extent by culture in the presence of IL-1alpha and IL-8. In contrast, blockade of IL-1alpha or IL-8 inhibited HUVEC proliferation and angiogenesis. CONCLUSIONS: The inflammatory cytokines IL-1alpha and IL-8 may have an important role in metastasis via vascular endothelial cell proliferation and angiogenesis.

Cell Division↗
PubMed2004

Glial cell line-derived neurotrophic factor enhances nuclear factor-kappaB activity and invasive potential in human pancreatic cancer cells.

OBJECTIVES: The invasive potential is increased by glial cell line-derived neurotrophic factor (GDNF) in human pancreatic cancer cell lines. We researched whether the signaling pathway activated by GDNF correlates with the nuclear factor-kappaB (NF-kappaB) in human pancreatic cancer cell lines and whether the inhibition of NF-kappaB activity is associated with suppression of invasive potential. METHODS: Proliferation of human pancreatic cancer cell lines (BxPC-3 and MIA PaCa-2) was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays (MTT assay). NF-kappaB activity was examined by dual luciferase assay and electrophoretic mobility shift assay. In addition, to investigate the invasive potential, an in vitro invasion assay was performed. RESULTS: Proliferation of both cell lines was decreased by a proteasome inhibitor, MG132, in a dose-dependent manner, but proliferation of control and IkappaBalphaM vector-transfected BxPC-3 cells was similar. The invasion cell number and the NF-kappaB activity were increased by GDNF stimulation. However, in the presence of MG132 or IkappaBalphaM, which blocks the nuclear localization of NF-kappaB, both were significantly suppressed. Furthermore, reduced activity of both remained unchanged by GDNF stimulation. CONCLUSION: These results indicate that GDNF promotes NF-kappaB activation and that the latter is involved in the invasive potential of human pancreatic cancer cells.

Cell Division↗
PubMed2004

Expression of integrins in tumour tissue of a patient with cancer of the Vater's ampulla complicated by pancreas divisum.

We present herein a rare case where cancer of the Vater's ampulla was complicated with pancreas divisum. Endoscopic retrograde cholangiopancreatography demonstrated the pancreas divisum and stenosis of the common channel due to the tumorous lesion of the Vater's ampulla. Magnetic resonance cholangiopancreatography demonstrated that the Wirsung duct and Santorini duct were unconnected. The biopsy specimen at the upper gastrointestinal endoscopy revealed moderately differentiated tubular adenocarcinoma. The patient was diagnosed with cancer of the Vater's ampulla complicated with pancreas divisum, and underwent a pylorus-preserving pancreaticoduodenectomy. Immunohistochemical examination showed that the p53 protein and the alpha5beta1-integrin were expressed in tumour cells, and the proliferating cell nuclear antigen test was positive. Furthermore, the alpha5beta1-integrin was expressed in chronic pancreatitis tissue. We demonstrate that there is a risk that pancreas divisum will co-exist with malignant disease in the pancreaticobiliary area, causing a potential risk of complicating malignant diseases in the pancreas.

Adenocarcinoma↗
PubMed2004

[The QOL of the patient with advanced pancreatic carcinoma was changed for the better with combination therapy consisting of arterial chemotherapy and injection of interferon].

The prognosis of advanced pancreatic carcinoma with multiple liver metastases is extremely poor. The current methods of treating pancreatic carcinoma are far from satisfactory. The results of systemic and regional chemotherapies for pancreatic carcinoma are disappointing. The patient was a 68-year-old male with advanced pancreatic carcinoma. After an operation, he received a combination therapy consisting of arterial infusion (gemcitabine hydrochloride, GEM, 600 mg) and muscle injection of interferon (IFN, 300x10(4) U). A decrease in metastatic tumor of the liver was observed. In this report, we describe the case of a patient whose effective results were achieved by using a new combination of GEM and IFN.

Aged↗