Successful outcome of retrograde pancreatojejunostomy for chronic pancreatitis and infected pancreatic cysts: A case report.

Background: Chronic pancreatitis occasionally requires surgical treatment that can be performed with various techniques. Often, this type of surgery presents with postoperative complications. We report a case of a successful retrograde pancreatojejunostomy for chronic pancreatitis and infected pancreatic cysts.

The influence of the interval between percutaneous transhepatic gallbladder drainage and cholecystectomy on perioperative outcomes: a retrospective study.

Background: Percutaneous transhepatic gallbladder drainage (PTGBD) is recommended for acute cholecystitis patients at high risk for surgical treatment. However, there is no evidence about the best timing of surgery after PTGBD. Here, we retrospectively investigated the influence of the interval between PTGBD and surgery on perioperative outcomes and examined the optimal timing of surgery after PTGBD.

PI3K inhibitor LY294002, as opposed to wortmannin, enhances AKT phosphorylation in gemcitabine-resistant pancreatic cancer cells.

LY294002 and wortmannin are chemical compounds that act as potent inhibitors of phosphoinositide 3-kinases (PI3Ks). Both of them are generally used to inhibit cell proliferation as cancer treatment by inhibiting the PI3K/protein kinase B (AKT) signaling pathway. In this study, LY294002 (but not wortmannin) showed an abnormal ability to enhance AKT phosphorylation (at Ser472) specifically in gemcitabine (GEM)-resistant pancreatic cancer (PC) cell lines PK59 and KLM1-R.

Laparoscopic and Open Resection of Gastrointestinal Stromal Tumors of the Stomach.

Introduction: Laparoscopic resection has been reported as reasonable for patients with gastrointestinal stromal tumors (GISTs). In this study, we report the feasibility of the laparoscopic approach for GIST of the stomach. We also discuss the laparoscopic approach for GIST larger than 5 cm, which is reported to be difficult to treat by laparoscopic surgery.

Resistance to gemcitabine in the pancreatic cancer cell line KLM1-R reversed by metformin action.

Background/aim: The pancreatic cancer cell line KLM1 can gain chemoresistance following gemcitabine (GEM) treatment. Metformin was found to be a useful sensitising agent towards GEM treatment following gain of chemoresistance.

Materials And Methods: The proliferation of GEM-sensitive and -resistant cells was investigated over a range of metformin concentrations from 0.

The short term feasibility of abdominoperineal resection with prostatectomy for locally advanced rectal cancer: open and laparoscopic cases report.

Total pelvic exenteration is often selected for advanced rectal cancer with prostatic invasion. The aim of this study was to evaluate the short term feasibility of the abdominoperineal resection with prostatectomy for locally advanced rectal cancer. We performed abdominoperineal resection with prostatectomy for 3 patients with locally advanced rectal cancer, including 2 patients by totally laparoscopic procedure.

Comparative proteomic analysis of two stress-management strategies in pancreatic cancer.

Background: It is known that cancers adopt different strategies to cope with stress and overcome adverse micro-environmental conditions. Such strategies are also applicable to chemo-therapeutic treatment, which could subsequently result in chemo-resistance.

Materials And Methods: In order to investigate known stress-evasion strategies observed in pancreatic cancer, the stress-resistant KLM1-derived cell lines KLM1-R (Gemcitabine (GEM)-induced stress) and KLM1-S (growth factor restriction-induced stress) were employed.

Cofilin-phosphatase slingshot-1L (SSH1L) is over-expressed in pancreatic cancer (PC) and contributes to tumor cell migration.

Slingshot-1L (SSH1L), a cofilin-phosphatase, plays a role in actin dynamics and cell migration by reactivating cofilin-1. However, the expression of SSH1L in malignant diseases is poorly understood. The overexpression of SSH1L in cancerous tissue compared to the matched surrounding non-cancerous tissues from patients with late stages (III-IV) of PC was detected in 90% (9/10) of cases by western blotting.

Gemcitabine induces poly (ADP-ribose) polymerase-1 (PARP-1) degradation through autophagy in pancreatic cancer.

Poly (ADP-ribose) polymerase-1 (PARP-1) and autophagy play increasingly important roles in DNA damage repair and cell death. Gemcitabine (GEM) remains the first-line chemotherapeutic drug for pancreatic cancer (PC). However, little is known about the relationship between PARP-1 expression and autophagy in response to GEM.

Active hexose-correlated compound down-regulates sex-determining region Y-box 2 of pancreatic cancer cells.

Background/aim: Active hexose-correlated compound (AHCC) is an extract of basidiomycete mushroom. It has been used as health food due to its efficacy of enhancing antitumor effects and reducing adverse effects of chemotherapy. Our previous research showed that AHCC down-regulated heat-shock protein (HSP)-27 and exhibited cytotoxic effects against gemcitabine-resistant pancreatic cancer cells.

Active hexose-correlated compound down-regulates HSP27 of pancreatic cancer cells, and helps the cytotoxic effect of gemcitabine.

Background/aim: Active hexose-correlated compound (AHCC), an extract of basidiomycete mushroom, is used as health food to enhance the therapeutic effects and reduce the adverse effects of chemotherapy. Our previous proteomic analysis revealed that up-regulation of heat-shock protein 27 (HSP27) was responsible for gemcitabine resistance of pancreatic cancer cells. The aim of the present study was to investigate the effect of AHCC on the expression of HSP27 and the effect of combinatorial treatment of AHCC and gemcitabine on the gemcitabine-resistant pancreatic cancer cell line KLM1-R.

Human pancreatic cancer cells with acquired gemcitabine resistance exhibit significant up-regulation of peroxiredoxin-2 compared to sensitive parental cells.

Gemcitabine (2'-deoxy-2'-difluorodeoxycytidine) is the only clinically effective drug for pancreatic cancer. However, high levels of inherent and acquired tumor resistance to gemcitabine lead to difficulty of chemotherapy for pancreatic cancer. We have reported on a proteomic study of gemcitabine-sensitive KLM1 and -resistant KLM1-R pancreatic cancer cells, and identified some proteins which were shown to be up-regulated in KLM1-R compared to KLM1 cells.

Up-regulation of DDX39 in human pancreatic cancer cells with acquired gemcitabine resistance compared to gemcitabine-sensitive parental cells.

Intrinsic or acquired resistance of pancreatic cancer to gemcitabine (2'-deoxy-2'-difluorodeoxycytidine) is an important factor in the failure of gemcitabine treatment. Proteomic analysis of gemcitabine-sensitive KLM1 pancreatic cancer cells and -resistant KLM1-R cells identified heat-shock protein-27(HSP27) as a biomarker protein which is involved in gemcitabine resistance. However, a knock-down experiment showed that HSP27 was not the only protein implicated with gemcitabine-resistance.

Role of resection of the primary pancreatic neuroendocrine tumor in the multidisciplinary treatment of patients with unresectable synchronous liver metastases: a case series.

Context: Liver metastases have often existed in patients who have pancreatic neuroendocrine tumors (pNETs) at the time of diagnosis. In the management of patients of pNETs with unresectable liver metastases, the clinical efficacy of surgery to primary pancreatic tumor has been controversial. We presented four patients who were treated with resection of primary pancreatic tumor, trans-arterial hepatic treatment and systemic therapies.

Clinical significance of chemoradiotherapy and surgical resection for cT4 esophageal cancer.

Aim: To clarify the clinical significance of definitive chemoradiotherapy (CRT) and CRT followed by esophagectomy for cT4 esophageal cancer.

Patients And Methods: The treatment results for cT4 esophageal cancer were examined in 81 patients who received definitive CRT [radiation 50-70 Gy, cisplatin and 5-fluorouracil; group I] and 19 patients who underwent esophagectomy after preoperative CRT [40Gy, Group II].

Results: Among the 81 patients in group I, toxicities (grade 3 or 4) were observed in 32 patients, while partial response and complete response were recognized in 8 and 47 patients, respectively.

Lamivudine treatment enabling right hepatectomy for hepatocellular carcinoma in decompensated cirrhosis.

A 69-year-old man was admitted to our hospital in October 2003, for further examination of two liver tumors. He was diagnosed with hepatocellular carcinoma (HCC) arising from decompensated hepatitis B virus (HBV)-related cirrhosis. Long-term lamivudine administration improved liver function dramatically despite repeated treatment for HCC.

KNK437 downregulates heat shock protein 27 of pancreatic cancer cells and enhances the cytotoxic effect of gemcitabine.

Background: Our previous proteomic study demonstrated that expression of heat shock protein 27 (HSP27) is upregulated in gemcitabine (GEM)-resistant pancreatic cancer cells and that it suppressed the cytotoxic effect of GEM on the cells. This report describes the benefits of a treatment strategy combining the HSP inhibitor KNK437 with GEM for GEM-resistant pancreatic cancer cells.

Methods: We used 2 human pancreatic cancer cell lines, GEM-sensitive KLM1 and GEM-resistant KLM1-R.

Identification of up- and down-regulated proteins in gemcitabine-resistant pancreatic cancer cells using two-dimensional gel electrophoresis and mass spectrometry.

The prognosis of patients with pancreatic cancer is very poor because of late diagnosis and the lack of response to various therapies. Pancreatic cancer is generally resistant to chemotherapy and is highly fatal. Gemcitabine (GEM) appears to be the only effective agent for treatment of pancreatic cancer.

Heat-shock protein 27 is phosphorylated in gemcitabine-resistant pancreatic cancer cells.

Background: Gemcitabine (2'-deoxy-2'-difluorodeoxycytidine: Gemzar) (GEM) appears to be the only effective anticancer drug for pancreatic cancer, but it has little impact on outcome due to a high level of inherent and acquired tumor resistance. Our previous proteomic study demonstrated that the expression of three spots of heat-shock protein 27 (HSP27) was increased in GEM-resistant pancreatic cancer cells and could play a role in determining the sensitivity of pancreatic cancer to GEM.

Materials And Methods And Results: In the present study, using one-dimensional and two-dimensional Western blotting, we elucidated that these three spots of HSP27 were phosphorylated in GEM-resistant pancreatic cancer cell line, KLM1-R.

Surgical radiofrequency ablation for treatment of hepatocellular carcinoma: an endoscopic or open approach.

Radiofrequency ablation (RFA) is widely used for the treatment of unresectable hepatocellular carcinoma (HCC) with cirrhosis, however, unexpected injuries to the adjacent organs remains the most critical problem after endoscopic radiofrequency ablation (RFA) using a percutaneous approach. The endoscopic RFA is a minimally invasive treatment for HCC with difficultly in the location due to limited percutaneous access. In this study, it was used an endoscopic approach or an open surgical approach for the treatment of 46 patients with unresectable HCC.

Intrathoracic ganglioneuroma in an elderly patient over 70 years of age.

We herein present an exceedingly rare case of intrathoracic ganglioneuroma that was surgically resected in an elderly patient over 70 years of age. A 74-year-old woman was asymptomatic, but a computed tomography (CT) scan of the thorax indicated the presence of a posterior mediastinal mass paravertebrally. A thoracotomy was thus performed under a strongly suggested diagnosis of a neurogenic tumor because of the appearance and position of the mass on the chest CT and magnetic resonance imaging findings, and measuring 6.

Proteomics finding heat shock protein 27 as a biomarker for resistance of pancreatic cancer cells to gemcitabine.

Pancreatic cancer remains a devastating disease and >96% of patients with pancreatic cancer do not survive for more than 5 years. Gemcitabine (2'-deoxy-2'-difluoro-deoxycytidine: Gemzar) appears to be the only clinically effective drug for pancreatic cancer, but it has little impact on outcome. Proteomic analysis of gemcitabine-sensitive cells (KLM1) and resistant pancreatic cells (KLM1-R) was performed to identify target proteins of the gemcitabine.