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This phase II study evaluated the efficacy and safety of combination chemotherapy with paclitaxel, cisplatin, and 5-fluorouracil (5-FU) in advanced gastric cancer. Patients with histologically confirmed gastric adenocarcinoma were eligible for the study. Paclitaxel (175 mg/㎡) and cisplatin (75 mg/㎡) were given as a 1-hr intravenous infusion on day 1, followed by 5-FU (750 mg/㎡) as a 24-hr continuous infusion for 5 days. This cycle was repeated every 3 weeks. Forty-five eligible patients (median age, 56 yr) were treated in this way. Of the 41 patients in whom efficacy was evaluable, an objective response rate (ORR) was seen in 51.2% (95% CI, 0.35-0.67), a complete response in two, and a partial response in 19 patients. The median progression free survival was 6.9 months (95% CI, 5.86-7.94 months), and the median overall survival was 12.7 months (95% CI, 9.9-15.5). The main hematological toxicity was neutropenia and greater than grade 3 neutropenia was observed in twelve patients (54%). Febrile neutropenia developed in three patients (6.8%). The major non-hematological toxicities were asthenia and peripheral neuropathy, but most of patients showed grade 1 or 2. In conclusion, combination chemotherapy with paclitaxel, cisplatin, and 5-FU is a promising regimen, and was well tolerated in patients with advanced gastric cancer.
Primary pancreatic lymphoma (PPL) is a rare form of extranodal lymphoma, and this accounts for less than 0.5% of all pancreatic tumors. Differentiating PPL from pancreatic adenocarcinoma is important because the prognosis and survival of PPL is much better than those of pancreatic adenocarcinoma. Although the treatment usually consists of a combination of chemotherapy and radiation therapy, PPL patient with biliary tract or gastrointestinal obstruction should undergo biliary or gastric bypass to relieve the symptoms. Herein, we describe a case of PPL with acute pancreatitis and obstructive jaundice, and the patient was successfully managed with endoscopic retrograde pancreatic and biliary drainage. 췌장에 발병하는 악성 종양은 대부분 선암으로, 원발성 췌장 림프종은 췌장 종양의 0.5% 이하에서 발생하는 드문 질환이다. 질환의 예후, 치료 방법이 다르기 때문에 췌장 선암과 감별 진단이 중요하다. 원발성 췌장 림프종의 치료는 대부분 항암 화학 요법 및 방사선 치료 등이 주가 되나, 담관이나 위 장관 폐색이 있는 경우 증상의 호전 등을 위해 담관 혹은 위 장관 배액술을 시행하여야 한다. 저자들은 상복부 통증, 황달을 주소로 내원한 젊은 남자에서 플라스틱 스텐트를 이용한 담관 및 췌관 배액을 통해 증상 호전 후 수술적 절제를 통해 원발성 췌장 림프종으로 진단한 1예를 경험하여 보고 한다.
KITENIN (KAI1 C-terminal interacting tetraspanin) promotes invasion and metastasis in mouse colon cancer models. In the present study, we evaluated the effects of KITENIN knockdown by intravenous administration of short hairpin RNAs (shRNAs) in an orthotopic mouse colon cancer model, simulating a primary or adjuvant treatment setting. We established orthotopic models for colon cancer using BALB/c mice and firefly luciferaseexpressing CT-26 (CT26/Fluc) cells. Tumor progression and response to therapy were monitored by bioluminescence imaging (BLI). In the primary therapy model, treatment with KITENIN shRNA substantially delayed tumor growth (P = 0.028) and reduced the incidence of hepatic metastasis (P = 0.046). In the adjuvant therapy model, KITENIN shRNA significantly reduced the extent of tumor recurrence (P = 0.044). Mice treated with KITENIN shRNA showed a better survival tendency than the control mice (P = 0.074). Our results suggest that shRNA targeting KITENIN has the potential to be an effective tool for the treatment of colon cancer in both adjuvant and metastatic setting.
Purpose: Hypoxia-inducible factor-1α (HIF-1α) increases transcription of the vascular endothelial growth factor (VEGF) gene. Inhibition of VEGF abolishes VEGF mediated induction of HIF-1α. Recent reports suggested that HIF-1α also mediated the induction of class III β-tubulin (TUBB3) in hypoxia. TUBB3 confers resistance to taxanes. Inhibition of VEGF may decrease the expression of HIF-1α and TUBB3. This study was undertaken to investigate the roles of vascular endothelial growth factor receptor (VEGFR) in gastric cancer cell behavior and to identify methods to overcome paclitaxel resistance in vitro. Materials and Methods: The protein expression levels of HIF-1α and TUBB3 were measured in human gastric cancer cell lines (AGS) under normoxic and hypoxic conditions. The relationship between TUBB3 and paclitaxel resistance was assessed with small interfering TUBB3 RNA. AGS cells were treated with anti-VEGFR-1, anti-VEGFR-2, placental growth factor (PlGF), bevacizuamb, and paclitaxel. Results: Hypoxia induced paclitaxel resistance was decreased by knockdown of TUBB3. Induction of HIF-1α and TUBB3 in AGS is VEGFR-1 mediated and PlGF dependent. Hypoxia-dependent upregulation of HIF-1α and TUBB3 was reduced in response to paclitaxel treatment. Expressions of HIF-1α and TUBB3 were most decreased when AGS cells were treated with a combination of paclitaxel and anti-VEGFR-1. AGS cell cytotoxicity was most increased in response to paclitaxel, anti-VEGFR-1, and anti-VEGFR-2. Conclusion: We suggest that blockade of VEGFR-1 and VEGFR-2 enhances paclitaxel sensitivity in TUBB3-expressing gastric cancer cells.
Necrotizing fasciitis is a life-threatening soft tissue infection involving skin, subcutaneous tissue, and superficial fascia. We report a case of necrotizing fasciitis that developed in a 76- year-old female patient taking low-dose methotrexate and prednisolone for rheumatoid arthritis (RA). A computed tomography scan of the neck during the initial work-up showed soft tissue swelling, loss of fat planes, and mild heterogeneous enhancement in the right lateral neck, suggesting cellulitis. The lesions were associated with skin necrosis and multiple bullae rapidly expanded to the right anterior chest in spite of empirical antibiotic therapy. Surgical debridement was immediately performed, and soft tissue biopsy from the lesions showed the pathologic finding consistent with necrotizing fasciitis. The skin wound defect was reconstructed by a flap operation with split-thickness skin graft. This case shows the development of necrotizing fasciitis in a elderly patient taking methotrexate and low-dose steroid for RA and highlights early recognition and prompt surgical debridement for successful management.
The purpose of this study was to determine the effects of stroke parameter and upper limb muscle power level by swim performance of competitive swimmers. Fourteen male college swimmers were performed swim trials and muscle power analysis. All swimmers were measured swim stoke parameters during maximal effort each swim stroke trails 50m and individual medley(IM) 200m. The result showed that 50m swim record was significantly different from IM 200m(p<.01). DPS(stroke per distance)(p<.01) and Lactate level(p<.05) were significantly difference between 50m and 200m swim. Moreover, there was more related to swim velocity in all swim trials (p<.05). Relationship of muscle power and swim performance were significantly difference between freestyle and butterfly. In conclusion, efficiency of swim stroke and muscle power were increased a beneficial effect on swim performance. Decrease in lactate concentration with swimming velocity may possibly contribute to improvement of swim performance for stroke efficiency, development of anaerobic capacity in elite swimmers.