• Asian Pacific Journal of Cancer Prevention
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• v.15 no.18
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• pp.7925-7928
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• 2014

Purpose: Renal cell carcinoma (RCC) is increasingly being recognized as a metabolic disease in recent studies. The aim of the present study was to identify the prevalence of metabolic syndrome (MetS) and its association with RCC among urologic patients. Materials and Methods: The study included a total of 355 participants (117 adult RCC patients and 238 age matched controls) divided into groups, with and without MetS diagnosed using the criteria of the American Heart Association/The National Heart Lung and Blood Institute. Groups were compared statistically and logistic regression analysis was performed to investigate the impact of MetS criteria on RCC risk. Results: Of the 117 RCC patients, 52 (44.4%) and of the 238 controls, 37 (15.5%) had MetS. A significant association (p<0.001) was found between the presence of MetS and RCC (OR: 4.35; 95% CI=2.62-7.21). As the number of MetS components accumulated from 3 to 5, RCC risk increased likewise from 4 to 6 times. Conclusions: MetS is more prevalent in RCC patients in Turkey compared to controls. Risk increases with the number of coexisting MetS components.

• Biomolecules & Therapeutics
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• v.23 no.1
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• pp.31-38
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• 2015

Histone acetylation plays a critical role in the regulation of transcription by altering the structure of chromatin, and it may influence the resistance of some tumor cells to tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) by regulating the gene expression of components of the TRAIL signaling pathway. In this study, we investigated the effects and molecular mechanisms of trichostatin A (TSA), a histone deacetylase inhibitor, in sensitizing TRAIL-induced apoptosis in Caki human renal carcinoma cells. Our results indicate that nontoxic concentrations of TSA substantially enhance TRAIL-induced apoptosis compared with treatment with either agent alone. Cotreatment with TSA and TRAIL effectively induced cleavage of Bid and loss of mitochondrial membrane potential (MMP), which was associated with the activation of caspases (-3, -8, and -9) and degradation of poly (ADP-ribose) polymerase (PARP), contributing toward the sensitization to TRAIL. Combined treatment with TSA and TRAIL significantly reduced the levels of the cellular Fas-associated death domain (FADD)-like interleukin-$1{\beta}$-converting enzyme (FLICE) inhibitory protein (c-FLIP), whereas those of death receptor (DR) 4, DR5, and FADD remained unchanged. The synergistic effect of TAS and TRAIL was perfectly attenuated in c-$FLIP_L$-overexpressing Caki cells. Taken together, the present study demonstrates that down-regulation of c-FLIP contributes to TSA-facilitated TRAIL-induced apoptosis, amplifying the death receptor, as well as mitochondria-mediated apoptotic signaling pathways.

• The Korean Journal of Cytopathology
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• v.2 no.2
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• pp.79-89
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• 1991

Metastatic tumors occur more frequently in the liver than in any other organ. Guided percutaneous fine-needle aspiration (FNA) of the liver is often recommended for confirmative diagnosis of the metastatic lesion, because of its simplicity, high yield, and reasonable safety. The authors studied retrospectively cytologic findings of 110 cases of metastatic tumors to the liver. The frequent primary sites were the stomach (23 cases), pancreas(19 cases), gallbladder(12 cases), and periampullary lesions(6 cases). Most of the metastases were carcinoma (106 cases). There were only 4 cases of sarcoma. The characteristic cytologic findings of FNA of meatastatic tumors were dirty background, abrupt change between hepatocytes and malignant cells, and desmoplasia. Some tumors displayed rather distinctive cytologic appearance that suggests primary sites. For example, the colonic adenocarcinoma showed tall columnar cells with a palisading arrangement, adenocarcinoma of gallbaldder showed focal squamous differentiation in some cases, and metastatic renal cell carcinoma and neuroblastoma showed also distinctive cytologic findings. Because the cytologic features of metastatic tumor are very similar to those of primary tumor, correct cytologic typing may be helpful in pursuit of an occult primary site of metastatic liver lesions, reducing extensive diagnostic investigation in poor prognostic patients.

• Journal of Nutrition and Health
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• v.34 no.2
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• pp.150-157
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• 2001

Intestinal absorption of dietary taurine is one of the regulatory component maintaining taurine homeostasis along with renal reabsorption, bile acid conjugation and secretion, and de nobo synthesis of taurine in mammals. Recent observations of decreased enterocytic levels of taurine in response to trauma, infection and surgical insults, postulate the possibility that intestinal taurine absorption might be impaired in such stressed conditions. The aim of the present study was to evaluate changes in enterocytic taurine transporter activity using the human intestinal colon carcinoma cell line, HT-29, in various stress-induced conditions. Pretreatment of the HT-29 cells with dexamethasone, a stress hormone(0.1,1,10 or 100$\mu$M) for 3 hrs, or with E coli heat-stable enterotoxin(10, 100, or 200nM) for 30 minutes in order to induce the condition of enterotoxigenic infection did not influence taurine uptake as compared to the value found in control cells. In contrast, pretreatment of the cells with cholera toxin(10, 100, 500, or 1000ng/ml)for 3hr or 24hr significantly decreased taurine uptake by HT-29 cells to 40~50% of the value found in untreated control cells. Kinetic studies of the taurine transporter activity were conducted in control and cholera toxin treated HT-29 cells with varying taurine concentrations(2~60$\mu$M) in the uptake medium. Pretreatment of the cells with cholera toxin(100ng/ml) for 3hr did not influence the Vmax, but resulted in a 55% increase in the Michaelis-Menten constant(Km) of the taurine transporter compared to those in control cells. These results suggest that cholera toxin-induced reduction in taurine transporter activity in HT-29 cells is associated with decreased affinity of the taurine transporter without altering the amount of transporter protein. Intestinal taurine absorption appears to be reduced in the condition of water-borne diseases caused by bacteria such as V. cholerae. This might influence the taurine status of infants and young children more readily, an age group in which the prevalence of intestinal infection is high and the role of intestinal absorption is crucial for maintaining the body taurine pool. (Korean J Nutrition 34(2) : 150-157, 2001)

• Korean Journal of Head & Neck Oncology
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• v.13 no.1
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• pp.40-44
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• 1997

Background: Lateral rhinotomy and medial maxillectomy, an en bloc resection of the medial maxillary sinus, ethmoid sinus with the lamina papyracea, medial orbital floor, and lacrimal fossa-duct, have been advocated for lateral nasal wall neoplasms as a standard approach method. Objective: This report was conducted to investigate the clinical efficacy of lateral rhinotomy and medial maxillectomy for lateral nasal wall neoplasms. Materials and Methods: We retrospectively analyzed clinical data of 31 patients who were treated at department of otolaryngology-head and neck surgery, Catholic university of Korea, school of medicine between 1990 and 1996. Results: Twenty five patients had benign lesions(80.6%). By far, the largest percentage was inverted papillomas(80%, 20/25). Of the six malignant lesions(19.4%), 33.3%(2/6) was squamous cell carcinoma and other lesions were metastatic renal cell carcinoma, adecarcinoma, transitional cell cacinoma, and hemangiopericytoma. There were a 4% recurrence for benign tumors(1/25), 5% especially for inverted papilloma(1/20), and 50% for malignant neoplasms(3/6). The overall complication rate was 9.7%. Conclusion: Despite the various approach for treatment of lateral nasal wall neoplasms including inverted papilloma, we continue to advocate a lateral rhinotomy and medial maxillectomy as the treatment of choice.

• Biomolecules & Therapeutics
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• v.27 no.1
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• pp.34-40
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• 2019

Transglutaminase 2 (TGase 2) plays a key role in p53 regulation, depleting p53 tumor suppressor through autophagy in renal cell carcinoma. We found that microtubule-associated protein 1A/1B-light chain 3 (LC3), a hallmark of autophagy, were tightly associated with the level of TGase 2 in cancer cells. TGase 2 overexpression increased LC3 levels, and TGase 2 knockdown decreased LC3 levels in cancer cells. Transcript abundance of LC3 was inversely correlated with level of wild type p53. TGase 2 knockdown using siRNA, or TGase 2 inhibition using GK921 significantly reduced autophagy through reduction of LC3 transcription, which was followed by restoration of p53 levels in cancer cells. TGase 2 overexpression promoted the autophagy process by LC3 induction, which was correlated with p53 depletion in cancer cells. Rapamycin-resistant cancer cells also showed higher expression of LC3 compared to the rapamycin-sensitive cancer cells, which was tightly correlated with TGase 2 levels. TGase 2 knockdown or TGase 2 inhibition sensitized rapamycin-resistant cancer cells to drug treatment. In summary, TGase 2 induces drug resistance by potentiating autophagy through LC3 induction via p53 regulation in cancer.

• Journal of Life Science
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• v.29 no.3
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• pp.318-324
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• 2019

Squamous cell carcinoma is the primary tumor type in head and neck cancers, the fifth most common malignant neoplasm world-wide. Survivin, a member of the inhibitor of apoptosis family, is highly expressed in head and neck carcinoma patients and correlated with more aggressive forms. In this study, we investigated whether YM155, a specific survivin inhibitor, could induce apoptosis in head and neck AMC-HN4 cells. YM155 was found to markedly induce apoptosis and cleavage of PARP, a marker of apoptosis. Furthermore, YM155 promoted apoptosis in other cancer cells, such as glioma (U251MG) and renal carcinoma (Caki) cells. In contrast, YM155 had no effect on apoptosis in normal mesangial cells. YM155 significantly induced caspase activation, and pan caspase inhibitor z-VAD-fmk markedly blocked apoptosis, PARP cleavage, and caspase-3 cleavage. Therefore, YM155 was seen to instigate caspase-dependent apoptosis in head and neck AMC-HN4 cells, inducing downregulation of survivin as well as other apoptotic proteins such as c-FLIP and Mcl-1. In addition, the induction of apoptosis and PARP cleavage by YM155 treatment was effectively inhibited in survivin-, c-FLIP- and Mcl-1-over-expressing head and neck AMC-HN4 cells. In conclusion, YM155 is a potent candidate for inducing cell death in head and neck AMC-HN4 cells.

• Journal of Yeungnam Medical Science
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• v.30 no.2
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• pp.101-104
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• 2013

Von Hippel-Lindau (VHL) disease is an autosomal dominant hereditary disorder caused by a germline mutation of the VHL gene. It is a multi-systemic disorder that is predisposed to benign or malignant tumors of visceral organs such as hemangioblastoma of the central nervous system, renal cell carcinoma, retinal angioma and pheochromocytoma. We report herein a case of VHL disease that initially manifested with aortic valve insufficiency.

• Journal of Korean Neurosurgical Society
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• v.54 no.5
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• pp.415-419
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• 2013

Hemangioblastomas are sporadic tumors found in the cerebellum or spinal cord. Supratentorial hemangioblastomas are rare, and those with meningeal involvement are extremely rare and have been reported in only approximately 130 patients. Here, we report the case of a 51-year-old female patient with supratentorial meningeal hemangioblastoma detected 5 years after surgical resection of an infratentorial hemangioblastoma associated with von Hippel-Lindau disease. Patients with von Hippel-Lindau syndrome are at risk for developing multiple hemangioblastomas, with new tumor formation and growth and possible meningeal infiltration. Regular lifelong follow-up in at-risk patients is recommended and should include the differential diagnosis of dural-based tumors such as angioblastic meningioma and metastatic renal cell carcinoma.

• Journal of Chest Surgery
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• v.45 no.5
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• pp.323-325
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• 2012

Pulmonary tumor embolism can be a cause of respiratory failure in patients with cancer even though it occurs rarely. We describe a 56-year-old man who underwent a pulmonary tumor embolectomy using cardiopulmonary bypass on beating heart combined with inferior vena cava embolectomy and right radical nephrectomy. Aggressive surgical treatment in this severe case is necessary not only to reduce the fatal outcome of pulmonary embolism in the short run, but also to improve the oncological prognosis in the long term.