• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.31 no.6
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• pp.468-473
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• 2005

Head and neck squamous cell carcinoma (HNSCC) is the sixth most common malignancy worldwide. The molecular mechanisms involved in the development and progression of these carcinomas are not well known. Abnormalities of genomic methylation patterns have been attributed a role in carcinogenesis and local de novo methylation at tumor suppressor loci was held to be involved in silencing of tumor suppressor genes. Using Ms APPCR, we previously isolated a hypermethylated fragment corresponded to the 5' end of TPEF gene from primary liver and lung cancer cells. To confirm the inactivation of TPEF gene by hypermethylation in HNSCC, we investigated correlation between methylation pattern and expression of TPEF in 10 HNSCC cell lines. In methylation analysis such as combined-bisulfite restriction analysis(COBRA) and bisulfite sequencing, only RPMI 2650 showed none methylated pattern and another 9 cell lines showed dense methylation. The TPEF gene expression level analysis using RT-PCR showed that these 9 cell lines had not or significantly low expression levels of TPEF as compared with RPMI 2650. In addition, the increase of TPEF reexpression by 5-AzaC as demethylating agent in 9 cell lines also indicated that TPEF expression was regulated by hypermethylation. These results of this study demonstrate that epigenetic silencing of TPEF gene by aberrant methylation could play an important role in HNSCC carcinogenesis.

• Journal of Chest Surgery
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• v.25 no.7
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• pp.732-735
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• 1992

We experienced a case of application of Gianturco Self-Expendable Metal vascular stent for S V.C. syndrome at the postoperative stae of pneumonectomy for Lung cancer[Squamous cell carcinoma, stage IIIa] Placement was performed under fluoroscopic guidance. Clinical problem for patient was resolved satisfactorily Long-term follow-up is required to determine restenosis, complication, and recurrence of cancer, etc.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.7
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• pp.4279-4282
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• 2013

Background: The activation and inactivation of receptor tyrosine kinases are tightly regulated to ensure faithful replication of cells. After having transduced extracellular growth activating signals, activated EGFR is subjected to downregulation either by clathrin mediated endocytosis or c-Cbl mediated proteasome degradation depending on the ligand concentration. c-Cbl is an ubiquitin ligase which requires a phosphorylated tyrosine residue at position 1045 in the cytoplasmic domain of EGFR to interact and add ubiquitin molecules. While activating mutations in exons 19 and 21 have been associated with the development of several cancers, the status of mutations at tyrosine 1045 coding exon 27 of EGFR remain to be investigated. Consistently, defective phosphorylation at 1045 has been associated with sustained phosphorylation of EGFR in non-small lung carcinomas. Hence in the present study we investigated the genetic status of the tyrosine 1045 coding site within exon 27 of EGFR gene to explore for possible occurrence of mutations in this region, especially since no studies have addressed this issue so far. Materials and Methods: Tumor chromosomal DNA isolated from thirty five surgically excised oral squamous cell carcinoma tissues was subjected to PCR amplification with intronic primers flanking the tyrosine 1045 coding exon 27 of EGFR gene. The PCR amplicons were subsequently subjected to direct sequencing to elucidate the mutation status. Results: Sequence analysis identified no mutations in the tyrosine 1045 codon of EGFR in any of the thirty five samples that were analyzed. Conclusions: The lack of identification of mutation in the tyrosine 1045 codon of EGFR suggests that mutations in this region may be relatively rare in oral squamous cell carcinomas. To the best of our knowledge, this study is the first to have explored the genetic status of exon 27 of EGFR in oral squamous cell carcinoma tissue samples.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.12
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• pp.7315-7319
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• 2013

Background: The metastasis gene osteopontin (OPN) is subject to alternative splicing, which yields three messages, osteopontin-a, osteopontin-b and osteopontin-c. Osteopontin-c is selectively expressed in invasive, but not in noninvasive tumors. In the present study, we examined the expression of OPN-c in esophageal squamous cell carcinomas (ESCCs) and assessed its value as a diagnostic biomarker. Methods: OPN-c expression was assessed by immunohistochemistry in 63 ESCC samples and correlated with clinicopathologic factors. Expression was also examined in peripheral blood mononuclear cells (PBMCs) from 120 ESCC patients and 30 healthy subjects. The role of OPN-c mRNA as a tumor marker was investigated by receiver operating characteristic curve (ROC) analysis. Results: Immunohistochemistry showed that OPN-c was expressed in 30 of 63 cancer lesions (48%)and significantly associated with pathological T stage (P=0.038) and overall stage (P=0.023). Real time PCR showed that OPN-c mRNA was expressed at higher levels in the PBMCs of ESCC patients than in those of healthy subjects (P<0.0001) with a sensitivity as an ESCC biomarker of 86.7%. Conclusion: Our findings suggest that expression of OPN-c is significantly elevated in ESCCs and this upregulation could be a potential diagnostic marker.

• Journal of Microbiology and Biotechnology
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• v.5 no.5
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• pp.264-268
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• 1995

Sulforhodamine B(SRB) assay was performed on the human lung carcinoma, A549 cell line to screen soil microorganisms for production of anti-cancer agent. Among 4, 265 microorganisms, 45 isolates were selected for their cytotoxicity and tested for their effects on the expression of c-myc by RNA slot blot and Northern blot analysis resulting in selection of No.2303 isolate. This No.2303 was identified as Streptomyces sp. by ISP classification and the chemotaxonomic analysis method. NO.2303 inhibited the expression of cmyc in Col0320 DM and A549 cell lines. The culture extract of No. 2303 also inhibited the progression of the cell cycle of Go in NIH 313 cells, implying that the extract also inhibited the expression of c-myc in NIH 313 cell.

• Biomedical Science Letters
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• v.10 no.3
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• pp.195-202
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• 2004

Lung cancer is a leading cause of cancer death worldwide; however, despite major advances in cancer treatment during the past two decades, the prognostic outcome of lung cancer patients has improved only minimally. This is largely due to the inadequacy of the traditional screening approach of diagnosis in lung cancer, which detects only well­established overt cancers and fails to identify precursor lesions in premalignant conditions of the bronchial tree. In recent years this situation has fundamentally changed with the identification of molecular abnormalities characteristic of premalignant changes; these concern tumour suppressor genes, loss of heterozygosity at crucial sites and activation of oncogenes. Basic knowledge at the molecular level has extremely important clinical implications with regard to early diagnosis, risk assessment and prevention, and therapeutic targets. In this study we used a 'cap-finder' subtractive hybridization method, 'long distance' polymerase chain reaction (PCR), streptavidin magnetic beads mediated subtraction, and spin column chromatography to detect differential expression genes of human small cell lung carcinoma. We have now isolated ninety two genes that expressed differentially in the human small cell lung carcinoma cells and analyzed of 12 clones with sequencing, nine cDNAs include tapasin (NGS-17) mRNA, BC200 alpha scRNA, chromosome 12q24 PAC RPCI3-462E2, protein phosphatase 1 (PPPICA), translocation protein 1 (TLOC1), ribosomal protein S24 (RPS24) mRNA, protein phosphatase (PPEF2), cathepsin Z, MDM2 gene and three novel genes. They may be oncogenesis­related proteins.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.5
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• pp.2253-2255
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• 2012

Objective: The objective of our present study was to assess the role of serum amyloid A (SAA) in stages and prognosis of renal cell carcinoma. Material and Methods: It was a hospital based retrospective study carried out in the Department of Medicine and Biochemistry of Manipal Teaching Hospital, Pokhara, Nepal between $1^{st}$ January 2008 and $31^{st}$ December 2011. The variables collected were SAA, CRP. Approval for the study was obtained from the institutional research ethical committee. Quantitative analysis of human SAA and C-reactive protein (CRP) was performed by radial immune diffusion (RID) assay for all cases. Results: Of the 422 total cases of renal cell carcinoma, 218 patients had normal and 204 abnormal SAA. SAA levels were grossly elevated in T3 stage ($122.3{\pm}SD35.7$) when compared to the mean for the T2 stage ($84.2{\pm}SD24.4$) (p value: 0.0001). Similarly, SAA levels were grossly elevated in M1 stage ($190.0{\pm}SD12.7$) when compared to the M0 stage ($160.9{\pm}SD24.8$) (p: 0.0001). There was no significant association with elevated CRP levels ($209.1{\pm}SD22.7$, normal $199.0{\pm}SD19.5$). Conclusion: The validity of SAA in serum as being of independent prognostic significance in RCC was demonstrated with higher levels in advanced stage disease.

• Preventive Nutrition and Food Science
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• v.11 no.3
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• pp.177-183
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• 2006

Methanolic and aqueous extracts of 26 red algae species collected from Jeju Island coast were prepared at a high $(70^{\circ}C)$ and a room temperature $(20^{\circ}C)$ and were examined for their cytotoxic activity against 4 tumor cell lines: U-937 (human monoblastoid leukemia cell line), HL-60 (human promyelocytic leukemia cell line), B-16 (murine melanoma cell line) and HeLa (woman cervical carcinoma cell line). $20^{\circ}C$ methanolic extract of Polysiphonia japonica showed cytotoxic activity of over 50% against U-937, HL-60 and B-16 cells. On the other hand, the $20^{\circ}C$ aqueous extract of Scinaia okamurae and $70^{\circ}C$ aqueous extract of Chondrus crispus showed cell growth inhibition activity of more than 50% against HL-60 and B-16 cells. The highest cytotoxic activity was observed in the $20^{\circ}C$ aqueous extract of Scinaia okamurae against B-16 cells (80.55%).

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.1
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• pp.27-31
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• 2012

Objectives: Expression of vascular endothelial growth factor C (VEGF-C)and vascular endothelial growth factor feceptor-3 (VEGFR-3) in laryngeal squamous carcinoma and its relationship to lymph node metastasis were investigated. Methods: VEGF-C and VEGFR-3 gene expression in 30 cases of normal laryngeal mucosa tissue (NLM), primary laryngeal carcinoma cell carcinomas (PLC) and cervical lymph nodes (CLN) was examined by reverse transcription polymerase chain reaction (RT-PCR). Protein levels of VEGF-C expression were determined by immunohistochemical staining in 60 cases of PLC. Results: Expression of VEGF-C and VEGFR-3 different among NLM, PLC and CLN in the same patient. In PLC, expression was significantly higher in lymph node positive group than in the lymph node negative group and associated with histological grade of differentiation; Expression of VEGF-C and VEGFR-3 was not linked with age, sex, site or T stage. Conclusions: A close correlation was found between VEGF-C/VEGFR-3 expression and lymph node metastasis in PLC, suggesting a role in metastasis of laryngeal carcinomas.

• Korean Journal of Head & Neck Oncology
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• v.27 no.1
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• pp.3-11
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• 2011

Hepatocyte growth factor(HGF) and c-Met play an important role in the control of tumor growth and invasion, and they are known to be good prognostic indicators of patient outcome. Epigallocatechin-3-gallate (EGCG) has been shown to have chemopreventive and therapeutic properties by modulating multiple signal pathways regarding the control of proliferation and invasion of cells. In this study, we evaluated the role of c-Met in EGCG-induced inhibition of invasion and apoptosis in an oral cancer cell line. In KB cells where c-Met was knocked down with siRNA, we performed invasion assay and FACS with Annexin V-FITC/PT staining. In addition, we checked the change of mitochondrial membrane potential(MMP) and the generation of reactive oxygen species(ROS). EGCG-induced inhibition of invasiveness was significantly decreased after the knock-down of c-Met. EGCG-induced apoptosis, MMP change and ROS generation was also reduced in c-Met knock-ed-down KB cells. These results suggest that c-Met is involved in EGCG-induced apoptosis and inhibition of invasiveness of oral cancer cell line.