• Journal of Gastric Cancer
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• v.17 no.4
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• pp.374-383
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• 2017

Purpose: Bleeding is one of the most serious complications of advanced gastric cancer (AGC) and is associated with a poor prognosis. This study aimed to evaluate the clinical outcomes of endoscopic hemostasis for bleeding in patients with unresectable AGC. Materials and Methods: This study included 106 patients with bleeding associated with gastric cancer who had undergone endoscopic hemostasis between January 2010 and December 2013. Clinical characteristics, treatment outcomes, including rates of successful endoscopic hemostasis and rebleeding, risk factors for rebleeding, and overall survival (OS) were investigated. Results: Successful initial hemostasis was achieved in 83% of patients. Rebleeding occurred in 28.3% of patients within 30 days. The median OS after initial hemostasis was lower in patients with rebleeding than in those without rebleeding (2.7 and 3.9 months, respectively, P=0.02). There were no significant differences in disease status and rebleeding rates among patients with partial response or stable disease (n=4), progressive disease (n=64), and first diagnosis of disease (n=38). Univariate and multivariate analyses (P=0.038 and 0.034, respectively) revealed that transfusion of ${\geq}5$ units of RBCs was a significant risk factor for rebleeding. Conclusions: Despite favorable success rates of endoscopic hemostasis for bleeding associated with gastric cancer, the 30-day rebleeding rate was 28.3% and the median OS was significantly lower in patients with rebleeding than in those without rebleeding. Massive transfusion (${\geq}5$ units of RBCs) was the only significant risk factor for rebleeding. Patients with bleeding associated with AGC who have undergone massive transfusion should be observed closely following endoscopic hemostasis. Further research on approaches to reduce rebleeding rate and prevent death is needed.

• Tuberculosis and Respiratory Diseases
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• v.51 no.6
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• pp.550-558
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• 2001

Background : It has been reported that younger patients with lung cancer have characteristic features that differ from those in older patients. The prognosis for young patients with this disease is controversial. This study aimed to determine the clinicopathological characteristics, the survival rate, and the risk factors associated with the overall survival rate in younger patients with lung cancer. Methods : The records of 120 young(age${\leq}40$) patients with histologically confirmed lung cancer in the Korea Caneer Center Hospital(KCCH) between Jan. 1992 and Dec. 1998 were retrospectively reviewed. Of 5,082 lung cancer patients registered at the KCCH from 1992 to 1998, 120 older(age>40) patients were randomly selected as the controls. Results : More female patients(45.0% vs. 20.0%, p<0.001) and more adenocarcinoma cases(64.2% vs.38.3%, p<0.001) were found in the younger group, when compared to the older patients. In NSCLC, advanced disease(stage IIIB and IV) was more common in the younger patients(90.2%) than in the older patients(62.7%) (p<0.001). The Median survival was 8.6 months in the younger patients and 12.2 months in the older(p=0.003). In a multivariate analysis, only the advanced-stage was an independent negative prognostic factor. Conclusions : Lung cancer in the younger age group presents with a more advanced stage resulting in a poor survival rate, which suggests that lung cancer in this population is more aggressive than in older patients.

• Tuberculosis and Respiratory Diseases
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• v.43 no.6
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• pp.1008-1018
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• 1996

Primary mediastinal nonseminomatous germ cell tumor is extremely rare. Apart from rarity and large size, mediastinal germ cell tumors show striking similarity to testicular tumors in age, incidence, and tumor type. The symptoms associated with these tumors are related mainly to size, invasion of neighboring structures, and distant metastases. Tissue diagnosis is obtained by biopsy of the primary lesion or by biopsy of metastatic sites. Tumors often present with advanced bulky disease, which are unresectable. So these tumors require an aggressive multidisciplinary approach to management. Optimal management includes aggressive surgical debulking and early use of cisplatin-bleomycin-based combination chemotherapy. Serial biomarker measurements permit early recognition of recwrence and improved timing of surgical intervention. The prognosis for mediastinal germ cell tumors is poor, not only because they are far advanced at the time of diagnosis but also because some of the tumors-such as embryonal carcinomas, choriocarcinomas, and endodermal sinus tumors-are very aggressive. In these cases, we present three young male patients with large mass on anterior mediastinum. Tissue diagnosis was obtained by primary lesion biopsy. All patients received surgical debulking and combination chemotherapy and experienced a brief response and eventually had relapses. We report these cases with a review of literatures.

• Journal of Ginseng Research
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• v.44 no.5
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• pp.725-737
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• 2020

Background: T-cell acute lymphoblastic leukemia (T-ALL) is a kind of aggressive hematological cancer, and the PI3K/Akt/mTOR signaling pathway is activated in most patients with T-ALL and responsible for poor prognosis. 20(S)-Ginsenoside Rh2 (20(S)-GRh2) is a major active compound extracted from ginseng, which exhibits anti-cancer effects. However, the underlying anticancer mechanisms of 20(S)-GRh2 targeting the PI3K/Akt/mTOR pathway in T-ALL have not been explored. Methods: Cell growth and cell cycle were determined to investigate the effect of 20(S)-GRh2 on ALL cells. PI3K/Akt/mTOR pathway-related proteins were detected in 20(S)-GRh2-treated Jurkat cells by immunoblotting. Antitumor effect of 20(S)-GRh2 against T-ALL was investigated in xenograft mice. The mechanisms of 20(S)-GRh2 against T-ALL were examined by cell proliferation, apoptosis, and autophagy. Results: In the present study, the results showed that 20(S)-GRh2 decreased cell growth and arrested cell cycle at the G1 phase in ALL cells. 20(S)-GRh2 induced apoptosis through enhancing reactive oxygen species generation and upregulating apoptosis-related proteins. 20(S)-GRh2 significantly elevated the levels of pEGFP-LC3 and autophagy-related proteins in Jurkat cells. Furthermore, the PI3K/Akt/mTOR signaling pathway was effectively blocked by 20(S)-GRh2. 20(S)-GRh2 suppressed cell proliferation and promoted apoptosis and autophagy by suppressing the PI3K/Akt/mTOR pathway in Jurkat cells. Finally, 20(S)-GRh2 alleviated symptoms of leukemia and reduced the number of white blood cells and CD3 staining in the spleen of xenograft mice, indicating antitumor effects against T-ALL in vivo. Conclusion: These findings indicate that 20(S)-GRh2 exhibits beneficial effects against T-ALL through the PI3K/Akt/mTOR pathway and could be a natural product of novel target for T-ALL therapy.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.29 no.5
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• pp.394-404
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• 2007

Oral squamous cell carcinoma is the most prevalent oral cancer, which is characterized by its high metastasis and recurrent rates and poor prognosis. Taxol is an anticancer agent which is microbial products extracted from jew tree. It combines with the tubulin and induces apoptosis by inhibiting mitosis of cell with microtubule stabilization. Recently, it was reported to be effective in various solid tumors, but only very slight effect has been seen in oral squamous cell carcinomas due to its cell-specific potencies. Cyclosporin A is used as immune suppressant and is being applied in anticancer therapy as its mechanism of induction of change of apoptotic process in various cells have been known. In this study, oral squamous cell carcinoma HN22 cell line was used for in vitro experiment and as for the experimental group taxol and cyclosporin A were applied alone and to observe the synergistic effect of apoptosis, Taxol and cyclosporin A were coadministered with different concentration of taxol for comparison. The results were obtained as follow: 1. There was no difference in Bcl-2, Bax, caspase 3, 8, 9 mRNA expression when cyclosprin A or taxol was applied alone to HN 22 cell line. 2. Caspase 3, 9 mRNA expression was prominently increased when cyclosprin A and taxol were applied together to cancer cell. 3. No significant difference was observed when cyclosporin A and taxol($1{\mu}g/ml$ and $3{\mu}g/ml$) were applied together to cancer cell line. 4. No significant difference was seen in Bcl-2, Bax, and caspase 8 mRNA expression in all the groups of in vitro experiments. 5. When cyclosporin A was applied alone in vivo study on the nude mice, histopathologi cal findings was similar to those of the control group. Oral squamous cell carcinoma induced by inoculation of HN 22 cell line was not reduced after treatment of cyclosporin A. 6. When taxol was applied alone, the islands of squamous cell carcinoma still remained, which meant insignificant healing effect. There was a lesser volume increase compared with the cyclosporin A alone. 7. When taxol and cyclosporin A were applied together, the connective tissue and calcification were seen in the histopathologic findings. Oral squamous cell carcinoma was decreased and cancer cell was disappeared. In observing the tumor mass change with time, there was a gradual decreased size and healing features. As the results of the in vitro experiment, it could conclud that only when the two agents are applied together, mitochondria-mediated apoptosis occurred by considerable increase of caspase 3, 9 mRNA expression, irrespectable of the concentration of taxol. In vivo experiment, there was a discrete synergistic effect when the two agents were applied together. But single use of cyclosporin A was not effective in this study. Based on the results of this experiment, if further clinical studies are done, taxol and cyclosporin A could be effectively used in treatment of oral squamous cell carcinomas.

• Korean Journal of Bronchoesophagology
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• v.6 no.1
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• pp.80-86
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• 2000

Background : Stomal recurrence that occasionally follows total laryngectomy is associated with very poor prognosis regardless of treatment modality, so it is very important to identify high risk patients to prevent stomal recurrence. Objectives : We attempted to select an optimal management method to prevent stomal recurrence by analyzing risk factors in each patient who was found to have stomal recurrence following total laryngectomy. Materials and Methods : Risk factors in each of eleven patients who had stomal recurrence out of 159 patients who underwent total laryngectomy in the last ten years were analyzed retrospectively. Data were gathered on risk factors such as the presence of subglottic extension, extralaryngeal extension, thyroid gland invasion, lymph node metastasis, timing of tracheotomy, tumor stage, postoperative radiotherapy, and inclusion of the stoma in the radiotherapy field. Results : There were eight cases of subglottic extension, six cases of extralaryngeal invasion, one case of pharyngocutaneous fistula that occurred as a postoperative complication, and one case who was taken completion laryngectomy following conservation surgery. With the exception of one case who was taken tracheotomy prior to total laryngectomy, all tracheotomies were performed intra-operatively after endotracheal intubation. There was no evidence of paratracheal lymph node or prelaryngeal lymph node metastasis on preoperative neck CT scan. There were six cases of T4 tumors, four cases of T3 tumors, and one case of T2 tumor. Salvage surgery was performed following radiotherapy in three cases, and aside from one case who was not taken post-operative radiotherapy, postoperative radiotherapy including the stoma was performed in the remaining seven cases within one month after surgery. Conclusion : Total laryngectomy with wide paratracheal lymph node dissection, thyroidectomy, and tracheotomy should be performed for patients who have high risk factors such as subglottic extension and advanced stage. We believe that tracheotomy should be precede endotracheal intubation. Efforts should be made to prevent stomal recurrence by utilizing postoperative radiotherapy and by minimizing postoperative complications such as infection and fistula.

• Molecules and Cells
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• v.41 no.5
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• pp.390-400
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• 2018

Studies have revealed that miR-103a-3p contributes to tumor growth in several human cancers, and high miR-103a-3p expression is associated with poor prognosis in advanced gastric cancer (GC) patients. Moreover, bioinformatics analysis has shown that miR-103a-3p is upregulated in The Cancer Genome Atlas (TCGA) stomach cancer cohort. These results suggest that miR-103a-3p may function as an oncogene in GC. The present study aimed to investigate the role of miR-103a-3p in human GC. miR-103a-3p expression levels were increased in 33 clinical GC specimens compared with adjacent nontumor stomach tissues. Gain- and loss-of-function studies were performed to identify the correlation between miR-103a-3p and tumorigenesis in human GC. Inhibiting miR-103a-3p suppressed GC cell proliferation and blocked the S-G2/M transition in MKN-45/SGC-7901 cells, whereas miR-103a-3p overexpression improved GC cell proliferation and promoted the S-G2/M transition in vitro. Bioinformatics and dual-luciferase reporter assays confirmed that ATF7 is a direct target of miR-103a-3p. Analysis of the TCGA stomach cancer cohort further revealed that miR-103a-3p expression was inversely correlated with ATF7 expression. Notably, silencing ATF7 showed similar cellular and molecular effects as miR-103a-3p overexpression, namely, increased GC cell proliferation, improved CDK2 expression and decreased P27 expression. ATF7 overexpression eliminated the effects of miR-103a-3p expression. These findings indicate that miR-103a-3p promotes the proliferation of GC cell by targeting and suppressing ATF7 in vitro.

• Molecules and Cells
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• v.41 no.5
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• pp.423-435
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• 2018

This investigation was aimed at working out the combined role of lncRNA H19, miR-29b and Wnt signaling in the development of colorectal cancer (CRC). In the aggregate, 185 CRC tissues and corresponding para-carcinoma tissues were gathered. The human CRC cell lines (i.e. HT29, HCT116, SW480 and SW620) and normal colorectal mucosa cell line (NCM460) were also purchased. Si-H19, si-NC, miR-29b-3p mimics, miR-29b-3p inhibitor, si-PGRN and negative control (NC) were, respectively, transfected into the CRC cells. Luciferase reporter plasmids were prepared to evaluate the transduction activity of $Wnt/{\beta}-catenin$ signaling pathway, and dual-luciferase reporter gene assay was arranged to confirm the targeted relationship between H19 and miR-29b-3p, as well as between miR-29b-3p and PGRN. Finally, the proliferative and invasive capacities of CRC cells were appraised through transwell, MTT and scratch assays. As a result, overexpressed H19 and down-expressed miR-29b-3p displayed close associations with the CRC patients' poor prognosis (P < 0.05). Besides, transfection with si-H19, miR-29b-3p mimic or si-PGRN were correlated with elevated E-cadherin expression, decreased snail and vimentin expressions, as well as less-motivated cell proliferation and cell metastasis (P < 0.05). Moreover, H19 was verified to directly target miR-29b-3p based on the luciferase reporter gene assay (P < 0.05), and miR-29b-3p also bound to PGRN in a direct manner (P < 0.05). Finally, addition of LiCl ($Wnt/{\beta}-catenin$ pathway activator) or XAV93920 ($Wnt/{\beta}-catenin$ pathway inhibitor) would cause remarkably altered E-cadherin, c-Myc, vimentin and snail expressions, as well as significantly changed transcriptional activity of ${\beta}-catenin/Tcf$ reporter plasmid (P < 0.05). In conclusion, the lncRNA H19/miR-29b-3p/PGRN/Wnt axis counted a great deal for seeking appropriate diagnostic biomarkers and treatment targets for CRC.

• The Journal of the Korean bone and joint tumor society
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• v.15 no.1
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• pp.13-25
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• 2009

Purpose: The DNA repair protein, $O^6$-methylguanine-DNA methyltransferase (MGMT), removes alkyl adducts from the $O^6$ position of guanine. Epigenetic inactivation of MGMT has been found in human neoplasia and considered one of the implicated factors in chemoresistance. Materials and Methods: Sixty-two patiensts with soft tissue sarcomas (STS) were analyzed for the status of MGMT protein expression by immunohistochemistry and the promoter hypermethylation of the MGMT gene using methylation-specific PCR. Result: The loss of MGMT expression was found in 20 cases (32.3%) of total 62 STS. MGMT promoter hypermethylation rate was 25.0% (11/44 cases). The loss of MGMT expression showed significant association with high AJCC stage, high FNCLCC grade, and aggressive behavior. However,when the group who received chemotherapy was analyzed (n=27), loss of MGMT expression was correlated with worse survival in multivariate analysis (p=0.024). MGMT promoter hypermethylation is associated with high FNCLCC grade. MGMT promoter hypermethylation status had a strong correlation with loss of MGMT expression (p=0.000). Conclusion: Our results suggest that MGMT promoter hypermethylation and loss of MGMT expression had a tendency to be associated with poor prognosis and that loss of MGMT protein expression is frequently occurs via MGMT promoter hypermethylation.

• The Journal of the Korean bone and joint tumor society
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• v.15 no.1
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• pp.7-12
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• 2009

Purpose: This study was aimed to assess TLE1 as a target molecule of synovial sarcoma. Method: We obtained tissue samples and clinical data from 36 patients who were diagnosed and treated for synovial sarcoma in our hospital. Immunohistochemical staining was performed to detect the expression of TLE1 in synovial sarcoma and normal tissues such as fat, skeletal muscle, peripheral nerve, vascular endothelium, and epithelium. Univariate survival analysis was performed to find whether overexpression of TLE1 is correlated to poor prognosis. Results: TLE1 was expressed in 35 (97%) cases (grade 1 was 5 cases, grade 2 was 28 cases, grade 3 was 2 cases.). Normal tissues from mesenchymal origin did not express TLE1. However, epithelial and endothelial cells showed weak expression (grade 1) of TLE1. The level of TLE1 expression did not have any prognostic significance according to univariate survival analysis. Conclusion: TLE1 may be a new molecular target of synovial sarcoma that differentiates synovial sarcoma from normal mesenchymal cells.