• Journal of Chest Surgery
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• v.26 no.10
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• pp.815-820
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• 1993

We experienced a case of esophageal leiomyoma combined with achalasia that is very rare. Patient had suffered from severe dysphagia and postprandial vomiting and diagnosis was accomplished by esophagography, esophagoscopy, chest CT, and esophageal motility test. The operative treatment was done through left lateral thoracotomy by enucleation of the submucosal tumor and esophagomyotomy. By histopathological findings, the diagnosis of leiomyoma was confirmed and LES biopsy revealed absence of the ganglion cells of myenteric and Auerbach`s plexus. Symptoms of the patient were completely relieved and postoperative course was uneventful.

• The Korean Journal of Physiology and Pharmacology
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• v.16 no.5
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• pp.313-320
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• 2012

In this study, we focused to identify whether eupatilin (5,7-dihydroxy-3',4',6-trimethoxyflavone), an extract from Artemisia argyi folium, prevents $H_2O_2$-induced injury of cultured feline esophageal epithelial cells. Cell viability was measured by the conventional MTT reduction assay. Western blot analysis was performed to investigate the expression of 5-lipoxygenase by $H_2O_2$ treatment in the absence and presence of inhibitors. When cells were exposed to 600 ${\mu}M$ $H_2O_2$ for 24 hours, cell viability was decreased to 40%. However, when cells were pretreated with 25~150 ${\mu}M$ eupatilin for 12 hours, viability was significantly restored in a concentration-dependent manner. $H_2O_2$-treated cells were shown to express 5-lipoxygenase, whereas the cells pretreated with eupatilin exhibited reduction in the expression of 5-lipoxygenase. The $H_2O_2$-induced increase of 5-lipoxygenase expression was prevented by SB202190, SP600125, or NAC. We further demonstrated that the level of leukotriene $B_4$ ($LTB_4$) was also reduced by eupatilin, SB202190, SP600125, NAC, or nordihydroguaiaretic acid (a lipoxygenase inhibitor) pretreatment. $H_2O_2$ induced the activation of p38MAPK and JNK, this activation was inhibited by eupatilin. These results indicate that eupatilin may reduce $H_2O_2$-induced cytotoxicity, and 5-lipoxygenase expression and $LTB_4$ production by controlling the p38 MAPK and JNK signaling pathways through antioxidative action in feline esophageal epithelial cells.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.248.1-248.1
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• 2002

It has been shown that C2-ceramide (C2), short chain ceramide, plays a role in mediating contraction of cat esophageal smooth muscle cells. We examined the effect of newly synthesized ceramide analogues on the C2-ceramide induced contraction in esophageal smooth muscle cells isolated with collagenase. C2-ceramide produced contraction of smooth muscle cells in a dose dependent manner. (omitted)

• Biomolecules & Therapeutics
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• v.26 no.6
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• pp.546-552
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• 2018

A comprehensive collection of proteins senses local changes in intracellular $Ca^{2+}$ concentrations ($[Ca^{2+}]_i$) and transduces these signals into responses to agonists. In the present study, we examined the effect of sphingosine-1-phosphate (S1P) on modulation of intracellular $Ca^{2+}$ concentrations in cat esophageal smooth muscle cells. To measure $[Ca^{2+}]_i$ levels in cat esophageal smooth muscle cells, we used a fluorescence microscopy with the Fura-2 loading method. S1P produced a concentration-dependent increase in $[Ca^{2+}]_i$ in the cells. Pretreatment with EGTA, an extracellular $Ca^{2+}$ chelator, decreased the S1P-induced increase in $[Ca^{2+}]_i$, and an L-type $Ca^{2+}$-channel blocker, nimodipine, decreased the effect of S1P. This indicates that $Ca^{2+}$ influx may be required for muscle contraction by S1P. When stimulated with thapsigargin, an intracellular calcium chelator, or 2-Aminoethoxydiphenyl borate (2-APB), an $InsP_3$ receptor blocker, the S1P-evoked increase in $[Ca^{2+}]_i$ was significantly decreased. Treatment with pertussis toxin (PTX), an inhibitor of $G_i$-protein, suppressed the increase in $[Ca^{2+}]_i$ evoked by S1P. These results suggest that the S1P-induced increase in $[Ca^{2+}]_i$ in cat esophageal smooth muscle cells occurs upon the activation of phospholipase C and subsequent release of $Ca^{2+}$ from the $InsP_3$-sensitive $Ca^{2+}$ pool in the sarcoplasmic reticulum. These results suggest that S1P utilized extracellular $Ca^{2+}$ via the L type $Ca^{2+}$ channel, which was dependent on activation of the $S1P_4$ receptor coupled to PTX-sensitive $G_i$ protein, via phospholipase C-mediated $Ca^{2+}$ release from the $InsP_3$-sensitive $Ca^{2+}$ pool in cat esophageal smooth muscle cells.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.9
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• pp.5427-5433
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• 2013

5-Azacytidine (5-azaC) was originally identified as an anticancer drug (NSC102876) which can cause hypomethylation of tumor suppressor genes. To assess its effects on runt-related transcription factor 3 (RUNX3), expression levels and the promoter methylation status of the RUNX3 gene were assessed. We also investigated alteration of biologic behavior of esophageal carcinoma TE-1 cells. MTT assays showed 5-azaC inhibited the proliferation of TE-1 cells in a time and dose-dependent way. Although other genes could be demethylated after 5-azaC intervention, we focused on RUNX3 gene in this study. The expression level of RUNX3 mRNA increased significantly in TE-1 cells after treatment with 5-azaC at hypotoxic levels. RT-PCR showed 5-azaC at $50{\mu}M$ had the highest RUNX3-induction activity. Methylation-specific PCR indicated that 5-azaC induced RUNX3 expression through demethylation. Migration and invasion of TE-1 cells were inhibited by 5-azaC, along with growth of Eca109 xenografts in nude mice. In conclusion, we demonstrate that the RUNX3 gene can be reactivated by the demethylation reagent 5-azaC, which inhibits the proliferation, migration and invasion of esophageal carcinoma TE-1 cells.

• Journal of Chest Surgery
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• v.37 no.3
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• pp.261-266
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• 2004

Although significant progress has been made in the surgical treatment of esophageal carcinoma as well as in the detection of early stage esophageal carcinoma by diagnostic techniques, the prognosis of the esophageal carcinoma patients remain poor. The p53 gene product is known to regulate cell growth and proliferation. And the nm23 gene was identified originally as an anti-metastatic influence whose expression was correlated inversely with tumor metastatic potential in murine melanoma cell lines. This experiment was intended to know the relationship among the p53 and nm23 gene expression versus clinicopahologic characteristics of the esophageal cancer. Total 40 cases were collected from patients who had undergone esophagectomy at St. Mary's Hospital, Catholic university of Korea. Immunohistochemical stain for p53 mutant-type protein and nm23 protein was graded as <10% positive tumor cells: negative; 10∼30% positive tumor cells: ＋ ; 30∼50% positive tumor cells: ＋＋, and >50% positive tumor cells: ＋＋＋. The tumor invasion was grades as none:－ ; mild:＋ ; moderate:＋＋ ; severe: ＋＋＋. Overexpression of p53 protein and nm23 was not associated with the survival and cliniocopathologic characteristics of the esophageal cancer. Moreover, the combination analysis of p53 and nm23 revealed that there was no relationship between the gene expression and the clinicopatholic characteristics of the esophageal cancer.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.12
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• pp.6327-6332
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• 2012

Esophageal cancer is a common malignant tumor occurring in human esophageal epithelial tissue. The primary purpose of this paper was to define the effects of ${\beta}$-carotene and 1,25-dihydroxyvitamin $D_3$, alone and in combination, on cell proliferation, cell cycle and apoptosis of human esophageal cancer EC9706 cells. Treatment with different concentrations of ${\beta}$-carotene and/or 1,25-dihydroxyvitamin $D_3$. MTT assay showed that ${\beta}$-carotene and 1,25-dihydroxyvitamin $D_3$ significantly inhibited proliferation of EC9706 cells in a dose- and time-dependent manner. Further studies also demonstrated that ${\beta}$-carotene alone or 1,25-dihydroxyvitamin $D_3$ alone caused a marked increase on the induction of apoptosis in EC9706 cells. The percentage of G0/G1-phase cells significantly increased on addition of 1,25-dihydroxyvitamin $D_3$ alone, but there were no significant changes with ${\beta}$-carotene alone. These two agents in combination synergistically inhibited cell growth and induced apoptosis. Therefore, our results indicate that ${\beta}$-carotene and 1,25-dihydroxyvitamin $D_3$ in combination may provide a novel strategy for preventing and treating esophageal cancer.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.3
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• pp.1397-1401
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• 2014

Aim: To investigate the mechanisms of induction of apoptosis of esophageal cancer cells by esophageal cancer-related gene 2 (ECRG2) in combination with cisplatin (DDP). Methods: Hoechest staining was performed to analyze the effects of single ECRG2 and ECRG2 in combination with DDP on apoptosis of EC9706 cells. The expression levels of p53 and bcl-2 mRNA and protein were determined by RT-PCR and Western blotting, respectively. Results: The number of apoptotic cells after the treatment with ECRG2 in combination with DDP for 24 hours was more than that after the treatment with single ECRG2. RT-PCR and Western blotting showed that the expression levels of bcl-2 mRNA and protein were both down-regulated, while p53 mRNA and protein were both up-regulated in the cells treated with ECRG2 in combination with DDP compared with those given ECRG2 alone. Conclusion: ECRG2 in combination with DDP can enhance the apoptosis of EC9706 cells, possibly by down-regulating bcl-2 expression and up-regulating p53.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.5
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• pp.2359-2362
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• 2014

Background: To investigate the effects of double radiofrequency hyperthermia on Th1/Th2 cells in esophageal cancer patients treated with radiotherapy. Materials and Methods: 22 patients with esophageal cancer were divided into a radiotherapy group (10 cases) and a combined group (double radiofrequency hyperthermia combined with radiotherapy group, 12 cases). Both groups received conventional radiotherapy using a cobalt-60 therapy apparatus (TD60-66Gy/30-33F). Patients in the combined group also underwent double radiofrequency hyperthermia (2F/W, 8-10F). Before and after treatment, Th1, Th2, Tc1 and Tc2 cells in peripheral blood were determined with flow cytometry. Results: In the radiotherapy group, Th1 cell contents before and after radiotherapy were $17.5{\pm}5.26%$ and $9.69{\pm}4.86%$, respectively, with a significant difference (p<0.01). The Th1/Th2 ratio was significantly decreased from $28.2{\pm}14.3$ to $16.5{\pm}10.4 $(p<0.01). In the combined group, Th1 cell content before radiotherapy was $15.9{\pm}8.18%$, and it increased to $18.6{\pm}8.84$ after radiotherapy (p>0.05), the Th1/Th2 ratio decreasing from $38.4{\pm}36.3$ to $28.1{\pm}24.0$ (p>0.05). Changes in Th2, Tc1 and Tc2 cell levels were not significant in the two groups before and after therapy (p>0.05). Conclusions: Double radiofrequency hyperthermia can promote the conversion from Th2 to Th1 cells, and regulate the balance of Th1/Th2 cells.

• Journal of Chest Surgery
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• v.27 no.9
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• pp.812-814
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• 1994

The esophageal cyst result from a wrong cleavage of the primitive gut in the 4 weeks embryo. In embryo and after seperation of the tracheal diverticulum, the esophagus is lined with ciliated cells which are able cover a "cystic duplication". It is often difficult to distinguish between the bronchogenic and the esophageal cyst. Pathological findings showed the presence of a ciliated epithelium without cartilage which was diagnosed as an esophageal cyst. The patient was 21 year old man for evaluation of the cyst in the posterior mediastinum. The cyst was located the intramural esophagus. Microscopically, the cyst was lined with ciliated columnar epithelium and there was no evidence of cartilage. The cyst was confirmed as the intramural esophageal cyst.geal cyst.