Jin Wang Park;Won Gi Jeong;Jong Eun, Lee;Hyo-jae Lee;So Yeon Ki;Byung Chan Lee;Hyoung Ook Kim;Seul Kee Kim;Suk Hee Heo;Hyo Soon Lim;Sang Soo Shin;Woong Yoon;Yong Yeon Jeong;Yun-Hyeon Kim
Korean Journal of Radiology
/
v.22
no.1
/
pp.139-154
/
2021
Magnetic resonance imaging (MRI) has become a crucial tool for evaluating mediastinal masses considering that several lesions that appear indeterminate on computed tomography and radiography can be differentiated on MRI. Using a three-compartment model to localize the mass and employing a basic knowledge of MRI, radiologists can easily diagnose mediastinal masses. Here, we review the use of MRI in evaluating mediastinal masses and present the images of various mediastinal masses categorized using the International Thymic Malignancy Interest Group's three-compartment classification system. These masses include thymic hyperplasia, thymic cyst, pericardial cyst, thymoma, mediastinal hemangioma, lymphoma, mature teratoma, bronchogenic cyst, esophageal duplication cyst, mediastinal thyroid carcinoma originating from ectopic thyroid tissue, mediastinal liposarcoma, mediastinal pancreatic pseudocyst, neurogenic tumor, meningocele, and plasmacytoma.
Purpose: Since preoperative staging in esophageal cancer is important in both therapy and prognosis, there had been many efforts to improve its accuracy. Recent studies indicate that whole body FDG-PET has high sensitivity in detection of metastasis in esophageal cancer. Therefore, we added FDG-PET to other conventional methods in staging esophageal cancer to evaluate the usefulness of this method. Materials & Methods: Subjects were 142 esophageal cancer patients (average $62.3{\pm}8.3$ yrs) who received CT and PET just before operation. First, we compared N stage and M stage of the CT or PET with those of the post-operative results. Then we compared the stage according to the EUS (T stage) and CT (N and M stage) or SUS (T stage) and CT & PET (N and M stage) to that according to the post-operative results. Results: Among 142 patients, surgical staging of 69 were N0 and 73 were N1. In M staging, 128 were M0 and 14 were M1. Sensitivity, specificity, and accuracy of N staging were 35.6%, 89.9%, 62.0% with CT and 58.9%, 71.0%, 64.7% with PET, respectively. In M staging, 14.3%, 96.9%, 88.7% with CT and 50.0%, 94.5%, 90.1%, with PET, respectively. The concordances of [EUS+CT] and [EUS+CT+PET] with post-operative results were 41.2% and 54.6%, respectively and there was significant improvement of staging with additional PET scan (p<0.005). Conclusion: The concordance of [EUS+CT+PET] with post-operative result was significantly increased compared to that of [EUS+CT]. Thus, the addition of FDG-PET with other conventional methods may enable more accurate preoperative staging.
Background: Weight loss during chemotherapy has not been exclusively investigated. Macrophage inhibitory cytokine-1 (MIC-1) might play a role in its etiology. Here, we investigated the prognostic value of weight loss before chemotherapy and its relationship with MIC-1 concentration and its occurrence during chemotherapy in patients with advanced esophageal squamous cell carcinoma (ESCC). Materials and Methods: We analyzed 157 inoperable locally advanced or metastatic ESCC patients receiving first-line chemotherapy. Serum MIC-1 concentrations were assessed before chemotherapy. Patients were assigned into two groups according to their weight loss before or during chemotherapy:>5% weight loss group and ${\leq}5%$ weight loss group. Results: Patients with weight loss>5% before chemotherapy had shorter progression-free survival period (5.8 months vs. 8.7 months; p=0.027) and overall survival (10.8 months vs. 20.0 months; p=0.010). Patients with weight loss >5% during chemotherapy tended to have shorter progression-free survival (6.0 months vs. 8.1 months; p=0.062) and overall survival (8.6 months vs. 18.0 months; p=0.022), and if weight loss was reversed during chemotherapy, survival rates improved. Furthermore, serum MIC-1 concentration was closely related to weight loss before chemotherapy (p=0.001) Conclusions: Weight loss both before and during chemotherapy predicted poor outcome in advanced ESCC patients, and MIC-1 might be involved in the development of weight loss in such patients.
Microsatellites are short tandem repeated nucleotide sequences that are present throughout the human genome. Variations in the repeat number or a loss of heterozygosity around the microsatellites have been termed a microsatellite alteration (MA). A MA reflects the genetic instability caused by an impairment in the DNA mismatch repair system and is suggested to be a novel tumorigenic mechanism. A number of studies have reported that MA in the DNA extracted from the plasma occurs at varying frequencies among patients with a non-small cell lung carcinoma (NSCLC). The genomic DNA from 9 subjects with a non-small cell lung cancer (squamous cell cancer 6, adenocarcinoma 2, non-small cell lung cancer1) and 9 age matched non-cancer control subjects (AMC: tuberculosis 3, other inflammatory lung disease 6) and 12 normal control subjects (NC) were extracted from the peripheral blood leukocytes and plasma. Three microsatellite loci were amplified with the primers targeting the Gene Bank sequence D21S1245, D3S1300, and D3S1234. MA in the form of an allelic loss or a band shift was examined with 6% polyacrylamide gel electrophoresis and silver staining. None (0/12) of the NC subjects less than 40 years of age showed a MA in any of the three markers, while 88.9%(8/9) of the AMC above 40 showed a MA in at least one of the three markers (p<0.05). Sixty percent(6/10) of the control subjects with a smoking history showed a MA in one of the three markers, while 9.1%(1/11) of the control subjects without smoking history showed a MA (p<0.05). However, not only did 66.7%(6/9) of lung cancer patients show a MA in at least one of the three markers but so did 88.9%(8/21) of the AMC patients (p>0.05). In conclusion, a MA in the D21S1245, D3S1300, and D3S1234 loci using DNA extracted from the plasma was detected in 66.7% of lung cancer while no MA was found in the young non-smoking control subjects. However, many of the non-cancer control subjects (aged smokers) also showed a MA, which compromised the specificity of the MA analysis as a screening test. Therefore, a further study with a larger sample size will be needed.
Background: The origin site of carcinoma invading esophagogastric junction is variable. It may arise from squamous cell carcinoma of low esophagus, adenocarcinoma arising from Barrett's esophagus, adenocarcinoma of gastric cardia, or extension from proximal stomach cancer. In Korea, the majority of adenocarcinoma invading esophago-gastric junction seems to arise from proximal gastric carcinoma. Material and Method: We reviewed the data of surgically-resected gastric adenocarcinoma involving esophagogastric junction in KCCH between 1988 and 1999. Result: There were 212 cases. Male to female ratio was 156 to 56. Age distribution was between 22 and 78. Variable surgical approaches including median laparotomy, laparotomy with left or right thoracotomy, left thoracotomy, and thoracoabdominal approach were used. Postoperative pathologic stages were : Stage IA-7, IB-11, Ⅱ-25, ⅢA-73, ⅢB-34, and Ⅳ-57. Curative resection was performed in 199 patients, and total gastrectomy was performed in 200 patients. There were 77.4%(164 cases) with esophageal involvement, 74.1%(157 cases) with tumor involvement in the abdominal LN, and 8%(17 cases) with mediastinal LN metastasis. Operative mortality was 3.3%, and over-all 5 year survival rate was 35%. Conclusion: There are various surgical approaches and many things to consider for surgical resection, thoracic and abdominal approach may need for obtain proper resection margin and adequate lymph node dissection in stomach cancer invading esophagogastric junction.
Licochalcone C (LCC; PubChem CID:9840805), a chalcone compound originating from the root of Glycyrrhiza inflata, has shown anticancer activity against skin cancer, esophageal squamous cell carcinoma, and oral squamous cell carcinoma. However, the therapeutic potential of LCC in treating colorectal cancer (CRC) and its underlying molecular mechanisms remain unclear. Chemotherapy for CRC is challenging because of the development of drug resistance. In this study, we examined the antiproliferative activity of LCC in human colorectal carcinoma HCT116 cells, oxaliplatin (Ox) sensitive and Ox-resistant HCT116 cells (HCT116-OxR). LCC significantly and selectively inhibited the growth of HCT116 and HCT116-OxR cells. An in vitro kinase assay showed that LCC inhibited the kinase activities of EGFR and AKT. Molecular docking simulations using AutoDock Vina indicated that LCC could be in ATP-binding pockets. Decreased phosphorylation of EGFR and AKT was observed in the LCC-treated cells. In addition, LCC induced cell cycle arrest by modulating the expression of cell cycle regulators p21, p27, cyclin B1, and cdc2. LCC treatment induced ROS generation in CRC cells, and the ROS induction was accompanied by the phosphorylation of JNK and p38 kinases. Moreover, LCC dysregulated mitochondrial membrane potential (MMP), and the disruption of MMP resulted in the release of cytochrome c into the cytoplasm and activation of caspases to execute apoptosis. Overall, LCC showed anticancer activity against both Ox-sensitive and Ox-resistant CRC cells by targeting EGFR and AKT, inducing ROS generation and disrupting MMP. Thus, LCC may be potential therapeutic agents for the treatment of Ox-resistant CRC cells.
The classic approach for esophagectomy is via the combined thoracic and abdominal approach. Controversy exists whether patients with esophageal carcinoma are best managed with Ivor-Lewis esophagectomy(ILO) as combined thoracic and abdominal approach or transhiatal esophagectomy(THO). The THO approach is known to be superior with respect to operative time, severity of leak, morbidity/mortality, and length of stay, but may represent an inferior cancer operation as a result of survival disadvantage due to inadequate mediastinal clearance compared with ILO. Accordingly, we reviewed the results of our esophageal resections to compare these outcome parameters for each operative approach. Material and Method: From January 1993 to July 2001, We performed a retrospective review of all esophagectomies performed at Keimyung University Dongsan ·Medical Center; 27 underwent THO, and 45 underwent ILO Result: The two groups were comparable in terms of age, sex, and stage of the disease. Mean tumor length and mean operative time were 3.81cm and 354 minutes for THO versus 5.31cm and 453 minutes for ILO, respectively (p<0.01 and p<0.001). Respiratory complications were 11.1% for THO versus 35.6% for ILO(p<0.05). Hospital mortality was 11.1% for THO versus 22.2% for ILO. There were no significant differences between THO and ILO with respect to other types of complications, amount of blood transfusion, leak and stricture rates, and hospital stay. Overall long-term survival at 5 years was 37%, respectively. Conclustion: There was no significant difference in long-term survival of patients of both operative approach. ILO had significant difference in respiratory complications associated with hospital mortality. Hence, THO is a valid alternative to ILO for well selected patients. And either approach appears to be acceptable depending on the surgeons, preferences and experiences.
Purpose :We peformed the retrospective analysis to find the outcome of external beam radiotherapy alone in advanced esophageal cancer patients. Methods and Materials : One hundred and six Patients treated with external beam radiotherapy alone between July 1990 and December 1996 were analyzed retrospectively. We limited the site of the lesions to the thoracic esophagus and cell type to the squamous cell carcinoma. Follow-up was completed in 100 patients (94$\%$) and ranged from 1 month to 92 months (median; 6 months). Results :The median age was 62 years old and male to female ratio was 104 2. Fifty-three percent was the middle thorax lesion and curative radiotherapy was peformed in 83$\%$. Mean tumor dose delivered with curative aim was 58.6 Gy (55$\~$70.8 Gy) and median duration of the radiation therapy was 53 days. The median survival of all patients was 6 months and )-year and 2-year overall survival rate was 27$\%$ and 12$\%$, respectively, Improvement of dysphagia was obtained in most patients except for 7 patients who underwent feeding gastrostomy. The complete response rate immediately after radiation therapy was 32$\%$ (34/106). The median survival and 2-year survival rate of the complete responder was 14 months and 30$\%$ respectively, while those of the nonresponder was 4 months and 0$\%$ respectively (p=0.000). The median survival and 2-year survival rate of the patients who could tolerate regular diet was 9 months and 16$\%$ while those of the patients who could not tolerate regular diet was 3 months and 0$\%$, respectively (p=0.004). The survival difference between the patients with S cm or less tumor length and those with more than 5 cm tumor length was marginally statistically significant (u=0,06). However, the survival difference according to the periesophageal invasion or mediastinal tyrnphadenopathy in the chest CT imaging study was not statistically significant in this study. In a multivariate analysis, the statistically significant covariates to the survival were complete response to radiotherapy, tumor length, and initial degree of dysphagia in a decreasing order. The complication was observed in 10 patients (9$\%$). Conclusion :The survival outcome for advanced esophageal cancer patients treated by external beam radiotherapy alone was very poor. In the treatment of these patients, the brachytherapy and chemotherapy should be added to improve the treatment outcome.
This is a retrospective study of 62 patients with unresected squamous cell carcinoma of the esophagus treated by radiotherapy alone (25 patients) or combined chemotherapy and radiotherapy (37 patients). Of these, 14 of 25 patients treated by radiation therapy alone and 25 of 37 patients treated by combined chemotherapy and radiotherapy completed radiotherapy consisting of 55 to 60 Gy in 5 to 6 weeks and were analyzed for local control rate and survival rate. Follow up ranged from 6 days to 58 months. Three ($8\%$) of 39 patients had a complete response, twenty-eight ($72\%$) a partial response and eight ($20\%$) minimal or no response. Overall median survival was 11 months for all stages. The 1 year and 2 year actuarial survival rates were $48.6\%$ and $13\%$ respectively. Age and stage had prognostic significances (p <0.05, p<0.05 respectively). The 1 year survival rate was $70.1\%$ for stage I, $47.6\%$ for stage II, and $28.4\%$ for stage III. The median survival was 19 months for stage I, 11 months for stage II, 6 months for stage III, and 5.5 months for stage III with distant metastases. The 1 year survival rate of patients 55 years and above was $69.6\%$, 54 years and below was $0\%$. There was no significant difference in survival rate between treatment modalities, locations of tumor, and responses of tumor.
Objective: To determine whether CDX2 and villin protein expression are associated with intestinal metaplasia (IM) in gastric cardiac mucosa and to explore the relationship with evolution of gastric cardiac adenocarcinoma (GCA). Methods: We studied 143 gastric cardiac biopsy or resection specimens from Henan province China, including 25 cardiac gastritis specimens with IM, 65 dysplasia specimens with IM and 35 gastric cardiac adenocarcinoma specimens and stained them for CDX2 and villin by the immunohistochemical SP method. 15 normal gastric cardiac biopsy specimens were also collected as control. Results: (1) Normal gastric mucosa presented no CDX2 and villin expression. The positive rates of CDX2 protein in cardiac gastritis with IM, dysplasia with IM, and carcinoma tissues were 84.0% (21/25), 66.7% (32/48) and 36.4% (20/55), respectively. While the positive rates of villin protein in cardiac gastritis with IM, dysplasia with IM, and carcinoma tissues were 76.0% (19/25), 70.8% (34/48) and 45.5% (25/55), respectively. There were significant differences among the three groups for both CDX2 and villin (P<0.01). Spearman's rank correlation coefficient(rho) showed a close correlation between the two proteins (r=0.843, P<0.01) and both were positively related with tumor differentiation (both P<0.05), but not associated with age, sex, invasion and metastasis of lymph node (P>0.05). Conclusion: Our results suggest that ectopic expression of CDX2 and villin may be involved in early-stage IM and tumorigenesis in gastric cardia and the expression of villin may be regulated by CDX2.
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