Older liver grafts from donation after circulatory death are associated with impaired survival and higher incidence of biliary non-anastomotic structure.

BACKGROUND: Grafts from older donors after circulatory death were associated with inferior outcome in liver transplants in the past. But it has seemed to remain controversial in the last decade, as a result of modified clinical protocols, selected recipients, and advanced technology of organ perfusion and preservation. The present study aimed to examine the impact of older donor age on complications and survival of liver transplant using grafts from donation after circulatory death (DCD). METHODS: A total of 944 patients who received DCD liver transplantation from 2015 to 2020 were included and divided into two groups: using graft from older donor (aged ≥ 65 years, n = 87) and younger donor (age < 65 years, n = 857). Propensity score matching (PSM) was applied to eliminate selection bias. RESULTS: A progressively increased proportion of liver transplants with grafts from older donors was observed from 1.68% to 15.44% during the study period. The well-balanced older donor (n = 79) and younger donor (n = 79) were 1:1 matched. There were significantly more episodes of biliary non-anastomotic stricture (NAS) in the older donor group than the younger donor group [15/79 (19.0%) vs. 6/79 (7.6%); P = 0.017]. The difference did not reach statistical significance regarding early allograft dysfunction (EAD) and primary non-function (PNF). Older livers had a trend toward inferior 1-, 2-, 3-year graft and overall survival compared with younger livers, but these differences were not statistically significant (63.1%, 57.6%, 57.6% vs. 76.9%, 70.2%, 67.7%, P = 0.112; 64.4%, 58.6%, 58.6% vs. 76.9%, 72.2%, 72.2%, P = 0.064). The only risk factor for poor survival was ABO incompatible transplant (P = 0.008) in the older donor group. In the subgroup of ABO incompatible cases, it demonstrated a significant difference in the rate of NAS between the older donor group and the younger donor group [6/8 (75.0%) vs. 3/14 (21.4%); P = 0.014]. CONCLUSIONS: Transplants with grafts from older donors (aged ≥ 65 years) after circulatory death are more frequently associated with inferior outcome compared to those from younger donors. Older grafts from DCD are more likely to develop NAS, especially in ABO incompatible cases.

Breast-conserving in centrally located breast cancer patients confirmed safe by SEER based study.

BACKGROUND: Due to the lack of high-level data, there is still controversy over the oncological safety of breast conservation in patients with centrally located breast cancer. This study aimed to assess the safety of breast-conserving surgery in patients with centrally located breast cancer based on the data from the Surveillance, Epidemiology, and End Results (SEER) database. METHODS: We collected data for all cases diagnosed with breast cancer who underwent breast-conserving surgery from 2012-2014 in the SEER database. The primary outcome of our study was disease-specific survival (DSS) and overall survival (OS). The PSM was used to eliminate the effects of non-random statistics. Chi-square test, Kaplan-Meier method and Cox proportional hazards regression model on univariate and multivariate analysis were used to analyze the data. RESULTS: Data from 79,214 patients who had undergone breast-conserving surgery were analyzed in this study, including those with breast cancer in the central region (n=3,128) and outside the central region (n=76,086). The DSS of central breast cancer patients and outside the central breast cancer patients was 58.1 months versus 58.0 months (P>0.05), respectively, while the OS of the 2 groups was 58.0 months versus 58.0 months (P>0.05), respectively. CONCLUSIONS: Breast cancer in the central region should not be contraindicated for breast conserving surgery and breast-conserving surgery can benefit a wider range of patients.

A Non-Linear Relationship between Preoperative Total Bilirubin Level and Postoperative Delirium Incidence after Liver Transplantation.

This study aimed to explore the correlation between preoperative total bilirubin (TBil) level and postoperative delirium (POD) in orthotopic liver transplantation (OLT). All the OLT consecutively performed between April 2019 and March 2021 were retrospectively reviewed with data retrieved from a prospectively collected database. Logistic regression model and generalized additive model were used to identify both linear and non-linear relationships between TBil and POD. A two-piecewise regression model was performed to calculate the saturation effect. Subgroup analyses were performed using stratified logistic regression models. A total of 402 recipients were enrolled. After fully adjusted for covariates, TBil was indicated to have a non-linear relationship with POD. The two-piecewise regression model showed the inflection point was 20 mg/dL. On the left side of the inflection point, the incidence of POD increased by 5% per 1 mg/dL increment of TBil (p = 0.026). On the right side of the inflection point, the effect size had no statistical significance (OR, 0.97; 95% CI, 0.90-1.05; p = 0.482). The relationship between preoperative TBil level and POD incidence is non-linear in OLT recipients. The incidence of POD is positively correlated with TBil level when it is below 20 mg/dL. A saturation effect is observed when TBil level reaches 20 mg/dL.

Liver Transplantation for Acute-on-Chronic Liver Failure Associated With Acute Necrotizing Pancreatitis: A Case Report.

Liver transplantation (LT) for acute-on-chronic liver failure (ACLF) accompanied by acute necrotizing pancreatitis is still unclear. We have a reported case of LT for ACLF associated with acute necrotizing pancreatitis. The postoperative multiorgan dysfunction and secondary infection were successfully managed under close supervision. The patient was a 47-year-old man with chronic hepatitis B virus infection presented with ACLF and acute necrotizing pancreatitis. After receiving LT from a deceased donor, the patient's liver functioning rapidly reverted to a normal level, and the acute pancreatitis was simultaneously stabilized. However, the patient later developed multiorgan dysfunction secondary to multidrug resistant bacteria infection, which was treated successfully with repeated percutaneous drainage, sensitive antibiotics, continuous renal replacement therapy, microbial balance, and best supportive care. LT can be considered for ACLF associated with acute necrotic pancreatitis without absolute contraindication. Moreover, we recommend a close observation of possible postoperative severe infection, and cautious multidisciplinary management was needed for the prevention of organ dysfunction.

Targeting MUC1-C reverses the cisplatin resistance of esophageal squamous cell carcinoma in vitro and in vivo.

BACKGROUND: The efficacy of chemotherapeutic treatment of esophageal squamous cell carcinoma (ESCC) is limited by drug resistance during. This severely compromises the long-term survival rate of patients. Therefore, reversing chemotherapy resistance in ESCC may improve the therapeutic outcome. Here, we investigated the molecular mechanism of MUC1-C, the C-terminal transmembrane subunit of MUC1 (a transmembrane heterodimer protein), and its role in the reversal of cisplatin sensitivity in ESCC cells. METHODS: We assessed the efficacy of GO-203, a cell-penetrating peptide, as a chemotherapeutic target of MUC1-C using cell proliferation, colony-forming, and transwell assays. Apoptosis was analyzed in GO-203-treated cells by flow cytometry. Tumor xenograft assay was performed in nude mice to corroborate our in vitro findings. RESULTS: GO-203 treatment inhibited cell proliferation and restrained the migration and invasion of cisplatin-resistant ESCC. Moreover, targeting MUC1 resulted in enhanced apoptosis in GO-203-treated cells. These in vitro pro-apoptotic and anti-proliferative effects of GO-203 in combination with cisplatin were validated by in vivo models. Significantly smaller tumor volumes were observed in ESCCs-xenografted nude mice treated with GO-203 in combination with cisplatin compared with mice treated with monotherapy or their control counterparts. We found that blocking MUC1-C with GO-203 significantly reversed the cisplatin resistance in ESCC via modulating Akt and ERK pathways. CONCLUSIONS: Our findings suggest that GO-203 may hold potential as an ancillary therapeutic molecule and a chemosensitizer to improve the outcomes of cisplatin-based chemotherapy especially in patients with cisplatin-resistant ESCC.

EFEMP2 Suppresses the Invasion of Lung Cancer Cells by Inhibiting Epithelial-Mesenchymal Transition (EMT) and Down-Regulating MMPs.

BACKGROUND: Epidermal growth factor-containing fibulin-like extracellular matrix protein 2 (EFEMP2), also known as fibulin-4, MBP1 and UPH1, is an extracellular matrix protein associated with a variety of tumors. The purpose of this study was to investigate the prognostic value and the function of EFEMP2 in lung cancer. METHODS: The mRNA and protein expression of EFEMP2 in lung normal and cancer tissues, lung cancer cell lines (A549, H460, H1299 and H1650) and normal epithelial cell line BEAS-2B were evaluated by immunohistochemistry, RT-qPCR and Western blotting. The Public databases (Oncomine and Kaplan-Meier plotter) were used to investigate the prognostic value of EFEMP2 in lung cancer. RNA interference (RNAi) and overexpression transfection were performed to detect the effects of EFEMP2 up- or down-regulation on lung normal and cancer cell proliferation, invasion and metastasis in vitro and in vivo. RESULTS: EFEMP2 was lowly expressed in lung cancer tissues and cells, and its low expression was associated with malignant phenotype and poor prognosis of lung cancer. The same conclusion had been drawn from the Public databases. EFEMP2 overexpression significantly inhibited the invasion of lung cancer cells, hampered the process of EMT, and decreased the expression and activity of MMP2 and MMP9, while EFEMP2 knockdown remarkably enhanced the invasion of lung cancer cells, promoted EMT, and increased the expression and activity of MMP2 and MMP9. CONCLUSION: The low expression of EFEMP2 was detected in lung cancer and was positively correlated with the poor prognosis of patients. EFEMP2 was a tumor suppressor gene that inhibited the progress of lung cancer, which suggested a new research objective for the future studies.

Signal transducer and activator of transcription 3 overexpression promotes lymph node micrometastasis in early-stage non-small cell lung cancer.

BACKGROUND: Signal transducer and activator of transcription 3 (STAT3) is constitutively activated in several malignancies. Here, we define the correlation between STAT3 expression and lymph node micrometastasis of early-stage non-small cell lung cancer. Then we highlight some possibilities associated with developing a way to detect tumor micrometastasis and an anticancer drug that might therapeutically inhibit the STAT3 signaling pathway. METHODS: The samples were collected from 50 patients with early-stage non-small cell lung cancer and 50 patients with benign lung tumors. Mucin 1 mRNA expression was evaluated to determine lymph node micrometastasis status. STAT3 mRNA, STAT3 protein, and phosphorylated STAT3 protein expression were evaluated through reverse transcription polymerase chain reaction, western blot, and immunohistochemistry, respectively. Measurement data was represented as mean ± standard deviation, and the t-rest or F-test were used. The χ2 -test was used in enumeration data. Logistic regression analysis was carried out to determine the independent risk factors influencing lymph node micrometastasis. RESULTS: STAT3 mRNA and proteins expression were correlated with lymph node micrometastasis (P < 0.05). Logistic regression analysis revealed STAT3 protein overexpression and the differentiation degree of tumors were independent risk factors for lymph node micrometastasis. CONCLUSION: Overexpression of STAT3 might promote lymphatic micrometastasis of early-stage non-small cell lung cancer and might be a clinical predictor of lymph node micrometastasis.

CCL21-CCR7 promotes the lymph node metastasis of esophageal squamous cell carcinoma by up-regulating MUC1.

BACKGROUND: CCR7 and MUC1 are correlated with lymph node metastasis in ESCC, but the role of MUC1 in the CCR7-induced lymphatic metastasis and the underlying molecular mechanism is still unclear. METHODS: The expression of CCR7 and MUC1 was detected in the ESCC samples by IHC, and the clinical significance of CCR7 and MUC1 in ESCC was analyzed. The expression of CCR7 and MUC1 in ESCC cell lines was detected by qRT-PCR and western blot. The effect of CCL21 on the migration and invasion of ESCC cells was determined by transwell assay. The activity of MUC1 promoter was determined by luciferase reporter assay. The activation of Erk, Akt and Sp1 was detected by western blot and the binding of Sp1 to the MUC1 promoter was determined by ChIP. RESULTS: The co-expression of CCR7 and MUC1 was detected in 153 ESCC samples by IHC, and both were correlated with lymph node metastasis, regional lymphatic recurrence and poor prognosis. Correspondingly, increasing levels of MUC1 mRNA and protein were detected in the ESCC cell lines KYSE410 and Eca9706 after treatment with CCL21 in a time- and dose-dependent manner. Furthermore, silencing MUC1 could remarkably suppress the invasion and migration of ESCC cells induced by CCL21. Moreover, heterologous CCR7 promoted the invasion and migration of KYSE150 and up-regulated MUC1 expression. Increasing levels of activated ERK1/2 and Akt were detected in KYSE410 after treating the cells with CCL21, and inhibiting the activation of ERK1/2 but not Akt caused the increased transcription of MUC1. Finally, the phosphorylation of Sp1 induced by ERK1/2 and subsequent increases in the binding of Sp1 to the muc1 promoter at -99/-90 were confirmed to cause the up-regulation of MUC1 induced by CCL21-CCR7. CONCLUSIONS: Our findings suggested that MUC1 plays an important role in CCL21-CCR7-induced lymphatic metastasis and may serve as a therapeutic target in ESCC.

Activated STAT3 correlates with prognosis of non-small cell lung cancer and indicates new anticancer strategies.

PURPOSE: Aberrant activation of the signal transducer and activator of transcription 3 (STAT3) occurs in many human tumors. Many studies have provided compelling evidence for the critical role of aberrant STAT3 activity in malignant transformation and tumor progression. But few of them provided data on whether activated STAT3 overexpression correlated with patients' prognosis. Here, we define the relationship between phosphorylated STAT3 (pSTAT3) function and prognosis of non-small cell lung cancer (NSCLC). METHODS: Immunohistochemical analyses were carried out on 82 surgically resected NSCLC tissues to evaluate the expression level of pSTAT3. The Kaplan-Meier method was used to calculate the survival rate, and the log-rank test was performed to compare the survival difference. Cox regression analysis was performed to identify prognostic risk factors. All statistic analyses were performed with SPSS11.5 statistical software. Differences were considered significant when the P value was <0.05. RESULTS: In this study, we identified nuclear pSTAT3 expression in 59.76 % of tumors. pSTAT3 expression was correlated with differentiation degree of tumors (P < 0.05), lymph node metastasis status (P < 0.01), clinical stage of tumors (P < 0.01) and the prognosis of NSCLC patients after surgical resection (P < 0.05). CONCLUSIONS: pSTAT3 overexpression is an important factor related to prognosis of NSCLC patients and indicates new anticancer strategies.

Therapeutic efficacy evaluation of postoperative adjuvant radiotherapy in mid-thoracic esophageal carcinoma patients underwent Ivor Lewis esophagectomy with two-field lymphadenectomy.

The objective of this paper is to study the treatment outcome of postoperative adjuvant radiation therapy in Ivor Lewis esophagectomy with two-field lymphadenectomy (2FL) and evaluate whether the method can replace three-field lymphadenectomy (3FL). We collected a consecutive series of 503 patients who had undergone Ivor Lewis esophagectomy with 2FL over a seven-year period in our department and evaluated the therapeutic efficacy of postoperative adjuvant radiation therapy. Recurrence and survival rates were calculated with the Kaplan-Meier method, and the differences were compared by the log-rank test. Logistic regression analysis was used to test risk factors for postoperative lymph node metastasis. Cox regression analysis was used to identify prognostic risk factors. The overall 3- and 5-year survival rates were 62.8 and 34.4 %, respectively. There was a significant difference in 5-year survival rate between patients received adjuvant radiation therapy and did not receive radiation therapy. Postoperative adjuvant radiation therapy for patients who underwent Ivor Lewis esophagectomy with 2FL may offer the patients significant survival benefits and reduces the incidence of recurrence in cervical and superior mediastinal lymph nodes.

Inactivation of RUNX3 predicts poor prognosis in esophageal squamous cell carcinoma after Ivor-Lewis esophagectomy.

The inactivation of RUNX3 in various cancers has been reported while the expression of RUNX3 on protein level in esophageal squamous cell carcinoma (ESCC) and its relationship with pathological parameters and prognosis still remained unclear. In this study, we examined the expression of RUNX3 in 158 ESCC samples and 20 normal esophageal mucosa samples by immunohistochemistry and qRT-PCR. The IHC result showed that RUNX3 was detected mainly in the nuclei of basal layer cells in 18 of 20 normal mucosa samples while in 158 ESCC samples, there were 46 with RUNX3 nuclei expression, 37 RUNX3 cytoplasmic expression, and 75 negative expression. The qRT-PCR confirmed the downregulation of RUNX3 mRNA in the RUNX3 protein negative group than in the RUNX3 nuclei and cytoplasmic expression group (P < 0.001), and the methylation-specific PCR showed a low methylation rate in the ESCC tissue samples with RUNX3 protein negative expression (6/40, 15%). The RUNX3 nuclei expression negatively correlated with the lymph node metastasis (P = 0.033) and recurrence status (P = 0.019), and the survival analysis showed that the patients with RUNX3 nuclei expression had a higher 5-year survival rate than the patients with RUNX3 cytoplasmic/negative expression (P = 0.022). The Cox regression analysis showed that the T classification (P = 0.001), lymph node metastasis (P < 0.001), and RUNX3 inactivation (negative/cytoplasmic expression, P = 0.039) were independent risk factor of poor prognosis. In conclusion, we found a frequent inactivation of RUNX3 due to low expression and cytoplasmic dislocalization in ESCC. The inactivation of RUNX3 may be involved in the progression of ESCC, and RUNX3 could be an indicator of prognosis for patients with ESCC after surgery.

microRNA­802 promotes lung carcinoma proliferation by targeting the tumor suppressor menin.

microRNAs play important roles in numerous biological processes, including tumorigenesis, by modulating critical gene transcripts. In the present study, the role of microRNA­802 (miR­802) in lung cancer was investigated. The results of the quantitative polymerase chain reaction revealed that expression levels of miR­802 were significantly upregulated in lung cancer tissues. In vitro experiments demonstrated that miR­802 promoted cell proliferation in A549, NCI­H358 and NCI­H1299 cells. Furthermore, it was indicated that miR­802 promoted the proliferation of lung carcinoma by targeting the tumor suppressor menin. Therefore, these results suggest a previously unknown miR­802/menin molecular network controlling lung carcinoma development.

Correlation between Vascular Endothelial Growth Factor C Expressior and Lymph Node Micrometastasis and Prognosis in Patients with pNO Esophageal Squamous Cell Carcinomas.

BACKGROUND/AIMS: The purpose of this study was to investigate the correlation between vascular endothelial growth factor C expression and lymph node micrometastasis and prognosis in patients with pN0 esophageal squamous cell carcinoma. METHODOLOGY: A total of 528 lymph nodes obtained from the 87 patients with pN0 esophageal squamous cell carcinoma who underwent Ivor-Lewis esophagectomy were reevaluated by reverse transcriptasepolymerase chain reaction to detect mucin 1 mRNA. Vascular endothelial growth factor C mRNA was detected in esophageal cancer issues also by re-evaluated by reverse transcriptasepolymerase chain reaction. RESULTS: Vascular endothelial growth factor C mRNA expression was correlated with tumor invasion (P < 0.01) and lymphatic invasion (P = 0.000). In univariate analysis by log-rank test, the 5-year survival rate in patients after operation was significantly associated with tumor invasion (P = 0.026), mucin 1 mRNA expression (P = 0.000) and vascular endothelial growth factor C mRNA expression (P = 0.020). The results of Cox regression multivariate analysis confirmed that tumor invasion status and mucin 1 mRNA expression were the independent relevant factors. CONCLUSION: Expression of vascular endothelial growth factor C is related to tumor invasion and lymphatic invasion and is not related to lymph node micrometastasis in patients with pN0 esophageal squamous cell carcinoma.

The relationship between KRAS gene mutations and HLA class I antigen downregulation in the metastasis of non-small cell lung cancer.

OBJECTIVE: To investigate the association between v-Ki-ras2 Kirsten rat sarcoma viral oncogene homologue (KRAS) gene mutations and levels of human leucocyte antigen (HLA) class I antigen in primary lung tumours and metastatic lymph nodes of patients with non-small cell lung cancer (NSCLC). METHODS: Patients with NSCLC undergoing tumour resection were enrolled. KRAS codon 12 mutations were analysed in normal lung and lymph node tissue, primary lung tumours and metastatic lymph nodes using polymerase chain reaction-restriction fragment length polymorphism analysis. HLA class I antigen immunostaining was examined using flow cytometry. RESULTS: A total of 65 patients participated in the study. All normal lung tissues had positive HLA class I antigen immunostaining. The majority of primary lung tumours (56/65) and all of the metastatic lymph nodes (31/31) had downregulated HLA class I antigen immunostaining. There was a positive correlation between downregulated HLA class I antigen in primary tumours and metastatic lymph nodes. There was a negative correlation between KRAS codon 12 mutations and the level of HLA class I antigen in primary and metastatic tumours. CONCLUSIONS: KRAS codon 12 mutations appear to be important in the downregulation of HLA class I antigen in NSCLC. Abnormal activation of the oncogenic KRAS pathway might provide a new treatment target for NSCLC.

Congruence in symptom assessment between hepatocellular carcinoma patients and their primary family caregivers in China.

OBJECTIVES: The aims of this cross-sectional study were to explore the agreement in symptom evaluation results between patients and their family caregivers and to search for the possible factors influencing the agreement. METHODS: A convenience sample of 280 dyads consisting of hepatocellular carcinoma patients and their family caregivers was included in this study. All of them completed the symptom checklist of Chinese version of the M. D. Anderson symptom inventory and the evaluations of six common symptoms of hepatocellular carcinoma. RESULTS: The levels of agreement ranged from moderate to substantial. A number of factors associated with caregivers (particularly depression state, age, others helping to care for the patient or not, and the relationship with patient) and patients (traditional Chinese medicine treatment, religion, KPS scores, and educational levels) were significantly correlated with levels of disparity on some symptoms. CONCLUSION: The study illustrates that family caregivers of hepatocellular carcinoma patients can provide reasonable reports on patients' symptoms. Healthcare providers need to pay special and sufficient attention to the caregivers' depression.

CCR7: A metastasis and prognosis indicator of postoperative patients with esophageal carcinoma.

BACKGROUND/AIMS: To investigate the expression of CC chemokine receptor 7 (CCR7) and its relationship to the metastasis and prognosis in esophageal squamous cell carcinoma (ESCC) after esophagectomy. METHODOLOGY: CCR7 expression was detected by immunohistochemistry. Kaplan-Meier method was performed to calculate the survival rate, Cox regression multivariate analysis was performed to determine independent prognostic factors. RESULTS: CCR7 expression rate in T1, T2 and T3 patients was 27.3%, 64.7% and 75.2%, respectively, the difference of CCR7 protein expression was statistically significant (p=0.000). The positive expression of CCR7 in patients with lymph node metastasis was significantly higher than those without metastasis (p=0.000). CCR7 expression correlated with significantly worsened 5-year survival for all patients as well as those with T2 and T3 tumors, N0 nodal status or N1 nodal status. The result of Cox analysis demonstrated that N stage, T stage and CCR7 expression were independent prognostic factors. CONCLUSIONS: CCR7 expression was detected in ESCC and was found to be significantly associated with T stage and lymph node metastasis. The 5-year survival rate was significantly lower in patients with CCR7 expression in those without. Invasion, lymph node metastasis and CCR7 expression were independent factors.

A 39-year-old man with dyspnoea, low forced expiratory volume and a large mass of the left hemithorax.

In patients with intrathoracic neoplasms, low forced expiratory volume (FEV1) can preclude surgical treatment. Here, we present a case of a giant solitary fibroma of the pleura (SFTP) successfully treated by surgical removal in spite of low FEV1. A 39-year-old male patient was referred to our hospital with dyspnoea and chest distress. Computed tomography (CT) showed a large mass in the left chest. Spirometry showed FEV1 1.4 L (39% of the expected value). Computed tomography scan-guided transcutaneous aspiration biopsy was performed on the patient, and microscopic examination of the specimen revealed spindle tumor cells with a background of abundant collagen. Complete surgical resection was accomplished. The tumor was large and encapsulated. It measured 28 cm × 20 cm × 18 cm. The definitive diagnosis obtained by histopathology after resection was benign SFTP. The patient felt no dyspnoea at discharge. Surgical treatment of SFTP should be considered even in patients with a huge tumor and with increased post-operative risk.

Curative effect comparison between Ivor-Lewis esophagectomy and left transthoracic esophagectomy in treatment of middle thoracic esophagus carcinoma.

BACKGROUND/AIMS: The aim of this study is to compare and evaluate the therapeutic efficacy of Ivor-Lewis esophagectomy and one incision esophagectomy through left thoracic and above aortic arch anastomosis approach (left transthoracic esophagectomy) in order to choose a proper surgical procedure to treat middle esophageal carcinoma. METHODOLOGY: Patients who underwent Ivor-Lewis esophagectomy (n=132) and who underwent left transthoracic esophagectomy (n=52) between January 2003 and June 2005 were included. The survival rate was calculated by Kaplan-Meier method and the prognostic risk factors were assessed by Cox regression analysis. RESULTS: Postoperative complications occurred in 43 patients (23.4%), with 31 patients (23.5%) and 12 patients (23.1%) in the Ivor-Lewis group and in the left transthoracic esophagectomy group, respectively. The overall 5-year survival rate was 36.4%, with 37.1% and 34.6% in the Ivor-Lewis group and in the left transthoracic esophagectomy group, respectively (p>0.05). In Cox regression analysis, T classification (HR=1.43, p=0.025) and N classification (HR=1.76, p=0.004) were the independent prognostic risk factors. CONCLUSIONS: Ivor-Lewis esophagectomy and left transthoracic esophagectomy are both feasible options to treat middle thoracic esophageal squamous cell carcinoma. Patients' individual condition is suggested to be taken into account when choosing the operative approach.

Mucin 1 and vascular endothelial growth factor C expression correlates with lymph node metastatic recurrence in patients with N0 esophageal cancer after Ivor-Lewis esophagectomy.

BACKGROUND: The purpose of the present study was to investigate the risk factors associated with lymph node metastatic recurrence in patients with N0 esophageal cancer after Ivor-Lewis esophagectomy based on the detection of Mucin 1 mRNA and vascular endothelial growth factor (VEGF) C mRNA. METHODS: The subjects were 82 patients with pN0 esophageal cancer who underwent Ivor-Lewis esophagectomy with two-field lymph node dissection from January 2001 to January 2005. A total of 501 lymph nodes obtained from these patients were re-evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR) to detect mucin l (MUC1) mRNA; VEGF-C mRNA was also detected in esophageal cancer issues by RT-PCR. The diagnosis of lymph node micrometastasis (LNMM) was based on the detection of MUC1 mRNA. The Kaplan-Meier method was used to calculate the survival rate and lymph nodal metastatic rate, the log-rank test was performed to compare the recurrence rate, and Cox regression multivariate analysis was performed to determine independent prognostic factors. RESULTS: MUC1 mRNA was detected in 29 lymph nodes from 23 patients, which accounted for 5.79% of all the 501 lymph nodes and 28.05% of all 82 patients, respectively. Vascular endothelial growth factor C mRNA was identified in esophageal cancer issues from 42 (51.22%) patients. The overall 3- and 5-year survival rates of 82 patients were 78.0 and 51.2%, respectively. First recurrence exhibiting lymph nodal metastasis was recognized in 37 patients (45.1%) in the first 3 years after operation. The lymph node metastatic rate in patients in the first 3 years after operation was significantly associated with T status (p < 0.05) and the lymph node metastatic rate of the patients with LNMM was significantly higher than that of the patients without LNMM (p < 0.01). The lymph node metastatic rate of the patients with VEGF-C mRNA expression in esophageal cancer tissues was significantly higher than that of the patients without VEGF-C mRNA expression (p < 0.01).The results of multivariate analysis confirmed that VEGF-C mRNA expression in esophageal cancer tissues, LNMM, and T status in patients with N0 esophageal cancer were independent relevant factors for 3-year lymph node metastatic recurrence after Ivor-Lewis esophagectomy. CONCLUSIONS: Vascular endothelial growth factor C mRNA expression in esophageal cancer tissues, LNMM, and T status in patients with N0 esophageal cancer were independent risk factors for 3-year lymph node metastatic recurrence after Ivor-Lewis esophagectomy. Adjunctive therapy might be beneficial in controlling the locoregional recurrence and elevated healing rates for certain patients.