crossing96/oncoscreening huggingface dataset:
PML protein as a prognostic molecular marker for patients with esophageal squamous cell carcinomas receiving primary surgery.	BACKGROUND AND OBJECTIVES: We evaluated the clinicopathological associations and prognostic implications of promyelocytic leukemia gene (PML) expressions in patients with esophageal squamous cell carcinomas (ESCC) receiving primary surgery. METHODS: Expression patterns of PML and tumor protein 53 (TP53) of 132 cases of ESCC were evaluated by immunohistochemistry and correlated with clinicopathological parameters. The Cox proportional hazards model was used to determine the prognostic influence of clinicopathological factors on progression-free survival (PFS) and overall survival (OS). RESULTS: Forty-two cases (31.82%) were classified as lost expression of PML, 25 (18.94%) as focally positive, and 65 (49.24%) as diffusely expressed. Sixty-three cases (47.73%) were classified as over-expression of TP53. High expression of TP53 and down-regulation of PML were often found in advanced disease; and, in together with high pathological staging, grading, and positive margin, were associated with poor survival. However, only tumor differentiation (P = 0.016), distant metastasis (P = 0.001), and PML expression (P = 0.001) could act as independent prognostic factors for PFS, and LN metastasis (P = 0.004), TP53 (P = 0.006), and PML expression (P = 0.029) were identified as independent prognostic factors for OS in multivariate analysis. CONCLUSIONS: Our study demonstrated PML protein as an independent prognostic marker for patients with ESCC receiving primary surgery.	esophagus
Risk of perforation during dilation for esophageal strictures after endoscopic resection in patients with early squamous cell carcinoma.	BACKGROUND AND STUDY AIMS: Growing evidence suggests that esophageal stricture frequently develops after endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD) in early esophageal cancer patients, with an incidence proportional to the greater extent of mucosal defects resulting from improved EMR/ESD techniques. There seems to be a potential risk of perforation during bougienage in such patients. PATIENTS AND METHODS: 648 stricture dilations for 78 lesions in 76 patients were consecutively included. The outcomes after combined use of Maloney and Savary wire-guided bougienage for esophageal strictures after EMR/ESD were analyzed in a single-institute retrospective case series study. The perforation rate was determined and risk factors for perforation were identified. RESULTS: Patients underwent a median of 5.0 dilation procedures performed over a median 3.0 months for post-EMR/ESD strictures. Initial dilation was done a median 14 days following endoscopic resection. Perforations developed in seven patients (7/648 dilation procedures, 1.1%), all in the lower esophagus, and bleeding occurred in one patient (0.1% dilations). Two independent risk factors for development of perforation during dilation therapy for post-EMR/ESD stricture were identified: multiple dilations (odds ratio [OR] 1.2; P=0.012), and lower site of stricture (OR 12.8; P=0.043). Dysphagia was ameliorated by the dilations, and no patient required surgery. CONCLUSIONS: A specific emerging risk of perforation in dilation therapy for post-EMR/ESD strictures was identified. Carefully planned treatment is necessary in patients with severe post-EMR/ESD strictures especially strictures requiring multiple dilations or located in the lower esophagus.	esophagus
[A case of small cell carcinoma of esophagus treated by chemotherapy with CDDP plus CPT-11 and radiotherapy].	We present a case of small cell carcinoma of esophagus treated by chemotherapy with CDDP plus CPT-11 and radiotherapy. A 73-year-old woman visited our hospital with complaints of neck mass and discomfort during swallowing. Upper gastrointestinal endoscopy revealed a type 3 tumor in the middle portion of the esophagus, which was pathologically diagnosed as small cell carcinoma. A computed tomography showed lymph node swelling from neck to mediastinum. Then she was administered chemotherapy with CDDP plus CPT-11 and radiotherapy. The main tumor and lymph node swelling was remarkably reduced by chemoradiotherapy. The prognosis of small cell carcinoma of the esophagus is extremely poor because it may cause a general metastasis in early stage. This case was for long-term survival with chemoradiotherapy, and we report our case with the literature cited.	esophagus
[A case successfully treated with subtotal esophagectomy after preoperative second-line chemotherapy for cT4 esophageal cancer].	A 69-year-old male was diagnosed with type 2 advanced esophageal cancer in the upper and middle thoracic esophagus which invaded the left main bronchus and the aorta. Radio-chemotherapy was administered since a radical resection could not be performed due to the invasion. Two courses of enforced FP combination therapy (5-FU and CDDP) were administered along with radiotherapy. Although this radio-chemotherapy was effective to some degree in tumor reduction, a radical resection still could not be performed due to the invasion of the left main bronchus and the aorta. Thus, we administered four more courses of DCF combination therapy (docetaxel, CDDP and 5-FU). This chemotherapy reduced the esophageal cancer mass significantly, and subtotal esophagectomy was performed. No complications were observed after the operation. We conclude that DCF combination therapy may be effective in the treatment of esophageal cancer in cases which the desired effect cannot be achieved by FP combination therapy alone.	esophagus
[Successful treatment of advanced esophageal cancer with lymph node metastases by docetaxel, cisplatin and 5-FU followed by salvage lymphadenectomy--a case report].	We present a case of advanced esophageal cancer with multiple lymph node metastases successfully treated by combination therapy of docetaxel, cisplatin and 5-FU (DCF) followed by salvage lymphadenectomy. The patient was a 60-year-old female with the diagnosis of squamous cell carcinoma of the middle thoracic esophagus. The clinical stage diagnosis was cT2N4M0, cStage IVa. Systemic chemotherapy with DCF was started as the initial treatment. The changes noted on endoscopy and CT scan in the primary lesion and lymph nodes after two cycles of DCF were judged as complete response (CR). However, recurrence was diagnosed in the left cervical lymph nodes based on FDG uptake on FDG-PET. Salvage cervical lymphadenectomy was performed. Thereafter, the patient again achieved CR after the second administration of DCF for upper mediastinal lymph node recurrence. At present, she is still alive three years after the first visit. Combination therapy of DCF and salvage lymphadenectomy is potentially effective for advanced esophageal cancer with lymph node metastases.	esophagus
[Effect of minimally invasive Ivor-Lewis esophagectomy on acute phase responses in patients with esophageal carcinoma].	OBJECTIVE: To explore the effect of minimally invasive Ivor-Lewis esophagectomy on acute phase responses in patients with esophageal carcinoma. METHODS: Forty-eight patients with middle or low thoracic esophageal carcinoma underwent Ivor-Lewis esophagectomy. The patients were divided into small incision group (n = 25) and conventional group (n = 23) according to the patients' will. Serum levels of acute phase proteins C reactive protein (CRP), haptoglobin (HPT), α₁-acid glycoprotein (α₁-AG), ceruloplasmin (CER), transferrin (TRF), β₂-microglobulin (β₂-MG), album protein (ALB), interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) were measured and compared on 1st day before operation, at 18 hours as well as 3rd and 7th day after operation. RESULTS: There was no significant difference in all the acute phase proteins indicators and IL-6 between the small incision and conventional groups at each time points after operation (P > 0.05). In both groups the levels of CRP, α₁-AG and HPT were significantly higher after operation than before operation (P < 0.05). The levels of ALB and TRF were significantly lower after operation than before operation (P < 0.05). The levels of CER and β₂-MG were not significantly different during perioperative period (P > 0.05). The level of TNF-α was significantly higher in the small incision group than that in the conventional group at the 18 hours postoperationally (P < 0.05), and were not significantly different on the other time points between the two groups (P > 0.05). CONCLUSION: Compared with conventional operation, the small incision Ivor-Lewis esophagectomy do not significantly alleviate the stress of the surgical trauma in patients. Unchanging the essence of operation, if one is trying to minimize the stress caused by surgery on patients, the key factor is not the size of incision. An effective approach should be found in other operation-related factors.	esophagus
c-Myc inhibits TP53INP1 expression via promoter methylation in esophageal carcinoma.	Tumor protein p53-induced nuclear protein 1 (TP53INP1) is a well known stress-induced protein that plays a role in both cell cycle arrest and p53-mediated apoptosis. Loss of TP53INP1 expression has been reported in human melanoma, breast carcinoma, and gastric cancer. However, TP53INP1 expression and its regulatory mechanism in esophageal squamous cell carcinoma (ESCC) remain unclear. Our findings are in agreement with previous reports in that the expression of TP53INP1 was downregulated in 28% (10/36 cases) of ESCC lesions, and this was accompanied by significant promoter methylation. Overexpression of TP53INP1 induced G1 cell cycle arrest and increased apoptosis in ESCC cell lines (EC-1, EC-109, EC-9706). Furthermore, our study showed that the oncoprotein c-Myc bound to the core promoter of TP53INP1 and recruited DNA methyltransferase 3A to methylate the local promoter region, leading to the inhibition of TP53INP1 expression. Our findings revealed that TP53INP1 is a tumor suppressor in ESCC and that c-Myc-mediated DNA methylation-associated silencing of TP53INP1 contributed to the pathogenesis of human ESCC.	esophagus
A multicenter phase II trial of single-agent cetuximab in advanced esophageal and gastric adenocarcinoma.	BACKGROUND: Epidermal growth factor receptor (EGFR) is overexpressed in a significant proportion of esophageal and gastric carcinomas. Although previous studies have examined tyrosine kinase inhibitors of EGFR, there remains limited data regarding the role of EGFR-directed monoclonal antibody therapy in these malignancies. We carried out a multi-institutional phase II study of cetuximab, a monoclonal antibody against EGFR, in patients with unresectable or metastatic esophageal or gastric adenocarcinoma. PATIENTS AND METHODS: Thirty-five patients with previously treated metastatic esophageal or gastric adenocarcinoma were treated with weekly cetuximab, at an initial dose of 400 mg/m(2) followed by weekly infusions at 250 mg/m(2). Patients were followed for toxicity, treatment response, and survival. RESULTS: Treatment with cetuximab was well tolerated; no patients were taken off study due to drug-related adverse events. One (3%) partial treatment response was noted. Two (6%) patients had stable disease after 2 months of treatment. Median progression-free survival and overall survival were 1.6 and 3.1 months, respectively. CONCLUSION: Although well tolerated, cetuximab administered as a single agent had minimal clinical activity in patients with metastatic esophageal and gastric adenocarcinoma. Ongoing studies of EGFR inhibitors in combination with other agents may define a role for these agents in the treatment of esophageal and gastric cancer.	esophagus
Single-access transhiatal esophagectomy for cancer: are we on the right way?	Minimally invasive surgery has gained wide application since its introduction and has been applied to all aspects of general surgery. The common denominator in minimally invasive surgery is to perform the same operation as in the open approach. Single access surgery has the same goal by reducing the number and the size of access incisions. We present the first case,to our knowledge,of single access transhiatal esophagectomy in a very compromised patient(chronic renal failure, diabetes on dialysis). The patient was not amenable to chemo or radiation therapy. Surgical technique is described step by step.	esophagus
Defining cure for esophageal cancer: analysis of actual 5-year survivors following esophagectomy.	BACKGROUND: Esophagectomy is the mainstay of curative treatment for localized esophageal cancer. However, what constitutes cure is not well defined. This study was undertaken to characterize actual 5-year survivors following esophagectomy and to determine prognostic factors for disease-specific survival (DSS) from 60 months. MATERIALS AND METHODS: Between 1987 and 2004, 398 consecutive patients underwent esophagectomy and had potential for 5 years follow-up. Clinicopathological factors associated with DSS from 5 years onward were analyzed. RESULTS: Median DSS was 25 months. Neoadjuvant therapy was administered to 159 of 398 (40%). There were 114 of 398 (29%) actual 5-year survivors. On multivariate analysis, 5-year survivors were significantly more likely to have lower T classification, N classification, and R0 resections compared with patients who died less than 5 years after surgery. There were 66 of 398 patients (17%) with positive margins, and 6 of these were 5-year survivors. Of the 114 5-year survivors, 17 (15%) subsequently died of esophageal cancer. Prognostic factors for DSS after surviving 5 years were age and T classification for patients treated with neoadjuvant therapy and surgery alone, respectively. Powerful prognostic factors from time of treatment, including nodal status, were no longer prognostic factors after surviving to 5 years. CONCLUSIONS: No single clinicopathological variable negated survival to 5 years. Prognostication once surviving 5 years is difficult. The majority of 5-year survivors can be considered cured of esophageal cancer.	esophagus
Identification of signature genes for detecting hedgehog pathway activation in esophageal cancer.	The hedgehog signaling pathway plays an important role in cell growth and differentiation both in normal embryonic development and in tumors. Our previous work shows that hedgehog pathway is frequently activated in esophageal cancers. To further elucidate the role of hedgehog pathway in esophageal cancers we examined the expression of the target genes, hedgehog-interacting protein (HIP) and platelet derived growth factor receptor alpha (PDGFRα) and hedgehog signaling molecules, smoothened (SMO), suppressor of fused (Su(Fu)) in the specimens using in-situ hybridization and RT-PCR. We found that HIP, PDGFRα, SMO and Su(Fu) gene highly expressed in the primary esophageal squamous cell carcinomas but not in normal esophageal tissue. The transcripts of HIP, PDGFRα and SMO were expressed in 13 of 15 esophageal cancers. Su(Fu) expression was missing in 2 esophageal cancers. The results from in-situ hybridization were further confirmed by RT-PCR. Our results revealed a set of genes for detecting hedgehog signaling activation in esophageal cancer.	esophagus
Lapatinib inhibits receptor phosphorylation and cell growth and enhances antibody-dependent cellular cytotoxicity of EGFR- and HER2-overexpressing esophageal cancer cell lines.	Lapatinib is a dual tyrosine kinase inhibitor of the EGFR and HER2 tyrosine kinase domains. EGFR is expressed in 33.3% and HER2 in 30.3% of esophageal squamous cell carcinomas (ESCCs). To explore the potential utility of Lapatinib for therapy of ESCC patients, we evaluated the effect of Lapatinib on a panel of ESCC cell lines. EGFR and HER2 expression by the cell lines was established, and the effects of Lapatinib on inhibition of the phosphorylation of HER2, antiproliferative effect, apoptosis-inducing activity and accumulation of HER2 and EGFR on cell surface were evaluated. Additionally, the combined effect of Lapatinib together with Herceptin or Cetuximab on cell-mediated cytotoxicity was evaluated. Lapatinib inhibited HER2 phosphorylation in HER2-overexpressing, HER2 gene amplification positive ESCC cell line. Lapatinib also inhibited cell proliferation, induced apoptosis and caused the surface accumulation of HER2 and EGFR in ESCC cell lines. Addition of Lapatinib increased Herceptin-mediated antibody-dependent cell-mediated cytotoxicity by 15-25% with three ESCC target cell lines. Similarly, Cetuximab-mediated antibody-dependent cell-mediated cytotoxicity also increased by 15-30% in two ESCC cell lines on addition of Lapatinib. Cumulatively, the data indicate that Lapatinib has activity in EGFR- and/or HER2-expressing ESCC cells, and the combination therapy of Lapatinib and Cetuximab/Herceptin is a promising strategy in ESCC.	esophagus
In-hospital mortality after a surgical resection for esophageal cancer: analyses of the associated factors and historical changes.	BACKGROUND: Resections for esophageal cancer are invasive, with high mortality and morbidity rates. The object of this study was to clarify the factors associated with in-hospital death while also evaluating any associated historical changes in the characteristics of such deaths. METHODS: The factors associated with mortality were examined by logistic regression analysis in 1106 patients who underwent an esophagectomy for esophageal cancer. The historical changes in the characteristics of in-hospital deaths were also evaluated. RESULTS: A multivariate analysis revealed that not only undergoing an esophagectomy before 1979, but also a patient's age (odds ratio 1.070 for every increase in age by year) and an incomplete resection (odds ratio 2.265) were independent factors associated with in-hospital death. The in-hospital mortality rates were 16.1%, 5.8%, 2.5%, and 3.1%, while the 30-day mortality rates were 9.2%, 2.2%, 0.8%, and 0.3% during 1964-1979, the 1980s, the 1990s, and the 2000s, respectively. Eight patients had preoperative comorbidities among 11 patients who died in the hospital after 1997. The mortality rate was 5.5% in patients with any comorbidities, while it was 1.3% in patients without any comorbidities (P = 0.026). The most common direct cause of in-hospital death was previous pulmonary complications; however, cancer progression has recently become the most common cause. CONCLUSIONS: To prevent in-hospital mortality after an esophagectomy, strict indications for surgery and careful perioperative management are important, especially in high-risk patients with advanced esophageal cancer.	esophagus
TS gene tandem repeats in esophageal cancer patients receiving chemoradiotherapy.	5-Fluorouracil (5-FU) interferes with tumor-cell proliferation by inhibiting thymidylate synthase (TS). We examined the relationship between tandem repeat (TR) variations in the TS gene and survival following concurrent chemoradiotherapy in patients with esophageal squamous cell carcinoma (ESCC). TS-TR variations were analyzed in 57 stage II-IV ESCC patients undergoing chemoradiotherapy combined with 5-FU and cisplatinum (CDDP), and in 106 controls. Pretreatment non-neoplastic biopsy specimens from ESCC patients and lymphocytes from controls were used for analysis. Variations were identified by the size of DNA fragments amplified by polymerase chain reaction. Two to five TRs were found in Japanese individuals. TR3 homozygotes were predominant in 74% of ESCC patients and 61% of controls. Three-year survival rates were significantly longer in patients with TR2/2 or TR2/3 genotypes (38%) than in patients with TR3/3, 3/4, or 3/5 genotypes (9%; p=0.011). In the Cox proportional hazard model, the TR2/2 or TR2/3 genotypes were the only independent predictor for survival (Hazard ratio, 2.647; 95% confidence interval, 1.271-5.513). The TS-TR variations exert an important influence on survival following chemoradiotherapy in ESCC patients.	esophagus
Control chart methods for monitoring surgical performance: a case study from gastro-oesophageal surgery.	Graphical methods are becoming increasingly used to monitor adverse outcomes from surgical interventions. However, uptake of such methods has largely been in the area of cardiothoracic surgery or in transplants with relatively little impact made in surgical oncology. A number of the more commonly used graphical methods including the Cumulative Mortality plot, Variable Life-Adjusted Display, Cumulative Sum (CUSUM) and funnel plots will be described. Accounting for heterogeneity in case-mix will be discussed and how ignoring case-mix can have considerable consequences. All methods will be illustrated using data from the Scottish Audit of Gastro-Oesophageal Cancer services (SAGOCS) data set.	esophagus
Synchronous primary oesophageal malignant melanoma and sigmoid adenocarcinoma.	The authors present a case of a gentleman in his 70s who was referred to the gastroenterology outpatient clinic with dysphagia. An oesophagogastroduodenoscopy was performed which showed a polypoidal black coloured mass in the oesophagus. Endoscopic biopsies confirmed malignant melanoma. Further staging investigations were organised to assess suitability for surgery which revealed a mass in the sigmoid colon. Subsequent colonoscopy and biopsy confirmed adenocarcinoma. As this was an unusual case to associate these two malignancies at the same time, there was no ideal or recognised management plan available. Different treatment options were considered and a consensus was developed regarding best surgical approach but due to the lapse in time a repeat staging CT scan was organised which unfortunately now demonstrated lymph node metastasis. Patient was managed conservatively from this point onwards and he died 12 months later.	esophagus
[Modern aspects of photodynamic therapy of esophageal].	This review presents the current possibilities of photodynamic therapy in the treatment of precancerous lesions and cancer of the esophagus. Mechanisms of photodynamic effects on tumor and especially the accumulation of photosensitizer in tumor tissue, results of studies on the use of photodynamic therapy in the treatment of early esophageal cancer, esophageal cancer stenosis and combinations with other treatment techniques. Results of treatment of Barrett's esophagus using photodynamic therapy were analyzed and a compared with other methods of treatment.	esophagus
p53 functional activation is independent of its genotype in five esophageal squamous cell carcinoma cell lines.	p53 mutations have been found in many esophageal squamous cell carcinoma (ESCC) clinical specimens and cell lines. We reasoned that functional inactivation of wild-type p53 or the functional activation of mutant-type p53 might exist in these specimens and cell lines. In this study, we identified the correlation between p53 functional activation and its genotype in five different ESCC cell lines. To examine the potential p53 activation in a certain ESCC cell line, DNA damage methods including X-ray exposure and cisplatin treatment were employed to treat cells. Further, the expression of p53 protein and four transcripts of well-known p53 target genes were investigated using Western blot and reverse transcriptionpolymerase chain reaction (RT-PCR) after cell exposure to DNA damage. The results showed that in KYSE 30 cell line with mutant p53 and KYSE 150 with wild-type p53, p53 could be activated by DNA damages. However, p53 could not be activated following the DNA damages in YES 2 with wild-type p53, KYSE 70 with mutant p53, and EC9706 with unknown p53 genotype. All our data indicated that p53 function in certain cells is not closely correlated with its genotype. To judge p53 function in a particular cell line, it is important to examine the p53 functional activation, but not to simply rely on the p53 genotype.	esophagus