crossing96/oncoscreening huggingface dataset:
Overexpression of p28GANK accelerates the metastasis of oesophageal squamous cell carcinoma.	The present study aimed to evaluate the effects of p28GANK expression on the metastasis of oesophageal squamous cell carcinoma (ESCC) tissues and to investigate its roles in the metastasis of highly invasive and non‑invasive ESCC cell lines. Quantitative polymerase chain reaction (qPCR) and immunohistochemical analyses were performed to assess p28GANK mRNA and protein expression in ESCC tissues and to analyse its significance in ESCC metastasis. qPCR and western blot analyses were used to detect p28GANK mRNA and protein expression in highly invasive and non‑invasive cell lines. Subsequently, lentivirus‑mediated p28GANK short interfering RNA (siRNA) was transfected into highly invasive ESCC cells, and Transwell assays were performed to analyse the effects of p28GANK knockdown on their migration and invasion. The mean expression levels of p28GANK mRNA in the ESCC tissues of patients with metastasis were signiﬁcantly higher than those in the ESCC specimens from patients without metastasis. p28GANK expression in ESCC tissues was correlated with T‑stage, lymph node metastasis and lymphatic invasion. The mRNA and protein expression levels of p28GANK were significantly higher in highly invasive cell lines compared with those of matched, non‑invasive cell lines. Lentivirus‑mediated siRNA knockdown of p28GANK markedly decreased p28GANK expression in EC109‑P and EC9706‑P cells and supressed the metastasis of ESCC cells in vitro. In conclusion, p28GANK expression was increased in metastatic ESCC tissues and cells, and p28GANK knockdown decreased the metastatic ability of ESCC cells. These results suggested that p28GANK may be a potential therapeutic marker for ESCC metastasis.	esophagus
NSAIDs, statins, low-dose aspirin and PPIs, and the risk of oesophageal adenocarcinoma among patients with Barrett's oesophagus: a population-based case-control study.	OBJECTIVES: Non-steroidal anti-inflammatory drugs (NSAIDs), proton pump inhibitors (PPIs), low-dose aspirin and statins may decrease the risk of oesophageal adenocarcinoma (OAC) among patients with Barrett's oesophagus (BO). However, previous studies did not adequately address bias and confounding. Our objective was to estimate the risk of OAC among patients with BO exposed to NSAIDs, statins and PPIs. DESIGN: Case-control study nested within a BO cohort. SETTING: Two primary care databases (the UK and the Netherlands (NL)). PARTICIPANTS: Cases were adults ≥18 years of age with OAC or high-grade dysplasia (HGD) diagnosis ≥1 year after BO diagnosis. Controls were matched on age, sex, year of BO diagnosis and database. EXPOSURE: Drug use was assessed from BO diagnosis until matching date. OUTCOME MEASURE: Adjusted ORs with 95% CI were calculated by conditional logistic regression. RESULTS: Within the BO cohort (n=15 134), 45 OAC (UK: 40, NL: 5) and 12 HGD cases (NL: 12) were identified. ORa for OAC during NSAID use was 1.2 (95% CI 0.6 to 2.5) and during statin use for >3 years 0.5 (95% CI 0.1 to 1.7). When including HGD cases (n=57), ORa for NSAID use was 0.9 (95% CI 0.5 to 1.8) and for statin use >3 years 0.5 (95% CI 0.1 to 1.7). Higher doses of statins showed lower estimates for OAC and HGD, though not statistically significant. Low-dose aspirin and PPIs did not significantly decrease the risk of OAC and HGD. CONCLUSIONS: In this population-based nested case-control study, use of NSAIDs, PPIs, low-dose aspirin or statins did not reduce the risk of HGD and OAC among patients with BO. These findings indicate that for an unselected group of patients with BO chemoprevention by use of drugs to reduce progression to HGD and OAC should not be directly considered as routine care.	esophagus
Hospital type- and volume-outcome relationships in esophageal cancer patients receiving non-surgical treatments.	"AIM: To study the ""hospital type-outcome"" and ""volume-outcome"" relationships in patients with esophageal cancer who receive non-surgical treatments. METHODS: A total of 6106 patients with esophageal cancer diagnosed between 2008 and 2011 were identified from a national population-based cancer registry in Taiwan. The hospital types were defined as medical center and non-medical center. The threshold for high-volume hospitals was based on a median volume of 225 cases between 2008 and 2011 (annual volume, >56 cases) or an upper quartile (>75%) volume of 377 cases (annual volume>94 cases). Cox regression analyses were used to determine the effects of hospital type and volume outcome on patient survival. RESULTS: A total of 3955 non-surgically treated patients were included in the survival analysis. In the unadjusted analysis, the significant prognostic factors included cT, cN, cM stage, hospital type and hospital volume (annual volume, >94 vs ≤94). The 1- and 3-year overall survival rates in the non-medical centers (36.2% and 13.2%, respectively) were significantly higher than those in the medical centers (33.5% and 11.3%, respectively; P=0.027). The 1- and 3-year overall survival rates in hospitals with an annual volume of ≤94 (35.3% and 12.6%, respectively) were significantly higher than those with an annual volume of >94 (31.1% and 9.4%, respectively; P=0.001). However, in the multivariate analysis, the hospital type was not statistically significant. Only cT, cN, and cM stages and hospital volume (annual volume>94 vs ≤94) were independent prognostic factors. CONCLUSION: Whether the treatment occurs in medical centers is not a significant prognostic factor. High-volume hospitals were not associated with better survival rates compared with low-volume hospitals."	esophagus
Concurrent radiotherapy and weekly chemotherapy of 5-fluorouracil and platinum agents for postoperative locoregional recurrence of oesophageal squamous cell carcinoma.	The most optimal management for postoperative locoregional recurrence of oesophageal squamous cell carcinoma is still controversial. Several studies have reported the feasibility and efficacy of concurrent chemoradiotherapy (CCRT), mostly with three-weekly or four-weekly schedule of chemotherapy. However, treatment compliance was not quite satisfactory, probably due to treatment-related toxicities. Since CCRT with weekly chemotherapy regimens have demonstrated a favorable toxicity profile as well as promising survival in certain types of cancer, we aimed to evaluate the efficacy and toxicity of radiotherapy concurrently with weekly chemotherapy with 5-fluorouracil (5-FU) and platinum agents for patients with postoperative locoregional recurrence of oesophageal squamous cell carcinoma in our center. Twenty-seven consecutive patients who were diagnosed with postoperative locoregional recurrence of oesophageal squamous cell carcinoma and received CCRT with weekly chemotherapy of 5-FU and platinum agents were retrospectively analyzed. Our data showed that the present protocol of radiotherapy combined concurrently with weekly chemotherapy of 5-FU and platinum agents was a safe and effective salvage treatment for postoperative locoregional recurrence of oesophageal squamous cell carcinoma.	esophagus
Primary esophageal mucosa-associated lymphoid tissue lymphoma diagnosed by using stacked forceps biopsy.	Non-Hodgkin lymphoma involving the esophagus is very rare. Only a few cases have been reported in the English literature to date, and it accounts for less than 1% of all cases of gastrointestinal lymphoma. As this malignancy manifests as a submucosal tumor, pathological diagnosis by using a simple endoscopic biopsy alone is difficult. Therefore, surgical biopsy, endoscopic mucosal resection, and endoscopic ultrasound-guided fine-needle aspiration have been used in most cases. Herein, we report a case of esophageal mucosa-associated lymphoid tissue lymphoma in a 49-year-old man, which involved the use of a stacked forceps biopsy to obtain adequate samples for pathological analysis; the use of the stacked forceps biopsy method is unlike those used in previous cases. The patient received cyclophosphamide, vincristine, and prednisolone chemotherapy; he achieved a complete response. In addition, we review the literature relevant to this case.	esophagus
Three-dimensional telomere architecture of esophageal squamous cell carcinoma: comparison of tumor and normal epithelial cells.	Telomeres are repetitive nucleotide sequences (TTAGGG)n located at the ends of chromosomes that function to preserve chromosomal integrity and prevent terminal end-to-end fusions. Telomere loss or dysfunction results in breakage-bridge-fusion cycles, aneuploidy, gene amplification and chromosomal rearrangements, which can lead to genomic instability and promote carcinogenesis. Evaluating the hypothesis that changes in telomeres contribute to the development of esophageal squamous cell carcinoma (ESCC) and to determine whether there are differences between young and old patients, we compared the three-dimensional (3D) nuclear telomere architecture in ESCC tumor cells with that of normal epithelial cells obtained from the same patient. Patients were equally divided by age into two groups, one comprising those less than 45 years of age and the other consisting of those over 80 years of age. Tumor and normal epithelial cells located at least 10 cm from the border of the tumor were biopsied in ESCC patients. Hematoxylin and eosin staining was performed for each sample to confirm and identify the cancer and normal epithelial cells. This study was based on quantitative 3D fluorescence in situ hybridization (Q-FISH), 3D imaging and 3D analysis of paraffin-embedded slides. The 3D telomere architecture data were computer analyzed using 100 nuclei per slide. The following were the main parameters compared: the number of signals (number of telomeres), signal intensity (telomere length), number of telomere aggregates, and nuclear volume. Tumor and normal epithelial samples from 16 patients were compared. The normal epithelial cells had more telomere signals and higher intensities than the tumor cells, with P-values of P < 0.0001 and P = 0.0078, respectively. There were no statistically significant differences in the numbers of telomere aggregates or the nuclear volumes between the tumor and normal epithelial cells. Secondary analyses examined the effects of age on 3D telomere architecture and found no statistically significant differences in any parameter tested between the young and old patients in either the tumor or epithelial cells. The 3D nuclear telomeric signature was able to detect differences in telomere architecture between the ESCC and normal epithelial tissues. However, there were no differences observed between the young and old patients.	esophagus
Simplified classification of capillary pattern in Barrett esophagus using magnifying endoscopy with narrow band imaging: implications for malignant potential and interobserver agreement.	The classification of Barrett esophagus (BE) using magnifying endoscopy with narrow band imaging (ME-NBI) is not widely used in clinical settings because of its complexity. To establish a new simplified available classification using ME-NBI.We conducted a cross-sectional study in a single-referral center. One hundred eight consecutive patients with BE using ME-NBI and crystal violet (CV) chromoendoscopy, and histological findings were enrolled. BE areas observed by ME-NBI were classified as type I or II on the basis of capillary pattern (CP), and as closed or open type on the basis of a mucosal pit pattern using CV chromoendoscopy; then, biopsy samples were obtained. We evaluated the relation between CP and pit pattern, expression of the factors with malignant potential, percentage of microvascular density, and interobserver agreement.One hundred thirty lesions from 91 patients were analyzed. Type II CP had more open type pit pattern areas and significantly greater microvascular density than type I. The presence of dysplasia, specialized intestinal metaplasia, expressions of COX-2, CDX2, and CD34, and PCNA index were significantly higher in type II, whereas the multivariate analysis showed that type II was the best predictor for the presence of dysplasia (OR 11.14), CD34 expression (OR 3.60), and PCNA (OR 3.29). Interobserver agreement for this classification was substantial (κ = 0.66).A simplified CP classification based on observation with ME-NBI is presented. Our results indicate that the classification may be useful for surveillance of BE with high malignant potential.	esophagus
Clinical impact of the interval between chemoradiotherapy and esophagectomy in esophageal squamous cell carcinoma patients.	BACKGROUND: The optimal interval between chemoradiotherapy (CRT) and esophagectomy in patients with esophageal squamous cell carcinoma is still undetermined. The aim of this study was to evaluate the association between different treatment intervals and clinical impact, including perioperative outcome and long-term survival. METHODS: We retrospectively reviewed data from 665 patients with esophageal squamous cell carcinoma who underwent CRT and esophagectomy between 2008 and 2011 in Taiwan. Based on the interval between CRT and esophagectomy, patients were divided into group 1, less than 30 days; group 2, 30 to 59 days; group 3, 60 to 89 days; or group 4, 90 days or more. The impact of the treatment interval on perioperative outcomes and overall survival were assessed. A Cox regression model was used to identify prognostic factors for overall survival. RESULTS: There were 90 patients in group 1, 385 patients in group 2, 141 patients in group 3, and 49 patients in group 4. The 30-day surgical mortality rate was 5.6%, 2.9%, 1.4%, and 10.2% for groups 1, 2, 3, and 4, respectively (p = 0.018). The 90-day surgical mortality rate was 12.2%, 6.8%, 5.7%, and 18.4% for groups 1, 2, 3, and 4, respectively (p = 0.012). The differences between surgical margin positivity rates were also significant: 2.2% in group 1, 4.9% in group 2, 9.2% in group 3, and 12.2% in group 4 (p = 0.032). The treatment interval was not associated with the complete response and the overall survival. CONCLUSIONS: Although early operation (less than 30 days) is associated with reduced rates of surgical margin positivity, the potential benefits appear to be outweighed by the significant increase in postoperative mortality. The surgical timing that optimizes both mortality and surgical margin positivity requires further study.	esophagus
[Expression of leptin and adiponectin in esophageal squamous cell carcinoma and their clinical significance].	OBJECTIVE: To preliminarily investigate the expression and clinical significance of leptin and adiponectin in esophageal squamous cell carcinoma (ESCC). METHODS: The expression of leptin and adiponectin in ESCC and normal esophageal mucosal tissue was detected by immunohistochemical staining with tissue microarray. The correlation between leptin, adiponectin and clinicalpathological features was statistically analyzed. RESULTS: The expression of leptin was significantly upregulated in the ESCC than in the normal esophageal mucosa tissue [65.6% (80/122) versus 27.5% (11/40), P < 0.001]. Expression of leptin was significantly correlated with lymph node involvement and advanced tumor stage (P = 0.009 and P = 0.043, respectively). Expression of adiponectin was significantly down-regulated in ESCC compared with that in normal esophageal mucosal tissue [22.1% (27/122) versus 47.5% (19/40), P = 0.002]. Expression of adiponectin was significantly correlated with lymph node involvement (P = 0.020). Correlation analysis showed a positive correlation between the expression of leptin and lymph node metastasis and TNM stage (r = 0.235 and r = 0.183, respectively), and a negative correlation between the expression of adiponectin and lymph node metastasis (r = -0.229). There was no significant correlation between the expressions of leptin and adiponectin (P > 0.05), and between the body mass index and the expression of leptin and adiponectin, and lymph node metastasis (P > 0.05 for all). CONCLUSIONS: An imbalanced expression of adipocytokines exits in ESCC. The expression of leptin and adiponectin is correlated with lymph node metastasis and/or tumor stage. Therefore, imbalanced expression of leptin and adiponectin may have a potential role in the carcinogenesis and disease progression of ESCC.	esophagus
[Expression and clinical significance of CCL5 in patients with esophageal carcinoma].	OBJECTIVE: To investigate the expression and significance of CCL5 in patients with esophageal carcinoma. METHODS: Using reverse transcriptase polymerase chain reaction (RT-PCR), the expressions of CCL5/CD8/granzyme B/perforin in tumor and corresponding adjacent tissues from esophageal carcinoma patients were examined. Flow cytometry (FACS) was used to detect the percentages of CD8(+) T cells and CCR5(+)CD8(+) T cells in TIL and PBMC from the patients. Transwell assay was performed to study the effect of CCL5 on the migration of T cells in vitro. T test and Spearman correlation analysis were performed. RESULTS: The mRNA expressions of CCL5 and perforin were 0.348 2 ± 0.300 1 and 0.181 9 ± 0.118 6, respectively, in the tumor samples, while their expressions in adjacent samples were 0.279 6 ± 0.138 0 and 0.118 0 ± 0.109 8, respectively, with no statistically significant differences between them (P > 0.05 for both). The mRNA expressions of CD8 and granzyme B were significantly higher in the tumor tissues than in adjacent tissues (0.464 9 ± 0.300 8 vs. 0.279 0 ± 0.173 4, 0.648 7 ± 0.516 0 vs. 0.469 7 ± 0.259 1; P < 0.05 for both). The relative expression of CCL5 was positively correlated with that of CD8, perforin and granzyme B (r(CD8) = 0.272, P = 0.034; r(perforin) = 0.305, P = 0.026; r(granzymeB) = 0.108, P = 0.012) in the tumor sites. FACS data revealed that the proportions of CD8(+) T cells in TIL and PBMC were (45.86 ± 16.09)% and (34.05 ± 15.07)%, respectively, showing a significant difference (P = 0.022). Similarly, CCR5(+)CD8(+) T cells fraction in TIL (48.12 ± 26.75)% was much higher than that in PBMC (19.53 ± 13.67) % (P < 0.001). Transwell assay showed that CCL5 protein enhanced the migration of T cells, supporting that CCL5 is crucial for CD8(+) T cells recruitment in vivo. Intriguingly, CCL5 expression was down-regulated in advanced patients (stage IIb-IV). The accumulation of CD8(+) T cells and CCR5(+)CD8(+) T cells was strongly reduced in advanced patients, suggesting that CCL5 expression may be involved in the local control of the disease and its reduction may be involved in disease progression. CONCLUSIONS: The current data indicate the involvement of CCL5 in the regulation of CD8(+) T cell entry into tumor lesions in esophageal carcinoma patients. This process may affect the disease status and potentially as a prognostic factor for cancer patients. Enhancing local CCL5 expression in tumor lesions may represent a novel strategy in esophageal cancer therapy.	esophagus
Cyr61 promotes CD204 expression and the migration of macrophages via MEK/ERK pathway in esophageal squamous cell carcinoma.	Tumor-associated macrophages (TAMs) are known to be involved in the progression of various human malignancies. We previously demonstrated that CD204 was a useful marker for TAMs contributing to the angiogenesis, progression, and prognosis of human esophageal squamous cell carcinoma (ESCC). We also showed that conditioned media of ESCC cell lines induced CD204 expression in THP-1 human monocytic leukemia cells. Here, we performed a cDNA microarray analysis between THP-1 cells stimulated with TPA (macrophage [MΦ]-like THP-1 cells) treated with and without conditioned medium of ESCC cell line to clarify the molecular characteristics of TAMs in ESCC. From the microarray data, we discovered that Cyr61 was induced in CD204-positive-differentiated THP-1 cells (TAM-like THP-1 cells). In the ESCC microenvironment, not only cancer cells but also TAMs expressed Cyr61. Interestingly, the expression levels of Cyr61 showed a significant positive correlation with the number of CD204-positive macrophages in ESCCs by immunohistochemistry. Recombinant human Cyr61 (rhCyr61) promoted cell migration and induced the expression of CD204 along with the activation of the MEK/ERK pathway in MΦ-like THP-1 cells. Pretreatment with a MEK1/2 inhibitor significantly inhibited not only the Cyr61-mediated migration but also the CD204 expression in the MΦ-like THP-1 cells. These results suggest that Cyr61 may contribute to the expression of CD204 and the promotion of cell migration via the MEK/ERK pathway in TAMs in the ESCC microenvironment.	esophagus
Lymphovascular invasion and nodal metastasis in intramucosal adenocarcinoma of the esophagus and esophagogastric junction.	OBJECTIVE: To evaluate the tumor parameters predictive of lymphovascular invasion (LVI) and nodal metastases in intramucosal adenocarcinoma (IMAC) of the esophagus and esophagogastric junction. METHODS: In all, 171 cases of IMAC from esophagectomy database (1986-2009) were reviewed. LVI was evaluated on HE and by immunohistochemistry stain for D2-40 (in selected cases). Univariate analysis was performed to identify predictors for LVI (in this cohort) and nodal metastasis (for pooled data from literature review). RESULTS: Altogether 150 IMAC were included in the study after histology review; 7 (4.7%) showed LVI and one (0.7%) had nodal metastasis. LVI-positive IMAC were thicker (tumor thickness 3.0 ± 2.8 mm vs 1.3 ± 1.2 mm, P = 0.01), and more likely to invade the outer muscularis mucosae (M3) (P = 0.004), be poorly differentiated (P < 0.001), and to show a nodular or plaque-like lesion (P = 0.04) compared with LVI-negative IMAC. Patients' age, gender, the frequency of tumor multifocality, ulceration and tumor size were not significantly different between these two groups. The pooled rates of LVI and nodal metastases in IMAC from five published studies and this cohort were 6.0% (range 2.9-16.7%) and 3.4% (range 0-10.0%), respectively. Pooled analysis of studies with histology review showed that LVI in IMAC was associated with a nodal metastases rate of 27.3%. CONCLUSION: For IMAC of the esophagus and esophagogastric junction, LVI is associated with tumor thickness, M3 invasion, poor differentiation and the presence of nodular or plaque-like lesion; by pooled analysis, it is associated with a risk of nodal metastasis of 27.3%.	esophagus