crossing96/oncoscreening huggingface dataset:
[A Patient with Basaloid Carcinoma of the Esophagus Removed Surgically after Pre-Operative Chemotherapy Who Developed TTP during Post-Operative Chemotherapy].	A 63-year-old man presented with the chief complaint of an unpleasant feeling in the chest after a meal.Esophagogastroduodenoscopy revealed interminglement of ulcer infiltration type lesions and protruding lesions in the lower esophagus.A large type 1 protruding lesion was located mainly in the esophagogastric junction(EGJ)and it progressed towards the stomach.A hypertrophic and protruding lesion on the lower esophageal wall and a 6 cm tumor in the major axis of the fornix were observed on thoracic and abdominal CT, and an endocrine cell carcinoma or basaloid carcinoma were suggested after biopsy.Finally, we diagnosed a basaloid carcinoma after immunohistochemistry analysis.We administered 4 courses of TS-1 plus CDDP as pre-operative chemotherapy.Because of a significant reduction in tumor size, approximately 5 months after first presentation, we performed esophageal resection by right thoracotomy and laparotomy, and reconstructive surgery for the thoracic gastric duct.The pathological diagnosis was basaloid carcinoma with multiple foci of squamous cell carcinoma.After surgery, we continued chemotherapy with TS-1 plus CDDP, which was previously effective, but a liver metastasis appeared 8 months later.We discontinued chemotherapy because of a prominent decline in platelets.Because of the clinical symptoms, we diagnosed secondary thrombotic thrombocytopenic purpura accompanied by a malignant tumor.We implemented plasma exchange and steroid pulse therapy, but this patient experienced no therapeutic effect and died.	esophagus
Effect of sinomenine hydrochloride on radiosensitivity of esophageal squamous cell carcinoma cells.	Radiation therapy is one of the most important treatments for unresectable and locally advanced esophageal squamous cell carcinoma (ESCC), however, the response to radiotherapy is sometimes limited by the development of radioresistance. Sinomenine hydrochloride (SH) has anticancer activity, but its effect on the radiosensitivity of ESCC is unclear. We determined the effect of SH on the radiosensitivity of ESCC cells and elucidated its potential radiosensitization mechanisms in vitro and in vivo. ESCC cells were subjected to SH and radiation, both separately and in combination. Untreated cells served as controls. The CCK‑8 assay was used to evaluate cell proliferation, and the clonogenic assay to estimate radiosensitization. Flow cytometry was used to investigate cell cycle phases and cell apoptosis. Bcl‑2, Bax, cyclin B1, CDK1, Ku86, Ku70, and Rad51 expression was evaluated using western blotting. In vivo, tumor xenografts were created using BALB/c nude mice. Tumor‑growth inhibition was recorded, and Ki‑67 and Bax expression in the tumor tissues was assessed using immunohistochemistry. SH inhibited ESCC cell growth and markedly increased their radiosensitivity by inducing G2/M phase arrest. SH combined with radiation therapy significantly increased ESCC cell apoptosis. The molecular mechanism by which SH enhanced radiosensitivity of ESCC cells was related to Bcl‑2, cyclin B1, CDK1, Ku86, Ku70, and Rad51 downregulation and Bax protein expression upregulation. SH combined with radiation considerably delayed the growth of tumor xenografts in vivo. Immunohistochemical analysis showed that in the SH combined with radiation group, the expression of Bax was significantly higher while that of Ki‑67 was lower than the expressions in the control groups. Taken together, our findings showed that SH could improve the sensitivity of radiation in ESCC cells by inducing G2/M phase arrest, promoting radiation‑induced apoptosis and inhibiting DSB‑repair pathways. SH appears to be a prospective radiosensitizer for improving the efficacy of radiotherapy for ESCC.	esophagus
RNF113A promotes the proliferation, migration and invasion, and is associated with a poor prognosis of esophageal squamous cell carcinoma.	Ring finger protein 113A (RNF113A) possesses a C3HC4 zinc finger domain and this domain is found in E3 ubiquitin ligase and is involved in tumorigenesis. To date, and at least to the best of our knowledge, there are no studies available which have investigated RNF113A in cancer. Thus, this study aimed to explore the role of RNF113A in the development of esophageal squamous cell carcinoma (ESCC). For this purpose, paraffin-embedded samples from 117 patients with ESCC were selected, as well as 41 pairs of fresh-frozen ESCC and adjacent normal tissue samples. RNF113A expression was examined by immunohistochemistry and reverse transcription-quantitative PCR (RT-qPCR). RNF113A was overexpressed or silenced in the EC9706 and Eca109 cells. The cells were examined for cell cycle progression, apoptosis, invasiveness and migration. Xenograft tumors were also created in mice using the Eca109 cells. Tumor differentiation (P=0.008) and T classification (P<0.001) were found to be significantly associated with RNF113A expression. No statistically significant association was observed between RNF113A expression and sex, age, histological type, tumor location and lymph node metastasis (N classification). Kaplan-Meier analysis revealed that the patients with ESCC with ahigh expression of RNF113A had a lower survival rate than those with a low expression (P=0.002). Multivariate analysis revealed that RNF113A expression (HR=2.406; 95% CI, 1.301-4.449, P=0.005) was independently associated with overall survival in patients with ESCC. The overexpression of RNF113A promoted proliferation, migration, and invasiveness of ESCC cell lines in vitro, and RNF113A silencing reversed these malignant behaviors. RNF113A knockdown inhibited tumor growth in vivo. Thus, these results indicate that RNF113A promotes the proliferation, migration and invasiveness of ESCC cell lines. RNF113A expression in ESCC is this associated with a poor prognosis of affected patients.	esophagus
TGF-β-induced NKILA inhibits ESCC cell migration and invasion through NF-κB/MMP14 signaling.	The transforming growth factor β (TGF-β) signaling pathway plays anti- and pro-tumoral roles in the vast majority of cancers, and long noncoding RNAs have been reported to play key roles in the highly contextual response process. However, the roles of long noncoding RNAs (lncRNAs) in TGF-β signaling in esophageal squamous cell carcinoma (ESCC) remain unknown. In this study, we performed RNA-seq to compare lncRNAs expression levels between TGF-β1-treated and untreated ESCC cells and observed that NF-kappaB-interacting lncRNA (NKILA) was remarkably upregulated by the classical TGF-β signaling pathway. RNA profiling of 39 pairs ESCC tumor and adjacent nontumor samples using RT-qPCR demonstrated that NKILA is significantly downregulated in ESCC tumor tissues, and NKILA expression levels were significantly decreased in advanced tumor tissues (III and IV) compared to early stages (I and II) (p < 0.01). Gain- and loss-of-function assays showed that NKILA inhibited ESCC cell metastasis in vitro and in vivo, and mechanism studies showed that NKILA repressed MMP14 expression by inhibiting IκBα phosphorylation and NF-κB activation. Collectively, these findings suggest that the TGF-β-induced lncRNA NKILA has potential as an antimetastasis therapy. KEY MESSAGES: Long noncoding RNA NKILA could be remarkably upregulated by classical TGF-β signal pathway in ESCC. NKILA was significantly downregulated in esophageal squamous cell carcinoma and negatively correlated with TNM stage. NKILA inhibits ESCC cell metastasis via repressing MMP14 expression by suppressing the phosphorylation of IκBα and NF-κB activation.	esophagus
LKB1 inactivation occurs in a subset of esophageal adenocarcinomas and is sufficient to drive tumor cell proliferation.	BACKGROUND: The incidence of esophageal adenocarcinoma (EAC) has increased over the last several decades. Apart from mutations in TP53 gene, there are little data on genetic drivers of EAC. Liver kinase B1 (LKB1) has emerged as a multifunctional tumor suppressor regulating cell growth, differentiation, and metabolism. Somatic inactivation of LKB1 has been described in several tumor types; however, whether LKB1 inactivation has a role in EAC is unknown. Here we analyzed patient tumors to assess the prevalence of LKB1 loss in EAC. METHODS: Chromosomal deletion and expression of LKB1 in EAC were investigated using publicly available genomic data. Protein expression was assessed by immunohistochemistry (IHC) analysis for LKB1 in a tissue microarray (TMA) containing esophageal tumor specimens, including EAC. LKB1 was suppressed in EAC cells to determine the effects on cell growth in vitro. RESULTS: Analysis of EAC data in The Cancer Genome Atlas dataset revealed significant deletion of chromosome 19p13.3, containing the LKB1 gene locus. Single copy loss (shallow deletion) of LKB1 was present in 58% of EAC samples. Expression of LKB1 was significantly lower in EAC tumors compared with normal esophagus. IHC analysis showed reduced LKB1 protein expression in EAC. Suppression of LKB1 was sufficient to enhance EAC cell growth in vitro. CONCLUSIONS: Our data suggest that inactivation of LKB1 frequently occurs in EAC. Based on the reported oncogenic effects of LKB1 inactivation, our data indicate that LKB1 loss may play a significant role in EAC tumorigenesis, and point to the need for future studies.	esophagus
[Clinical significance of NS1-BP expression in esophageal squamous cell carcinoma].	Objective: To investigate the clinical significance of NS1-BP expression in patients with esophageal squamous cell carcinoma (ESCC), and to study the roles of NS1-BP in proliferation and apoptosis of ESCC cells. Methods: A total of 98 tumor tissues and 30 adjacent normal tissues from 98 ESCC patients were used as study group and control group, and these samples were collected in Sun Yat-Sen University Cancer Center between 2002 and 2008. In addition, 46 ESCC tissues which were collected in Cancer Institute and Hospital of Tianjin Medical University were used as validation group. Expression of mucosal NS1-BP was detected by immunohistochemistry. Kaplan-Meier curve and log-rank test were used to analyze the survival rate. Multivariate Cox proportional hazard model was used to analyze the prognostic factors. Furthermore, NS1-BP was over expressed or knocked down in ESCC cells by transient transfection. Protein levels of c-Myc were detected by western blot. Cell viability and apoptosis was analyzed by MTT assay and flow cytometry. Results: Among all of tested samples, NS1-BP were down-regulated in 9 out of 30 non-tumorous normal esophageal tissues (30.0%) and 85 out of 144 ESCC tissues (59.0%), respectively, showing a statistically significant difference (P=0.012). In the study group, three-year disease-free survival rate of NS1-BP high expression group (53.2%) was significantly higher than that of NS1-BP low expression group (27.6%; P=0.009). In the validation group, the three-year disease-free survival rates were 57.8% and 25.5% in NS1-BP high and low levels groups, respectively, showing a similar results (P=0.016). Importantly, multivariate analyses showed that low expression of NS1-BP was an independent predictor for chemoradiotherapy sensitivity and shorter disease-free survival time in ESCC patients(P<0.05 for all). Furthermore, overexpressed NS1-BP in TE-1 cells repressed c-Myc expression, inhibited cell proliferation and promoted apoptosis. In contrast, knockdown NS1-BP in KYSE510 cells induced c-Myc expression, increased cell proliferation and repressed apoptosis. Conclusions: NS1-BP is an independent favorable prognostic factor in ESCC. It inhibits cell proliferation and enhances cell apoptosis via repressing c-Myc. Targeting NS1-BP may be a new therapeutic strategy for ESCC patients.	esophagus
[Clinical application of supraclavicular flap for oncologic reconstruction of hypopharynx and upper esophagus].	Objective: To assess the efficacy of supraclavicular artery island flap (SCAIF) for the reconstruction of hypopharynx and upper esophagus. Methods: The SCAIF procedure on was used in 10 patients, including 8 with hypopharygeal carcinomas, 1 with esophageal carcinoma and neck skin invasion and 1 with hypopharyngeal leiomyosarcoma, at the Otorhinolaryngology Hospital, the First Affiliated Hospital, Sun Yatsen University between December 2015 and June 2017. The sizes of the flaps were measured in (4-8) cm×(5-12) cm. Clinical indexes such as harvesting time and survival were recorded. Results: Harvesting time for SCAIF ranged from 20 to 30 minutes, averaging 26 minutes. Nine flaps survived, one flap had partially necrosis. Functional outcomes were excellent and the donor sites were direct closed without complications. Conclusions: SCAIF is a versatile, reliable, and easily harvested flap, with good cosmetic and functional outcomes for reconstructing the defects of hypopharynx and upper esophagus.	esophagus
A core matrisome gene signature predicts cancer outcome.	BACKGROUND: Accumulating evidence implicates the tumour stroma as an important determinant of cancer progression but the protein constituents relevant for this effect are unknown. Here we utilised a bioinformatics approach to identify an extracellular matrix (ECM) gene signature overexpressed in multiple cancer types and strongly predictive of adverse outcome. METHODS: Gene expression levels in cancers were determined using Oncomine. Geneset enrichment analysis was performed using the Broad Institute desktop application. Survival analysis was performed using KM plotter. Survival data were generated from publically available genesets. RESULTS: We analysed ECM genes significantly upregulated across a large cohort of patients with ovarian, lung, gastric and colon cancers and defined a signature of nine commonly upregulated genes. Each of these nine genes was considerably overexpressed in all the cancers studied, and cumulatively, their expression was associated with poor prognosis across all data sets. Further, the gene signature expression was associated with enrichment of genes governing processes linked to poor prognosis, such as EMT, angiogenesis, hypoxia, and inflammation. CONCLUSIONS: Here we identify a nine-gene ECM signature, which strongly predicts outcome across multiple cancer types and can be used for prognostication after validation in prospective cancer cohorts.	esophagus
Genetic and epigenetic alterations in normal tissues have differential impacts on cancer risk among tissues.	Genetic and epigenetic alterations are both involved in carcinogenesis, and their low-level accumulation in normal tissues constitutes cancer risk. However, their relative importance has never been examined, as measurement of low-level mutations has been difficult. Here, we measured low-level accumulations of genetic and epigenetic alterations in normal tissues with low, intermediate, and high cancer risk and analyzed their relative effects on cancer risk in the esophagus and stomach. Accumulation of genetic alterations, estimated as a frequency of rare base substitution mutations, significantly increased according to cancer risk in esophageal mucosae, but not in gastric mucosae. The mutation patterns reflected the exposure to lifestyle risk factors. In contrast, the accumulation of epigenetic alterations, measured as DNA methylation levels of marker genes, significantly increased according to cancer risk in both tissues. Patients with cancer (high-risk individuals) were precisely discriminated from healthy individuals with exposure to risk factors (intermediate-risk individuals) by a combination of alterations in the esophagus (odds ratio, 18.2; 95% confidence interval, 3.69-89.9) and by only epigenetic alterations in the stomach (odds ratio, 7.67; 95% confidence interval, 2.52-23.3). The relative importance of epigenetic alterations upon genetic alterations was 1.04 in the esophagus and 2.31 in the stomach. The differential impacts among tissues will be critically important for effective cancer prevention and precision cancer risk diagnosis.	esophagus
Chronic Smoking is Not Associated with Increased Postoperative Opioid Use in Patients with Lung Cancer or Esophageal Cancer.	BACKGROUND: Chronic smokers show differences in pain sensitivity compared to healthy non-smokers. Yet, no study to date has examined whether smoker status has an effect on postoperative pain. OBJECTIVE: We aim to examine a possible correlation between preoperative smoking and postoperative opioid dose based on the hypothesis that smokers would use higher doses of opioids to manage increased postoperative pain. STUDY DESIGN: A retrospective observational cohort study. SETTING: The National Cancer Center in Korea. METHODS: We examined medical record data for patients who had undergone curative resection for either lung or esophageal cancer (lobectomy or bilobectomy for lung cancer or an Ivor Lewis operation for esophageal cancer) between January 1, 2006 and December 31, 2010. We examined the correlation between the total preoperative average number of packs per day multiplied by years of cigarette smoking (pack-years) and morphine equivalent daily doses administered to patients after surgery, considering each type of cancer both individually and together. Partial correlation and regression analyses were performed to determine the causality of a possible relationship between pack-years of cigarette smoking and postoperative opioid dose. RESULTS: A total of 1,129 patients (871 patients with lung cancer and 258 patients with esophageal cancer) were included in the final analysis. There was no significant correlation between total pack-years of cigarette smoking and postoperative opioid dose for lung cancer, esophageal cancer, or both cancer types combined (r = 0.042, -0.012, and 0.037, respectively). In the analysis of both cancer types combined, video-assisted thoracic surgery (VATS) was associated with an 11.1% decrease in opioid dose (β = -0.111, P = 0.003) and epidural analgesia was associated with a 7.2% increase in opioid dose (β = 0.072, P = 0.042). LIMITATIONS: The retrospective design of this study is a limitation. CONCLUSION: Our study did not observe a correlation between preoperative smoking and postoperative opioid dose in patients with lung or esophageal cancer. KEY WORDS: Smoking, postoperative pain, opioid, lung cancer, esophageal cancer, analgesia.	esophagus
A mutational signature associated with alcohol consumption and prognostically significantly mutated driver genes in esophageal squamous cell carcinoma.	BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is often diagnosed at an advanced and incurable stage. Information on driver genes and prognosticators in ESCC remains incomplete. The objective was to elucidate significantly mutated genes (SMGs), mutational signatures, and prognosticators in ESCC. PATIENTS AND METHODS: Three MutSig algorithms (i.e. MutSigCV, MutSigCL and MutSigFN) and '20/20+' ratio-metric were employed to identify SMGs. Nonnegative matrix factorization was used to decipher mutational signatures. Kaplan-Meier survival analysis, multivariate Cox and logistic regression models were applied to analyze association between mutational features and clinical parameters. RESULTS: We identified 26 SMGs, including 8 novel (NAV3, TENM3, PTCH1, TGFBR2, RIPK4, PBRM1, USP8 and BAP1) and 18 that have been previously reported. Three mutational signatures were identified to be prevalent in ESCC including clocklike C>T at CpG, APOBEC overactive C>T at TpCp[A/T], and a signature featured by T>C substitution. The T>C mutational signature was significantly correlated with alcohol consumption (OR: 3.59; 95% CI: 2.30-5.67; P < 0.001). This alcohol consumption signature was also observed in liver cancer and head and neck squamous cell carcinoma, and its mutational activity was substantially higher in samples with mutations in TP53. Survival analysis revealed that TENM3 mutations (HR: 5.54; CI: 2.68-11.45; P < 0.001) and TP53 hotspot mutation p.R213* (HR: 3.37; CI: 1.73-8.06; P < 0.001) were significantly associated with shortened survival outcome. The association remained statistically significant after controlling for age, gender, TNM stage and tumor grade. CONCLUSIONS: We have uncovered several new SMGs in ESCC and defined an alcohol consumption related mutational signature. TENM3 mutations and the TP53 hotspot mutation p.R213* are independent prognosticators for poor survival in ESCC.	esophagus
Evaluation of respiratory motion-corrected cone-beam CT at end expiration in abdominal radiotherapy sites: a prospective study.	BACKGROUND: Cone beam computed tomography (CBCT) for radiotherapy image guidance suffers from respiratory motion artifacts. This limits soft tissue visualization and localization accuracy, particularly in abdominal sites. We report on a prospective study of respiratory motion-corrected (RMC)-CBCT to evaluate its efficacy in localizing abdominal organs and improving soft tissue visibility at end expiration. MATERIAL AND METHODS: In an IRB approved study, 11 patients with gastroesophageal junction (GEJ) cancer and five with pancreatic cancer underwent a respiration-correlated CT (4DCT), a respiration-gated CBCT (G-CBCT) near end expiration and a one-minute free-breathing CBCT scan on a single treatment day. Respiration was recorded with an external monitor. An RMC-CBCT and an uncorrected CBCT (NC-CBCT) were computed from the free-breathing scan, based on a respiratory model of deformations derived from the 4DCT. Localization discrepancy was computed as the 3D displacement of the GEJ region (GEJ patients), or gross tumor volume (GTV) and kidneys (pancreas patients) in the NC-CBCT and RMC-CBCT relative to their positions in the G-CBCT. Similarity of soft-tissue features was measured using a normalized cross correlation (NCC) function. RESULTS: Localization discrepancy from the end-expiration G-CBCT was reduced for RMC-CBCT compared to NC-CBCT in eight of eleven GEJ cases (mean ± standard deviation, respectively, 0.21 ± 0.11 and 0.43 ± 0.28 cm), in all five pancreatic GTVs (0.26 ± 0.21 and 0.42 ± 0.29 cm) and all ten kidneys (0.19 ± 0.13 and 0.51 ± 0.25 cm). Soft-tissue feature similarity around GEJ was higher with RMC-CBCT in nine of eleven cases (NCC =0.48 ± 0.20 and 0.43 ± 0.21), and eight of ten kidneys (0.44 ± 0.16 and 0.40 ± 0.17). CONCLUSIONS: In a prospective study of motion-corrected CBCT in GEJ and pancreas, RMC-CBCT yielded improved organ visibility and localization accuracy for gated treatment at end expiration in the majority of cases.	esophagus