crossing96/oncoscreening huggingface dataset:
Superficial primary small cell carcinoma of the esophagus: clinicopathological and immunohistochemical analysis of 15 cases.	Primary esophageal small cell carcinoma (PESCC) is a relatively rare and aggressive tumor with poor prognosis. Systemic spreading and metastasis often occur at diagnosis. Although 5-year survival rate of superficial squamous cell carcinoma of the esophagus can be 86.1%, 5-year survival rate of superficial PESCC is still relatively low. This study mainly retrospectively analyzed clinicopathological and immunohistochemical features of 15 cases of superficial PESCC in our hospital from 1990 to 2004, in order to find suitable diagnostic markers and applicable therapies for this disease. The records mainly included presenting symptoms, demographics, diagnostic method, histopathology, follow-up, and therapy. Immunohistochemical staining of chromogranin A (CgA), neuron-specific enolase (NSE), synaptophysin (Syn), neuronal cell adhesion molecules (CD56), thyroid transcription factor-1 (TTF-1), cytokeration 34betaE12 (CK34betaE12), cytokeratin (AE1/AE3), and cytokeratin 10/13 was performed. Incidence of superficial PESCC accounted for 4.8% of that of superficial carcinoma of the esophagus during the same period. Initial symptoms of all patients were dysphagia or accompanied with retrosternal pain and upper abdominal pain, and duration of these symptoms was 75 days averagely. Mean age of patients was 58.8 years old, and the male-to-female ratio was 2.75 : 1. Lesions were mainly located at middle thoracic esophagus. One, 2, and 5-year survival rates were 66.7, 33.3, and 6.7%, respectively. The median survival time was 19 months and mean survival time was 23.7 months after diagnosis. The percentages of PESCC samples with positive immunoreactivity were NSE 100%, Syn 100%, AE1/AE3 100%, CD56 93.3%, TTF-1 60%, CgA 53.3%, CK34betaE12 6.7%, and cytokeratin 10/13 0%, respectively. Our study suggested that PESCC was a rare and aggressive tumor with high malignancy. Superficial PESCC had rapid progression and poor prognosis compared with superficial squamous cell carcinoma of the esophagus at the same stage. The systemic therapy based on combination of postoperative chemotherapy and radiotherapy might be an effective approach for the treatment of superficial PESCC as a systemic disease. Higher proportion of positive labeling of NSE, Syn, AE1/AE3, CD56, TTF-1, and CgA in PESCC was valuably applied in diagnosis and differential diagnosis.	esophagus
Assessment of response to neoadjuvant therapy in esophageal cancer: an updated systematic review of diagnostic accuracy of endoscopic ultrasonography and fluorodeoxyglucose positron emission tomography.	For assessing response to neoadjuvant therapy in patients with esophageal cancer, both endoscopic ultrasonography (EUS) and fluorodeoxyglucose positron emission tomography (FDG-PET) are commonly used, and despite few controlled trials, it is not known if one imaging modality is superior to the other. Also, relative diagnostic accuracy of early (during the course of neoadjuvant therapy) and FDG-PET after completion of neoadjuvant therapy has not been reviewed. The aim of this study was to perform a systematic review of published information to compare diagnostic accuracy of EUS and FDG-PET in this setting. A search of the MEDLINE, EMBASE, and Cochrane databases was performed along with a manual search of cross-references of eligible articles. Data on the accuracy of the imaging modalities were compared by constructing summary receiver-operating characteristic curves. Seven studies with EUS and 15 with FDG-PET were included in the final analysis (N= 966). The sensitivity of EUS and FDG-PET ranged from 20 to 100% and 42 to 100%, respectively. The specificity ranged from 36 to 100% and 27 to 100%, respectively. The areas under the curve were 0.86 (95% confidence interval [CI]: 0.77-0.96) for EUS and 0.80 (95% CI: 0.72-0.89) for FDG PET (P= 0.37). The maximum joint sensitivity and specificity (Q* index) values for EUS and FDG-PET were 0.79 (95% CI: 0.70-0.88) and 0.74 (95% CI: 0.66-0.81), respectively (P= 0.38). There was no difference in accuracy between early FDG-PET and FDG-PET after completion of neoadjuvant therapy. EUS and FDG-PET have similar overall diagnostic accuracy for assessment of response to neoadjuvant therapy in patients with esophageal cancer.	esophagus
p12CDK2-AP1 is associated with tumor progression and a poor prognosis in esophageal squamous cell carcinoma.	p12 CDK2-associating protein 1 (p12CDK2-AP1) is a growth suppressor that negatively regulates cyclin-dependent kinase 2 (CDK2) activities. In addition, p12CDK2-AP1 has also been shown to interfere in DNA replication. A reduction of p12CDK2-AP1 expression is known to be a negative prognostic indicator in patients with oral squamous cell carcinoma. To elucidate the role of p12CDK2-AP1 expression in esophageal squamous cell carcinoma (ESCC), we immunohistochemically examined the expression of p12CDK2-AP1 protein in 120 resected ESCC specimens and determined its association with the clinicopathological characteristics and prognosis. Of the 120 ESCCs, 79 (65.8%) showed positive staining (>or=25% of cancer cells showing p12CDK2-AP1 expression), while 41 (34.2%) lacked the staining (<25% of cancer cells showing p12CDK2-AP1 expression). Negative staining for p12CDK2-AP1 was found to be significantly associated with advanced lesions [depth of tumor (P=0.001), lymph node metastasis (P<0.001), pathological stage (P<0.0001) and venous invasion (P<0.0001)], and a poor prognosis (disease-free survival and overall survival: log-rank P<0.05). The rate of lymph node metastasis in patients with p12CDK2-AP1 negative-T1 ESCC was significantly higher than that in patients with p12CDK2-AP1 positive one (P<0.05). These results suggest the down-regulation of p12CDK2-AP1 to be related to tumor aggressiveness and a poor prognosis in patients with ESCC.	esophagus
Role of the vitamin C in diethylnitrosamine-induced esophageal cancer in Wistar rats.	PURPOSE: To evaluate the inhibitory effect of vitamin C on the experimental esophageal carcinogenesis induced by diethylnitrosamine (NDEA). METHODS: Sixty Wistar male rats aged three months, with mean weight of 210 g were employed in the study and were divided into four different groups according to the drinking drugs: group I--controls: only water, seven days a week; group II--only vitamin C, seven days a week; group III--NDEA, three days a week and water during the other four days; group IV--NDEA, three days a week and vitamin C during the other four days; group V--NDEA together with vitamin C three days a week, and only water during the other four days and group VI--NDEA together with vitamin C three days a week and vitamin C during the other four days. The dosages of NDEA were: --10 mg./Kg/day and vitamin C--200 mg/animal/day, dissolved in drinking water. The animals were observed during 180 days and after that each one was sacrificed and its esophagus and the stomach were removed together and macro and microscopically analyzed to identify any tumors. RESULTS: The largest number of tumors was observed in the group III: 48 macroscopic lesions (4.8 lesions per animal) and 23 microscopic lesions (2.3 lesions per animal). The groups that received vitamin C (groups IV, V and VI) showed smaller number of tumors: group V--0.5 macroscopic lesions and 0.3 microscopic lesions per animal and group VI--0.1 macroscopic lesions and 0.1 microscopic lesions per animal. The incidence of tumors in the groups V and VI showed statistical significance (p<0.05), when compared to the other groups. CONCLUSION: The vitamin C administered together with diethylnitrosamine showed an inhibitory effect on the experimental esophageal carcinogenesis in Wistar rats.	esophagus
A novel approach to cancer staging: application to esophageal cancer.	A novel 3-step random forests methodology involving survival data (survival forests), ordinal data (multiclass forests), and continuous data (regression forests) is introduced for cancer staging. The methodology is illustrated for esophageal cancer using worldwide esophageal cancer collaboration data involving 4627 patients.	esophagus
Medical treatment of Barrett's esophagus: can it prevent cancer?	The challenge of the title of this article is attention getting. How can medical therapy prevent cancer if anti-reflux surgery cannot prevent the neoplastic progression of Barrett's esophagus? Can anything short of esophagectomy prevent cancer? In the face of the increasing incidence of adenocarcinoma of the esophagus into the twenty-first century, the medical therapy of Barrett's esophagus and its potential role in preventing cancer are explored.	esophagus
Risk factors for esophageal cancer development.	The incidence of esophageal adenocarcinoma is increasing at a rate greater than that of any other cancer in the Western world today. Barrett's esophagus is a clearly recognized risk factor for the development of esophageal adenocarcinoma, but the overwhelming majority of patients with Barrett's esophagus will never develop esophageal cancer. To date, dysplasia remains the only factor useful for identifying patients at increased risk for the development of esophageal adenocarcinoma in clinical practice. Other epidemiologic risk factors include aging, gender, race, obesity, reflux symptoms, smoking, and diet. Factors that may protect against the development of adenocarcinoma include infection with Helicobacter pylori, a diet rich in fruits and vegetables, and consumption of aspirin and NSAIDs.	esophagus
Appropriateness of the indication for upper endoscopy: a meta-analysis.	BACKGROUND: Application of appropriate indications for upper endoscopy (EGD) should conserve limited endoscopic resources. To perform a systematic review and meta-analysis to assess the efficacy of American Society for Gastrointestinal Endoscopy and European Panel on the Appropriateness of Gastrointestinal Endoscopy guidelines in selecting patients referred for an upper endoscopy relative to the detection of gastro-oesophageal cancer. METHODS: Studies comparing the appropriateness of EGD indication according to American Society for Gastrointestinal Endoscopy or European Panel on the Appropriateness of Gastrointestinal Endoscopy guidelines and the detection of relevant endoscopic findings and cancer were identified by searching the Medline (1982 to September 2008). Pre-defined outputs of the meta-analysis were sensitivity, specificity, and positive and negative likelihood ratios (LR+, LR-). RESULTS: We included eight cohort studies comprising 13,856 patients; 10,643 EGD indications were categorized as appropriate, and 3010 (22%) as inappropriate. For relevant findings, the adjusted sensitivity, specificity, LR+, and LR- were 85% (95% CI, 84-86%), 28% (95% CI, 27-29%), 1.18 (95% CI, 1.1-1.3) and 0.6 (95% CI, 0.5-0.7), respectively. For cancer detection, the adjusted sensitivity, specificity, LR+, and LR- were 97% (95% CI, 94-98%), 22% (95% CI, 22-23%), 1.2 (95% CI, 1.1-1.4), and 0.2 (95% CI, 0.05-0.9), respectively. CONCLUSIONS: For inappropriate EGD, the very low likelihood of cancer argues against endoscopic referral, whereas the low specificity substantially reduces the predictive value of an appropriate indication for both cancer and relevant endoscopic findings.	esophagus
Amelanotic malignant melanoma of the esophagus: report of two cases with immunohistochemical and molecular genetic study of KIT and PDGFRA.	The author reports herein two cases of amelanotic malignant melanoma of the esophagus. Case 1 is an 87-year-old woman who was admitted to our hospital because of nausea and vomiting. Endoscopic examination revealed an ulcerated tumor of the distal esophagus, and a biopsy was taken. The biopsy showed malignant polygonal and spindle cells. No melanin pigment was recognized. Immunohistochemically, the tumor cells were positive for melanosome (HMB45), S100 protein, KIT and Platelet derived growth factor receptor-alpha (PDGFRA). The patient was treated by chemotherapy and radiation, but died of systemic metastasis 12 mo after the presentation. Case 2 is a 56-year-old man presenting with dysphagia. Endoscopic examination revealed a polypoid tumor in the middle esophagus, and a biopsy was obtained. The biopsy showed malignant spindle cells without melanin pigment. Immunohistochemically, the tumor cells were positively labeled for melanosome, S100 protein, KIT and PDGFRA. The patient refused operation, and was treated by palliative chemotherapy and radiation. He died of metastasis 7 mo after the admission. In both cases, molecular genetic analyses of KIT gene (exons 9, 11, 13 and 17) and PDGFRA gene (exons 12 and 18) were performed by the PCR direct sequencing method, which showed no mutations of KIT and PDGFRA genes. This is the first report of esophageal malignant melanoma with an examination of the expression of KIT and PDGFRA and the mutational status of KIT and PDGFRA genes.	esophagus
CRP genetic polymorphism is associated with lymph node metastasis in thoracic esophageal squamous cell cancer.	BACKGROUND: Lymph node involvement is the most important prognostic factor in thoracic esophageal cancer. A more accurate molecular technique for diagnosing lymph node metastasis and a better understanding of the molecular mechanisms governing lymph node metastasis would be highly desirable. The purpose of this study is to examine the association between inflammation-related genetic polymorphisms and lymph node metastasis. METHODS: The study participants were 113 Japanese patients undergoing curative surgery for thoracic esophageal squamous cell cancer. DNA was extracted from blood samples and genetic polymorphisms in C-reactive protein (CRP), tumor necrosis factor (TNF)-alpha and -beta, interferon (IFN)-gamma, transforming growth factor (TGF)- beta, interleukin (IL)-1beta, IL-1 receptor antagonist, IL-2, IL-4, IL-6, IL-6 receptor, IL-10, and IL-12beta were investigated using the polymerase chain reaction-restriction fragment length polymorphism method. We then assessed the association between inflammation-related genes and lymph node metastasis. RESULTS: For CRP 1846C>T polymorphism, the frequency of the 1846T/T genotype was significantly higher in patients with lymph node metastasis (P = 0.0043), and the odds ratio (3.040) derived from logistic regression models indicated that the 1846T/T genotype significantly increases the likelihood of lymph node metastasis. In submucosal cancer, the utility of CRP 1846C>T polymorphism for predicting lymph node involvement was superior to usual methods (computed tomography and ultrasonography), with positive and negative predictive values of 69% and 75%, respectively. CONCLUSIONS: These findings suggest that CRP polymorphism is a potentially effective predictor of lymph node metastasis and may thus be useful for deciding on treatment strategy.	esophagus
Down-regulation of HLA class I antigen-processing machinery components in esophageal squamous cell carcinomas: association with disease progression.	OBJECTIVE: Lack of human leukocyte antigen (HLA) presentation has been proposed to contribute to the immune evasion of cancer cells in some cancers including esophageal cancer. The aim of this study was to examine the expression of HLA class I antigen and the antigen-processing machinery (APM) components in esophageal squamous cell carcinoma (ESCC) lesions and to assess their association with histopathological characteristics. MATERIAL AND METHODS: A total of 143 formalin-fixed, paraffin-embedded ESCC lesions collected in two hospitals in Shandong Province of China were studied. The expression levels were determined by immunohistochemistry. RESULTS: TAP1, TAP2, LMP2, LMP7, beta2m, and HLA class I antigen were lost or down-regulated in 30.8%, 35.0%, 45.0%, 48.0%, 56.0%, and 60.8% of the ESCC lesions tested, respectively. The loss of or down-regulated expressions of HLA class I, beta2m, TAP1, LMP2, and LMP7 in tumor lesions were all significantly correlated to tumor grade and lymph node status. Expression of HLA class I antigens was strongly correlated to the expression levels of beta2m, TAP1, TAP2, LMP2, and LMP7, suggesting APM component defects as a mechanism underlying HLA class I antigen down-regulation in ESCC lesions. Expression of APM components and HLA class I antigens was significantly associated with the extent of intratumoral T-cell infiltration. CONCLUSIONS: Our results indicate that lack or reduction of HLA class I antigens and expression of APM components in ESCC may render some tumor cells to escape the immunosurveillance mediated by CD8(+) T cells and contribute to the clinical course of ESCC.	esophagus
Assessment of familiality, obesity, and other risk factors for early age of cancer diagnosis in adenocarcinomas of the esophagus and gastroesophageal junction.	OBJECTIVES: Adenocarcinomas of the esophagus and adenocarcinomas of the gastroesophageal junction are postulated to be complex genetic diseases. Combined influences of environmental factors and genetic susceptibility likely influence the age at which these cancers develop. The aim of this study was to determine whether familiality and other recognized risk factors are associated with the development of these cancers at an earlier age. METHODS: A structured validated questionnaire was utilized to collect self-reported data on gastro-esophageal reflux symptoms, risk factors for Barrett's esophagus (BE) and family history, including age of cancer diagnosis in affected relatives from probands with BE, adenocarcinoma of the esophagus, or adenocarcinoma of the gastroesophageal junction, at five tertiary care academic hospitals. Medical records of all relatives reported to be affected were requested from hospitals providing this cancer care to confirm family histories. Familiality of BE/cancer, obesity (defined as body mass index >30), gastroesophageal reflux symptoms, and other risk factors were assessed for association with a young age of cancer diagnosis. RESULTS: A total of 356, 216 non-familial and 140 familial, cancers were studied. The study population consisted of 292 (82%) men and 64 (18%) women. Mean age of cancer diagnosis was no different in a comparison of familial and non-familial cancers, 62.6 vs. 61.9 years, P=0.70. There were also no significant differences in symptoms of gastroesophageal reflux, body mass index, race, gender, and smoking history between familial and non-familial cancers. Mean age of cancer diagnosis was significantly younger in those who were obese 1 year before diagnosis as compared to those who were non-obese, mean age 58.99 vs. 63.6 years, P=0.008. Multivariable modeling of age at cancer diagnosis showed that obesity 1 year before diagnosis was associated with a younger age of cancer diagnosis (P=0.005) after adjustment for heartburn and regurgitation duration. CONCLUSIONS: Obesity is associated with the development of esophageal and gastroesophageal junctional adenocarcinomas at an earlier age. Familial cancers arise at the same age as non-familial cancers and have a similar risk factor profile.	esophagus
HOXA13 promotes cancer cell growth and predicts poor survival of patients with esophageal squamous cell carcinoma.	Homeobox genes are known to be classic examples of the intimate relationship between embryogenesis and tumorigenesis. Here, we investigated whether inhibition of HOXA13, a member of the homeobox genes, was sufficient to affect the proliferation of esophageal cancer cells in vitro and in vivo, and studied the association between HOXA13 expression and survival of patients with esophageal squamous cell carcinoma (ESCC). HOXA13 expression was permanently knocked down using an RNA interference technique, and cell strain with stable knockdown of HOXA13 protein was established. Colony formation assay showed that the number of colonies in HOXA13 protein-deficient cells was significantly less than that of control cells (P < 0.01). Tumor growth in nude mice showed that the weight and volume of tumors from the HOXA13 knockdown cells was significantly less than that from the control cells (P < 0.01). Then, HOXA13 expression in ESCC specimens and paired noncancerous mucosa was detected by immunohistochemistry, and overexpression of HOXA13 was found to be more pronounced in ESCCs than paired noncancerous mucosa (P < 0.05). Furthermore, the association of HOXA13 expression and disease-free survival time was analyzed in 155 ESCC cases. The median survival time of patients expressing HOXA13 was significantly shorter than HOXA13-negative patients (P = 0.0006). Multivariate analysis indicated that tumor-node-metastasis (TNM) stage and HOXA13 expression were independent predictors of disease-free survival time of patients with ESCC. Our results showed that HOXA13 expression enhanced tumor growth in vitro and in vivo, and was a negative independent predictor of disease-free survival of patients with ESCC.	esophagus
Dietary vitamin D and cancers of the oral cavity and esophagus.	BACKGROUND: Data on the association between vitamin D and upper digestive tract neoplasms are limited. METHODS: In two case-control studies in Italy, we examined the relation between dietary vitamin D intake and squamous cell carcinoma of the esophagus (SCCE; 304 cases) and oral/pharyngeal cancer (804 cases). Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by multiple logistic regression. RESULTS: Adjusted ORs for SCCE and oral/pharyngeal cancer were 0.58 (95% CI 0.39-0.86) and 0.76 (95% CI 0.60-0.94), respectively, for the highest tertile of vitamin D intake. Using a reference group of those in the highest tertile of vitamin D who were never/former smokers, ORs were 8.7 (95% CI 4.1-18.7) for SCCE and 10.4 (95% CI 6.9-15.5) for oral/pharyngeal cancer among heavy smokers in the lowest vitamin D tertile; similarly, compared with those in the highest tertile of vitamin D who drank <3 alcoholic drinks/day, corresponding ORs were 41.9 (95% CI 13.7-128.6) for SCCE and 8.5 (95% CI 5.7-12.5) for oral/pharyngeal cancer, among heavy alcohol drinkers in the lowest vitamin D tertile. CONCLUSION: We observed inverse associations between dietary vitamin D intake and risk of SCCE and, perhaps, oral/pharyngeal cancer, which were most pronounced among heavy current smokers and heavy consumers of alcohol.	esophagus
Gastrointestinal stromal tumor of the esophagus.	Gastrointestinal stromal tumors (GISTs) are rare mesenchymal neoplasms that account for 0.2% of all GI neoplasms. We report a case of a 62-year-old male with a large esophageal GIST, and discuss the pathophysiology of the disease and the current management principles. This case is noteworthy because it documents a rare lesion in the esophagus that presents like other neoplastic diseases in this organ that usually carry a poor prognosis. An aggressive approach (e.g., more radical surgery, radiotherapy, and chemotherapy) might have been pondered based purely on the size of the lesion in this patient. It is important that primary care physicians and surgeons be aware of the possibility of the presence of this potentially curable lesion so as to avoid overtreatment.	esophagus