crossing96/oncoscreening huggingface dataset:
Sentinel lymph node mapping with GI cancer.	"Precise evaluation of lymph node status is one of the most important factors in determining clinical outcome in treating gastro-intestinal (GI) cancer. Sentinel lymph node (SLN) mapping clearly has become highly feasible and accurate in staging GI cancer. The lunchtime symposium focused on the present status of SLN mapping for GI cancer. Dr. Kitigawa proposed a new strategy using sentinel node biopsy for esophageal cancer patients with clinically early stage disease. Dr. Uenosono reported on whether the SLN concept is applicable for gastric cancer through his analysis of more than 180 patients with cT1-2, N0 tumors. The detection rate was 95%, the false negative rate of lymph node metastasis including micro-metastasis was 4%, and accuracy was 99% in gastric cancer patients with cT1N0. Dr. Bilchik recommended the best technique for identifying SLNs in colorectal cancer: a combination of radiotracer and blue dye method, emphasizing that this technique will become increasingly popular because of the SLN concept, with improvement in staging accuracy. He stressed that this novel procedure offers the potential for significant upstaging of GI cancer. Dr. Saha emphasized that SLN mapping for colorectal cancer is highly successful and accurate in predicting the presence or absence of nodal disease with a relatively low incidence of skip metastases. It provided the ""right nodes"" to the pathologists for detailed analysis for appropriate staging and treatment with adjuvant chemotherapy. Although more evidence from large-scale multicenter clinical trials is required, SLN mapping may be very useful for individualizing multi-modal treatment for esophageal cancer and might be widely acceptable even for GI cancer."	esophagus
[Stent insertion as palliation of cancer in the esophagus and cardia].	BACKGROUND: The insertion of self-expanding metal stents (SEMS) for palliation of dysphagia in patients with malignant stenosis of the esophagus and cardia, is a well-established procedure. The aim of this retrospective study was to evaluate the results of esophageal stenting in terms of functioning, need of retreatment and survival after stenting. PATIENTS AND METHODS: 37 patients with unresectable esophageal and cardial carcinoma treated with SEMS between January 1997 and May 2004 were retrospectively analysed. RESULTS: One patient died the day the stent was introduced. Otherwise, no major procedural complications were observed. The median time to repeated hospital contact was 25 days, most often due to recurrence of dysphagia. Tumor ingrowth or overgrowth was primarily treated with argon plasma coagulation (APC). Ten patients underwent repeat stent insertion. The median survival time after the first stent insertion was 88 days. CONCLUSION: Insertion of SEMS in patients with inoperable carcinoma in esophagus and cardia should be regarded as a safe procedure. In our study, many patients could stay at home for months without recurrence of dysphagia that needed treatment.	esophagus
Esophageal cancer: the role of integrated CT-PET in initial staging and response assessment after preoperative therapy.	Esophageal cancer, an uncommon neoplasm, has been increasing in incidence over the past few decades. Optimal management of patients is determined by the stage of disease at presentation, patient performance status, and location of the primary cancer. Recently, there has been increasing use of multimodality therapy in suitable candidates that employs preoperative chemotherapy and/or radiation followed by surgical resection. This evolving treatment strategy together with the substantial morbidity and mortality associated with esophagectomy makes appropriate patient selection critical. Computed tomography (CT) and endoscopy/endoscopic ultrasonography are usually carried out to initially stage patients with esophageal cancer, to determine primary tumor response, and to detect nodal and distant metastases after preoperative therapy. Positron emission tomography (PET) with [18F]-fluoro-2-deoxy-D-glucose and integrated CT-PET are useful in the initial staging of patients with esophageal cancer and in the prediction of pathologic response, disease-free interval, and overall survival after preoperative therapy. Importantly, integrated CT-PET imaging decreases the number of futile attempts at surgical resection, mainly because of the detection of occult distant metastases. The following sections review the use of integrated CT-PET imaging in determining the T, N, and M descriptors of the American Joint Commission on Cancer's 2002 guidelines for pathologic and clinical staging at initial diagnosis and after chemoradiation therapy in those patients being considered for surgical resection.	esophagus
Clinical consequences of silent gastroesophageal reflux disease.	Silent gastroesophageal reflux disease (GERD) is a very common phenomenon that involves the incidental finding of erosive esophagitis, Barrett's esophagus, and the evolution of esophageal adenocarcinoma in asymptomatic patients. The reasons for having advanced GERD without clearly identifiable symptoms are poorly understood, primarily due to lack of recognition of this important phenomenon. The clinical implications of silent GERD are vast and should provide the impetus for further research into this group of patients. Recent studies have suggested that sleep disturbances and poor quality of sleep could be the needed clues to identify individuals with silent GERD.	esophagus
Tamoxifen exposure and risk of oesophageal and gastric adenocarcinoma: a population-based cohort study of breast cancer patients in Sweden.	In a population-based cohort study of all women aged over 50 years with breast cancer in the Swedish Cancer Register in 1961-2003, those diagnosed before 31 December 1987 were regarded as unexposed to tamoxifen, whereas those diagnosed after that date were considered potentially exposed. Crosslinkages within the Cancer Register and the Registers of Death and Emigration enabled follow-up. Standardised incidence ratios (SIRs) of oesophageal and gastric cancer represented relative risks. Among 138 885 cohort members contributing with 1 075 724 person-years of follow-up, we found a nonsignificantly increased risk of oesophageal adenocarcinoma during the potential tamoxifen exposure period (SIR 1.60, 95% confidence interval (CI) 0.83-3.08), but the risk estimates decreased with increasing latency interval. No association was observed during the unexposed period. No increased risk of cardia adenocarcinoma was identified in either period. The risk of non-cardia gastric adenocarcinoma was increased in the potential tamoxifen period (SIR 1.27, 1.03-1.57), and almost doubled (SIR 1.86, 95% CI 1.10-3.14) in the period of longest latency (10-14 years). The corresponding overall SIR was increased in the unexposed group also, but here SIR did not increase with longer latency intervals. An increased risk of tobacco-related tumours, that is, oesophageal squamous-cell carcinoma and lung cancer, was limited to the unexposed cohort, indicating that confounding by smoking might explain the increased SIR during the unexposed period. We concluded that there might be a link between tamoxifen and risk of non-cardia gastric adenocarcinoma.	esophagus
Monitoring of response to pre-operative chemoradiation in combination with hyperthermia in oesophageal cancer by FDG-PET.	PURPOSE: To evaluate the use of positron emission tomography using 18F-fluorodeoxyglucose (FDG-PET) to assess early response to pre-operative chemoradiation therapy in combination with external locoregional hyperthermia in patients with oesophageal cancer by correlating the reduction of metabolic activity with histopathologic response. MATERIAL AND METHODS: Twenty-six patients with histopathologically proven intra-thoracic oesophageal cancer (with < or =2 cm gastric involvement), scheduled to undergo a 5-week course of pre-operative chemoradiation therapy and hyperthermia, were included. FDG-PET was performed before (n = 26) and 2 weeks after initiation of therapy (n = 17). FDG uptake was quantitatively assessed by standardized uptake values. RESULTS: After neoadjuvant therapy, 24 of the 26 patients underwent surgery. In 16 patients changes in FDG uptake were correlated to histopathologic response. In these patients, histopathologic evaluation revealed less than 10% viable tumour cells in eight patients (responders) and more than 10% viable tumour cells in eight patients (non-responders). In responders, FDG uptake decreased by a median -44% (-75 to 2); in non-responders, it decreased by a median of -15% (-46 to 40). At a threshold of 31% decrease of FDG uptake compared with baseline, sensitivity to detect response was 75%, with a corresponding specificity of 75%. The positive and negative predictive values were both 75%. CONCLUSION: FDG-PET is a promising tool for early response monitoring in patients undergoing chemoradiation therapy in combination with hyperthermia.	esophagus
Immunohistochemical and quantitative mRNA assessment of ghrelin expression in gastric and oesophageal adenocarcinoma.	BACKGROUND: Ghrelin is an orexigenic gut peptide produced predominantly by the stomach. Gastric mucosal ghrelin production could be compromised by an infiltrating adenocarcinoma. AIMS: To assess the expression of ghrelin mRNA and peptide in oesophagogastric adenocarcinomas and adjacent non-neoplastic mucosa. METHODS: 10 gastric and 22 oesophageal adenocarcinoma archival samples were randomly selected from a database. The presence of ghrelin-positive cells was assessed in cancer and corresponding non-neoplastic mucosa by immunohistochemistry. Quantitative reverse transcriptase polymerase chain reaction (PCR) for ghrelin mRNA was also performed on 24 gastric and 8 oesophageal adenocarcinoma specimens and adjacent non-neoplastic mucosa. RESULTS: Immunohistochemistry and reverse transcriptase PCR confirm a negligible expression of ghrelin in adenocarcinoma specimens. By contrast, non-neoplastic gastric mucosa was rich in ghrelin-positive cells and ghrelin mRNA. The number (median and range) of ghrelin-positive cells per 2 mm section of non-neoplastic mucosa was 73 (45-215) in the corpus; this was significantly higher than in cardia mucosa (9 (0-64), p<0.001) and antral mucosa (5 (0-14), p<0.001). CONCLUSIONS: Gastric and oesophageal adenocarcinomas have no ghrelin-producing cells. The highest level of ghrelin expression was noted in the non-neoplastic mucosa of the gastric corpus. Disruption of the gastric ghrelin-producing mechanism may occur during oesophagogastric malignancy.	esophagus
RhoA and RhoC proteins promote both cell proliferation and cell invasion of human oesophageal squamous cell carcinoma cell lines in vitro and in vivo.	There is growing evidence that Rho proteins are deregulated by overexpression in tumours; and according to some reports, this correlates with disease progression. Our previous clinical study had demonstrated a correlation between RhoA expression and tumour progression in oesophageal squamous cell carcinoma (ESCC). These findings prompted us to study, using nude mice, pathological roles of Rho proteins in human ESCC cells. Western blot analysis in ESCC cell lines, in addition to cell proliferation and in vitro migration assays, were performed to observe the malignant potential of RhoA and RhoC in untransfected and transfected cells. Constitutively active RhoA, RhoC and dominant negative RhoA (dnRhoA) proteins were transfected to ESCC (TE-1 and TE-2) cells. The stably transfected cells were injected into nude mice, and the growth and metastasis of these cells to the lungs were analysed. Tumour tissues were then examined using immunohistochemical methods for proteins Ki-67 (MIB-1), FAK, MMP-1, MMP-9 and TIMP-3. Protein levels of RhoA and RhoC in ESCC cell lines were visualised by Western blotting, and showed highest expression in TE-2 cells. Results from the migration assay illustrated that both RhoA and RhoC play a role in migration of ESCC cells. In TE-2 transfected cells, RhoC showed greater migration compared to RhoA. By using an experimental metastasis model in nude mice, RhoA was found to promote more tumour growth than RhoC, whereas RhoC induced lung metastasis in comparison to RhoA. Ki-67 labelling index was used to evaluate the proliferation potential of tumour tissue inoculated from nude mice. In TE-2 cells RhoA gave a proliferation capacity of 24.8+/-0.5, which was significantly higher than those of TE-2 RhoC 10+/-0.4 (P<0.01). Strong immunoreactivity for FAK, MMP-1 and MMP-9 proteins was present in all tumour cells. By contrast, loss of TIMP-3 expression was observed in all tumour cells. In conclusion, our results indicate that pro-oncogenic Rho proteins are involved in promoting tumour growth, cell migration and metastasis in human ESCC cells in nude mice. The results from this study suggest that active Rho proteins may induce a transforming effect that leads to a malignant phenotype.	esophagus
Leptin stimulates proliferation and inhibits apoptosis in Barrett's esophageal adenocarcinoma cells by cyclooxygenase-2-dependent, prostaglandin-E2-mediated transactivation of the epidermal growth factor receptor and c-Jun NH2-terminal kinase activation.	Obesity is an important risk factor for esophageal adenocarcinoma (EAC), and elevated serum leptin is characteristic of obesity. We hypothesized that leptin may have biological effects in promoting esophageal adenocarcinoma and examined the effects of leptin on the OE33 Barrett's-derived EAC line. Proliferation was assessed by dimethylthiazoldiphenyltetra-zoliumbromide and 5-bromo-2'-deoxyuridine incorporation assays and apoptosis by ELISA of intracellular nucleosomes. Intracellular signaling was examined using specific pharmacological inhibitors and direct detection of phosphorylated active kinases. Expression of the long and short leptin receptors by OE33 cells was confirmed by RT-PCR, Western blotting and immunocytochemistry. Leptin stimulated OE33 cell proliferation in a dose-dependent manner and inhibited apoptosis. These effects were dependent on cyclooxygenase (COX)-2 and replicated by adding prostaglandin E2 (PGE2). The effects of PGE2 and leptin were abolished by the EP-4 antagonist AH23848. ERK, p38 MAPK, phosphatidylinositol 3'-kinase/Akt, and Janus tyrosine kinase (JAK)-2 were activated upstream of COX-2 induction, whereas the epidermal growth factor receptor and c-Jun NH2-terminal kinase (JNK) were downstream of COX-2. The activation of ERK and Akt but not p38 MAPK was JAK2 dependent. PGE2 stimulated phosphorylation of JNK in an EGF receptor-dependent manner, and activation of the epidermal growth factor receptor required protein kinase C, src, and matrix metalloproteinase activities. We conclude that leptin stimulates cell proliferation and inhibits apoptosis in OAC cells via ERK, p38 MAPK, phosphatidylinositol 3'-kinase/Akt, and JAK2-dependent activation of COX-2 and PGE2 production. Subsequent PGE2-mediated transactivation of the epidermal growth factor receptor and JNK activation are essential to the leptin effects. These effects may contribute to the greatly increased risk of esophageal adenocarcinoma in obesity.	esophagus
[Association of adenocarcinoma of esophagus and breast cancer in a male with Madelung' disease].	The development of a cancer of the esophagus in women who previously had received radiotherapy for breast cancer is a known although infrequent event. The risk of apparition of the second neoplasia is greater in women who survive at least ten years after the exposition to the radiation. Squamous cell carcinoma is the histological subtype more frequent. We report a case of adenocarcinoma of the esophagus in a man diagnosed of benign symmetrical lipomatosis (Madelung' disease), who had received adjuvant radiotherapy three years before for breast cancer.	esophagus
Phase I/II adenoviral p53 gene therapy for chemoradiation resistant advanced esophageal squamous cell carcinoma.	We investigated the feasibility, safety, biological activity and therapeutic efficacy of adenovirus-mediated p53 gene transfer in patients with chemoradiation resistant advanced esophageal carcinoma. Eligible patients were not surgical candidates and had measurable, advanced squamous cell carcinoma of the esophagus that was resistant to chemoradiation therapy. On a 28-day cycle, intratumoral injections of Ad5CMV-p53 (INGN 201; ADVEXIN) were administered on days 1 and 3 at four dose levels (10 x 10(11) particles to 25 x 10(11) particles) and treated for up to five cycles. Ten patients received a total of 26 cycles with no dose-limiting toxicity. Administration of multiple courses was feasible and well-tolerated. Local tumor responses revealed stable disease in nine cases and progressive disease in one case. The overall responses were stable in six and progressive in four cases. Using polymerase chain reaction (PCR) analyses, gene transfer and p53 specific transgene expression were detected in tumor biopsy tissue from all patients. mRNA levels of p53, p21 and MDM2 increased in all but one case. Three patients showed absence of disease upon repeat biopsies. Substantial improvement in swallowing was observed in one patient with stenotic lesions. Intratumoral injection of Ad5CMV-p53 is safe, feasible and biologically active when administered in multiple doses to patients with esophageal cancer. Observations from this study indicate that this treatment results in local antitumor effects in chemoradiation resistant esophageal squamous cell carcinoma.	esophagus
Influence of F-fluorodeoxyglucose-positron emission tomography on computed tomography-based radiation treatment planning for oesophageal cancer.	The addition of positron emission tomography (PET) information to CT-based radiotherapy treatment planning has the potential to improve target volume definition through more accurate localization of the primary tumour and involved regional lymph nodes. This case report describes the first patient enrolled to a prospective study evaluating the effects of coregistered positron emission tomography/CT images on radiotherapy treatment planning for oesophageal cancer. The results show that if combined positron emission tomography/CT is used for radiotherapy treatment planning, there may be alterations to the delineation of tumour volumes when compared to CT alone. For this patient, a geographic miss of tumour would have occurred if CT data alone were used for radiotherapy planning.	esophagus
Preoperative laparoscopic ligation of the left gastric vessels in preparation for esophagectomy.	Anastomotic leak is a major cause for morbidity after esophagectomy. The cause is believed to be ischemia of the gastric conduit. Preoperative embolization of the left gastric vessels in preparation for esophagectomy has been shown to improve collateral blood flow of the gastric conduit and may reduce the frequency of anastomotic dehiscence after esophagectomy. This report describes the technique of laparoscopic division of the left gastric vessels in 9 patients who underwent pre-esophagectomy staging laparoscopy. Our initial experience demonstrates that laparoscopic ligation of the left gastric artery is a safe alternative to embolization and can be performed in conjunction with staging laparoscopy for patients with esophageal cancer.	esophagus
The role of radiation therapy in thoracic tumors.	Radiation plays an important role in the treatment of thoracic tumors. During the last 10 years there have been several major advances in thoracic RT including the incorporation of concurrent chemotherapy and the application of con-formal radiation-delivery techniques (eg, stereotactic RT, three-dimensional conformal RT, and intensity-modulated RT) that allow radiation dose escalation. Radiation as a local measure remains the definitive treatment of medically inoperable or surgically unresectable disease in NSCLC and part of a multimodality regimen for locally advanced NSCLC, limited stage SCLC, esophageal cancer, thymoma, and mesothelioma.	esophagus
Differences of onset age and survival rates in esophageal squamous cell carcinoma cases with and without family history of upper gastrointestinal cancer from a high-incidence area in North China.	BACKGROUND: Gene expression analyses indicate that there are 152 genes of which the expression differs significantly in esophageal squamous cell carcinoma (ESCC) cases with positive as opposed to those with negative family history of upper gastrointestinal cancer (FHUGIC) in the high-incidence area for ESCC in northern China. However, the question as to whether there is any difference of onset age or survival rates in the familial and sporadic cases of ESCC in the area is unknown. AIMS: To investigate the differences of onset age or survival rates in the familial and sporadic cases of ESCC for surgically treated ESCC patients from the high-incidence area. METHODS: Retrospective analyses were performed on the clinicopathologic and survival data of ESCC cases (N = 1715) who had undergone surgery alone from 1985 to 1994 in Hebei Cancer Center, a provincial cancer center established primarily to treat esophageal cancer in the high-incidence area, to investigate the differences. All the patients had been native residents of the high-incidence area in northern China. Student's t-test was used to test the difference of onset ages, and Cox Proportional Hazard Model was used to examine the differences of survival rates in the familial and sporadic cases of ESCC. RESULTS: Although the familial cases of ESCC had had a significantly earlier onset than the sporadic cases (P < 0.00), they experienced relatively lower survival rates than the sporadic cases after surgery. The differences of survival rates in the familial and sporadic cases were significant for patients above the age of 50 years (P(Wald) = 0.04) and for the T(is, 1)N(0)M(0) group (P(Wald) = 0.04), the differences were bigger for early-staged than for the later-stage groups, and the differences persisted when adjusted for or stratified by confounding factors such as sex, age (under versus above the age of 50 years), smoking, drinking, cancer segment location, surgery year (calendar year), stage (UICC 4th Ed, 1987), and Resection category. Overall, cases under the age of 50 years old showed a higher survival curve than cases above the age of 50 years old, and this was especially true for the familial case group where the difference was significant (P(Wald) = 0.03). CONCLUSION: The findings suggest that the familial ESCC may develop earlier, and may have a poorer prognosis than the sporadic ESCC. Both earlier onset and poorer outcome may be important features for the familial as opposed to the sporadic cases of ESCC. The association between younger onset age and higher survival rates found for the familial cases may indicate some survival benefit for early discovery for people with positive FHUGIC in the high-incidence area.	esophagus