crossing96/oncoscreening huggingface dataset:
Added value of PET and PET-CT in oesophageal cancer: a review of current practice.	Oesophageal carcinoma is a relatively rare form of cancer. However, it is also one of the most deadly forms of cancer, with a 5-year survival rate of only 3% for patients with nodal disease, and 42% for those without nodal disease. It is therefore very important to accurately stage the disease at diagnosis and before therapy. In this article, we review the role of commonly used investigative techniques in the diagnosis and staging of oesophageal carcinoma, with special emphasis on PET and PET-CT scanning. The literature is reviewed in the context of our recent experience. A retrospective review of 129 patients with oesophageal carcinoma, who underwent PET or PET-CT scanning over a 24-month period confirmed the incremental value of PET and PET-CT scanning in the staging of oesophageal carcinoma.	esophagus
Effect of proton pump inhibitors on markers of risk for high-grade dysplasia and oesophageal cancer in Barrett's oesophagus.	BACKGROUND: It has been shown that the presence on diagnosis of endoscopic macroscopic markers indicates a high-risk group for Barrett's oesophagus. AIM: To determine whether proton pump inhibitor therapy prior to diagnosis of Barrett's oesophagus influences markers for risk development of subsequent high-grade dysplasia/adenocarcinoma. METHODS: A review of all patients with Barrett's oesophagus entering a surveillance programme was undertaken. Five hundred and two patients diagnosed with Barrett's oesophagus were assessed on diagnosis for endoscopic macroscopic markers or low-grade dysplasia. Subsequent development of high-grade dysplasia/adenocarcinoma was documented. The relationship between the initiation of proton pump inhibitor therapy prior to the diagnosis of BE and the presence of macroscopic markers or low-grade dysplasia at entry was determined. RESULTS: Fourteen patients developed high-grade dysplasia/adenocarcinoma during surveillance. Patients who entered without prior proton pump inhibitor therapy were 3.4 times (95% CI: 1.98-5.85) more likely to have a macroscopic marker or low-grade dysplasia than those patients already on a proton pump inhibitor. CONCLUSIONS: Use of proton pump inhibitor therapy prior to diagnosis of Barrett's oesophagus significantly reduced the presence of markers used to stratify patient risk. Widespread use of proton pump inhibitors will confound surveillance strategies for patients with Barrett's oesophagus based on entry characteristics but is justified because of the lower risk of neoplastic progression.	esophagus
Palliation of malignant esophageal Dysphagia: would you like plastic or metal?	Advanced esophageal carcinoma has a rather dismal prognosis with dysphagia to solids and liquids as a common symptom. Self-expanding metal stents provide immediate and durable relief of dysphagia. Recently, self-expanding plastic stents have been developed for refractory benign esophageal strictures but may have applications in malignant strictures as well. In this issue of The American Journal of Gastroenterology, a multicenter, prospective, randomized, comparative trial evaluates the safety and efficacy of self-expanding metal versus plastic stents for palliation of dysphagia due to esophageal cancer. While the stents compared equivalently for symptom relief, complications were observed more commonly in the plastic stent group.	esophagus
Gastric pull-up reconstruction for the hypopharyngeal and cervical esophageal carcinoma in small thoracic unit.	The objective of this article is to review results of one surgical team for gastric pull-up reconstruction for carcinoma of the hypopharynx and cervical esophagus after pharyngolaryngo-esophagectomy in small thoracic unit. Between July, 2004 and December 2005, four patients underwent pharyngolaryngo-esophagectomy and gastric pull-up reconstruction for carcinoma of hypopharynx and esophagus. There were three female and one male patient with average age at the time of surgery 47 years. The study analyzed complications and mortality in early postoperative period after resections of the carcinoma. Squamous cell cancer in all patients was confirmed. There was no in-hospital mortality and non-fatal complications were occurred in 3 patients. It was recorded two year survival for two patients. Pharyngolaryngo-esophagectomy and gastric pull-up reconstruction can be performed for the patients with carcinoma of the hypopharynx and cervical esophagus with an acceptable operative mortality and morbidity rate even in small thoracic unit. Long term survival despite good early postoperative results still remains poor.	esophagus
Signet-ring cell carcinoma of the esophagus associated with Barrett's epithelium: report of a case.	We herein report a case of infiltrative esophageal signet-ring cell carcinoma resembling gastric signet-ring cell carcinoma. Grossly, the tumor was a diffusely infiltrative carcinoma involving the lower esophagus measuring 11 cm in diameter. The tumor extensively metastasized to the cervical, mediastinal, and abdominal lymph nodes, and the patient died of peritonitis and pleuritis carcinomatosa soon after undergoing a radical esophagectomy. Histologically, the tumor was signet-ring cell carcinoma covered with normal squamous epithelium. However, the most superficial part of the tumor center contained a region of Barrett's mucosa with incomplete-type intestinal metaplasia and a well-differentiated adenocarcinoma component with goblet cells. The expression of cytokeratins 7 and 20 also indicated that both the Barrett's mucosa and the signet-ring cell carcinoma had an esophageal origin. Esophageal signet-ring cell carcinoma with diffuse infiltrative growth is quite rare, and may need a special treatment strategy because of its highly aggressive behavior and poor treatment outcome.	esophagus
Association of combined CYP2E1 gene polymorphism with the risk for esophageal squamous cell carcinoma in Huai'an population, China.	BACKGROUND: Cytochrome P450 2E1 (CYP2E1) has an important role in the metabolic activation of precarcinogens such as N-nitrosoamines and other low relative molecular mass, organic compounds. This study examined whether CYP2E1 RsaI and DraI polymorphism are associated with susceptibility to esophageal squamous cell carcinoma and the correlation between the genotypes and expression levels of CYP2E1 mRNA. METHODS: Seventy-seven patients with newly diagnosed, untreated esophageal squamous cell carcinoma and 79 healthy controls matched in age, gender and residence were recruited for the control study. An RsaI polymorphism in the 5'-flanking region and a DraI polymorphism in the sixth intron of the CYP2E1 gene, which could possibly affect its transcription, were determined in this study by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and mRNA level of CYP2E1 was measured by quantitative real-time reverse transcription PCR. RESULTS: No significant association of RsaI or DraI polymorphism of CYP2E1 with susceptibility of esophageal squamous cell carcinoma were demonstrated (OR = 1.67, 95% CI: 0.89 - 3.15, P = 0.11; OR = 1.11, 95% CI: 0.59 - 2.09, P = 0.74, respectively). With SHEsis software, no linkage disequilibrium was detected between RsaI and DraI polymorphism (D' = 0.528, r(2) = 0.27). When combined RsaI polymorphism with DraI polymorphism, the association between that carrying c2 allele and DD genotype and the risk for esophageal squamous cell carcinoma were found (OR = 5.77, 95% CI: 1.65 - 20.22). Compared with the normal controls, the mRNA levels with RsaI polymorphism, DraI polymorphism, or any combined genotypes in cases showed no statistical difference. CONCLUSIONS: This study suggests that carrying c2 allele and DD genotype conferreded an elevated risk for esophageal squamous cell carcinoma. There was no significant statistical relationship between the genotypes c1/c2, D/C, or the combined allele and mRNA expression.	esophagus
Confocal endomicroscopy for in vivo detection of microvascular architecture in normal and malignant lesions of upper gastrointestinal tract.	BACKGROUND AND AIM: Confocal laser endomicroscopy allows subsurface analysis of gastrointestinal mucosa during ongoing endoscopy. The present study assessed the feasibility of in vivo detecting superficial vascular architecture by confocal endomicroscopy in normal upper gastrointestinal mucosa and malignant lesions. METHODS: Early gastric cancer in eight patients, superficial esophageal carcinoma in six patients, and asymptomatic normal control in 10 patients were studied by confocal endomicroscopy. The characteristic of endomicroscopic microvascular architecture from normal and malignant mucosa was described and images were evaluated. RESULTS: Confocal endomicroscopy enabled clear visualization of the vascular networks of gastroesophageal mucosa. Honeycomb-like and coil-shaped regular microvascular architecture surrounding gastric pits were visible in the normal gastric body and antrum, respectively. Differentiated gastric cancerous mucosa showed hypervascularity and various caliber microvessels with irregular shapes. Undifferentiated gastric cancers disclosed a hypovascularity and irregular short branch vessels. Normal squamous epithelium had regular intraepithelial papillary capillary loops (IPCLs) directed toward the luminal surface. In superficial esophageal squamous carcinoma, dilated IPCLs were visible at the upper layer of the squamous mucosa. In esophageal adenocarcinoma, abnormal microvascular architecture showed tortuous and various calibers blood vessels. Of all the images, 41% were graded as good quality. The mean kappa value for interobserver agreement for the prediction of cancerous mucosa was 0.792. CONCLUSIONS: Confocal laser endomicroscopy system could yield very clear images of superficial microvascular network in the gastroesophageal mucosal layer both in malignant and normal mucosa. Endomicroscopic observation of vascular architecture may be of assistance in the identification of early gastroesophageal cancers.	esophagus
Relationship between Helicobacter pylori infection and gastric atrophy and the stages of the oesophageal inflammation, metaplasia, adenocarcinoma sequence: results from the FINBAR case-control study.	OBJECTIVE: A number of studies have shown an inverse association between infection with Helicobacter pylori and oesophageal adenocarcinoma (OAC). The mechanism of the apparent protection against OAC by H pylori infection and, in particular, the role of gastric atrophy is disputed. The relationship between all stages of the oesophageal inflammation, metaplasia, adenocarcinoma sequence and H pylori infection and gastric atrophy was explored. METHODS: A case-control study involving 260 population controls, 227 OAC, 224 Barrett's oesophagus (BO) and 230 reflux oesophagitis (RO) patients recruited within Ireland was carried out. H pylori and CagA (cytotoxin-associated gene product A) infection was diagnosed serologically by western blot, and pepsinogen I and II levels were measured by enzyme immunoassay. Gastric atrophy was defined as a pepsinogen I/II ratio of <3. RESULTS: H pylori seropositivity was inversely associated with OAC, BO and RO; adjusted ORs (95% CIs), 0.49 (0.31 to 0.76), 0.35 (0.22 to 0.56) and 0.42 (0.27 to 0.65), respectively. Gastric atrophy was uncommon (5.3% of all subjects), but was inversely associated with non-junctional OAC, BO and RO; adjusted ORs (95% CIs), 0.34 (0.10 to 1.24), 0.23 (0.05 to 0.96) and 0.27 (0.08 to 0.88), respectively. Inverse associations between H pylori and the disease states remained in gastric atrophy-negative patients. CONCLUSION: H pylori infection and gastric atrophy are associated with a reduced risk of OAC, BO and RO. While use of the pepsinogen I/II ratio as a marker for gastric atrophy has limitations, these data suggest that although gastric atrophy is involved it may not fully explain the inverse associations observed with H pylori infection.	esophagus
Neoadjuvant cisplatin chemotherapy before chemoradiation: a flawed paradigm?	Effective chemotherapy (CT) treatment of solid tumors emerged with the introduction of anthracyclines and platinum CT in the late 1970s, at first with palliative intent, and later extended into the adjuvant setting. High response rates led to the belief that systemic CT might improve locoregional control and also decrease the risk of distant metastases. A new strategy advocated cisplatin-based neoadjuvant CT (NACT) before definitive local treatment-either surgery or radiotherapy (RT). Response to NACT was viewed as a favorable prognostic sign, which allows the selection of patients most likely to benefit from RT or chemoradiotherapy (CRT). The aim of this discussion is to raise the debate regarding NACT in reducing metastases, improving local control and selecting out good responders for nonsurgical treatment in the following sites: head and neck, esophagus, cervix, anus, nasopharynx, and bladder; as well as non-small-cell lung cancer. NACT has almost invariably failed to deliver an improved outcome in terms of disease-free survival (DFS) or overall survival (OS) when delivered before RT or CRT in all solid tumor sites. The evidence that NACT may improve outcome in terms of DFS or OS is strongest when it is administered before surgical resection, but remains scant before RT or CRT. Taxane-containing regimens look more promising than does cisplatin NACT, but have not been shown to improve on concurrent CRT. Future meta-analyses should compare induction CT followed by RT and induction followed by CRT versus RT or CRT alone.	esophagus
Correlation of matrix metalloproteinase suppressor genes RECK, VEGF, and CD105 with angiogenesis and biological behavior in esophageal squamous cell carcinoma.	AIM: To explore the expression of reversion inducing cysteine-rich protein with Kazal motifs (RECK), vascular endothelial growth factor (VEGF) and endoglin (CD105) protein and its correlation with occurrence, development, invasion and metastasis in esophageal squamous cell carcinoma (ESCC). METHODS: Streptavidin-peroxidase (SP) immunohisto-chemistry was used to detect expression of RECK and VEGF in 62 cases of ESCC, 31 cases of adjacent atypical hyperplastic epithelium and 62 cases of normal esophageal epithelium. CD105 Mb was used to assess microvessel density (MVD). RESULTS: The expression of RECK was closely correlated with histological grade, infiltrative depth and lymphatic metastasis in ESCC (P < 0.05). The expression of RECK decreased during cancer development: normal esophageal epithelium (85.5%, 53/62), adjacent atypical hyperplastic epithelium (71.0%, 22/31), and carcinoma (59.7%, 37/62). There was a significant difference among the groups (P < 0.05). The expression of VEGF protein was closely correlated with infiltrative depth and lymphatic metastasis in ESCC (P < 0.05). The expression of VEGF protein increased during cancer development: normal esophageal epithelium (29.0%, 18/62), adjacent atypical hyperplastic epithelium (54.8%, 17/31), and carcinoma (67.7%, 42/62). There was a significant difference among the groups (P < 0.05). MVDCD105 increased in accordance with histological grade, but there was no significant difference (grade I, 36.92 +/- 10.85; grade II, 37.65 +/- 9.50; and grade III, 38.06 +/- 12.19). The MVDCD105 was closely correlated with infiltration and lymphatic metastasis in ESCC (P < 0.05). The expression of RECK was inversely correlated with the expression of VEGF and CD105. CONCLUSION: RECK, VEGF and CD105 play important roles in the infiltration, metastasis and carcinogenesis in esophageal carcinoma. Angiogenesis in ESCC may be promoted by over-expression of CD105.	esophagus
Longitudinal study of insulin-like growth factor, insulin-like growth factor binding protein-3, and their polymorphisms: risk of neoplastic progression in Barrett's esophagus.	BACKGROUND: Insulin-like growth factor-I (IGF-I) is a potent mitogen. IGF-I and its main binding protein, IGF binding protein-3 (IGFBP-3), and their polymorphisms have been investigated in relation to risk of many cancers, but not esophageal adenocarcinoma. MATERIALS AND METHODS: We used data and specimens from a longitudinal study of persons with Barrett's esophagus (n=344; median, 5.4 years follow up) to determine whether baseline serum concentrations of IGF-I and IGFBP-3 and associated polymorphisms were related to the risk of developing esophageal adenocarcinoma or flow cytometric abnormalities. RESULTS: Overall, circulating concentrations of IGF-I and IGBP-3 were not associated with risk of esophageal adenocarcinoma or flow cytometric abnormalities, with the exception of an approximate tripling of risk of aneuploidy among participants with higher IGFBP-3 levels [above median; adjusted hazard ratio (HR) comparing subjects with levels lower than median versus higher of equal to median, 2.7; 95% confidence interval (95% CI), 1.2-6.0; P=0.01]. Genotypic analyses revealed that persons with the IGF-I [cytosine-adenine (CA)](19) or the IGFBP-3 A-202C C allele were associated with lower circulating concentrations of IGF-I (P(trend)=0.01) and IGFBP-3 (P(trend)=0.002), respectively. Persons with two copies of the IGF-I receptors 2-bp deletion allele had a nonsignificant 2-fold increased risk of tetraploidy (HR, 2.3; 95% CI, 0.9-5.9; P(trend)=0.11). After adjustment for IGFBP-3 levels, participants carrying two IGFBP-3 C alleles had a significantly higher risk of developing aneuploidy (HR, 3.8; 95% CI, 1.0-14.0; P(trend)=0.04) than carriers of A alleles; whereas no associations were observed between the outcomes studied and the IGF-I receptors AGG trinucleotide repeat polymorphism at position 97. CONCLUSION: Our findings, although based on a relatively small number of outcomes and subject to several limitations, indicate a potential role of the complex IGF system in neoplastic progression among persons with Barrett's esophagus.	esophagus
Squamous dysplasia and other precursor lesions related to esophageal squamous cell carcinoma.	Squamous cell carcinoma is the most common tumor of the esophagus worldwide, and it is believed to develop through a sequence of dysplastic precursor lesions, which can be detected both endoscopically and microscopically. There are no published guidelines regarding treatment for dysplasia; however, most authorities recommend increased endoscopic surveillance, with biopsies, for patients with flat low-grade dysplasia and endoscopic mucosal resection, endoscopic submucosal dissection, or esophagectomy for patients with high-grade dysplasia. Future studies are needed to define appropriate endoscopic surveillance frequencies for patients with premalignant lesions of the esophagus. This article discusses squamous dysplasia in detail, which is the most important and well-described risk factor for squamous cell carcinoma of the esophagus.	esophagus
Neoplastic precursor lesions in Barrett's esophagus.	Barrett's esophagus, currently defined as endoscopically apparent columnar metaplasia of the esophagus with histologic documentation of goblet cells, is the precursor to esophageal adenocarcinoma. However, not all patients with this disorder require intensive surveillance. Pathologic diagnosis and grading of dysplasia in mucosal biopsies remains the best and most widely used method of determining which patients are at highest risk for neoplastic progression. The task of diagnosing dysplasia suffers from considerable interobserver variability. Therefore, consultation with expert gastrointestinal pathologists to confirm the diagnosis of dysplasia before definitive management is highly advisable. Adjunctive methods to improve reproducibility, such as immunostaining for alpha-methylacyl-CoA racemase, show promise but require confirmation in larger studies. This article focuses on dysplasia in Barrett's esophagus in terms of its classification, pathologic diagnostic criteria, limitations, natural history, and treatment.	esophagus
Prevention of upper aerodigestive tract cancer in zinc-deficient rodents: inefficacy of genetic or pharmacological disruption of COX-2.	Zinc deficiency in humans is associated with an increased risk of upper aerodigestive tract (UADT) cancer. In rodents, zinc deficiency predisposes to carcinogenesis by causing proliferation and alterations in gene expression. We examined whether in zinc-deficient rodents, targeted disruption of the cyclooxygenase (COX)-2 pathway by the COX-2 selective inhibitor celecoxib or by genetic deletion prevent UADT carcinogenesis. Tongue cancer prevention studies were conducted in zinc-deficient rats previously exposed to a tongue carcinogen by celecoxib treatment with or without zinc replenishment, or by zinc replenishment alone. The ability of genetic COX-2 deletion to protect against chemically-induced forestomach tumorigenesis was examined in mice on zinc-deficient versus zinc-sufficient diet. The expression of 3 predictive biomarkers COX-2, nuclear factor (NF)-kappa B p65 and leukotriene A(4) hydrolase (LTA(4)H) was examined by immunohistochemistry. In zinc-deficient rats, celecoxib without zinc replenishment reduced lingual tumor multiplicity but not progression to malignancy. Celecoxib with zinc replenishment or zinc replenishment alone significantly lowered lingual squamous cell carcinoma incidence, as well as tumor multiplicity. Celecoxib alone reduced overexpression of the 3 biomarkers in tumors slightly, compared with intervention with zinc replenishment. Instead of being protected, zinc-deficient COX-2 null mice developed significantly greater tumor multiplicity and forestomach carcinoma incidence than wild-type controls. Additionally, zinc-deficient COX-2-/- forestomachs displayed strong LTA(4)H immunostaining, indicating activation of an alternative pathway under zinc deficiency when the COX-2 pathway is blocked. Thus, targeting only the COX-2 pathway in zinc-deficient animals did not prevent UADT carcinogenesis. Our data suggest zinc supplementation should be more thoroughly explored in human prevention clinical trials for UADT cancer.	esophagus
Ingestion of thioproline suppresses rat esophageal adenocarcinogenesis caused by duodenogastroesophageal reflux.	Duodenogastroesophageal reflux causes esophageal adenocarcinoma in rats without the use of a carcinogen. This etiology is unclear, but may be associated with endogenous nitrosation in the gastrointestinal tract. Thioproline (TPRO) is an effective nitrite-trapping agent and blocks endogenous nitrosation. We investigated how ingested TPRO affected esophageal adenocarcinogenesis in rats with duodenogastroesophageal reflux (DGER) or gastroesophageal reflux (GER). A series of 200 male Fischer 344 rats received surgery to induce reflux of duodenogastric contents or gastric contents alone into the esophagus. The rats were separated into two divisions according to the surgical procedure employed (DGER or GER), and each division was further subdivided into two groups: one group was fed a special diet (CRF-1 containing 0.5% of TPRO); the other group was fed a standard diet (CRF-1). The rats were given no carcinogen and sacrificed at ten-week intervals from the 25th to the 45th week after surgery. Pathological examination was carried out using hematoxylin-eosin or immunohistochemical staining. Erosion, regenerative thickening, basal cell hyperplasia and columnar-lined epithelium (CLE) were found in both groups of the DGER rats. Adenocarcinoma (AC) appeared only in the DGER rats sacrificed at 35 and 45 weeks following surgery. The incidence of AC at the 45th week was significantly lower in the group of rats fed the diet containing TPRO, as compared to those fed the standard diet, whereas the incidences of CLE were the same for both groups. iNOS protein and nitrotyrosine protein were identified in the CLE and macrophages of the DGER group using immunohistochemical staining. There were no remarkable pathological changes in the esophagi of the rats which underwent the GER procedure. In conclustion, TPRO has an inhibitory effect on esophageal reflux-induced adenocarcinogenesis in rats in that it prevents the progression from CLE to AC.	esophagus