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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although evidence has been mounting that obesity may be related to the increased incidence of oesophageal and gastric cardia malignancies, these reports (mainly case-control studies) have relied on imperfect measures of obesity such as body mass index (BMI), and generally have not clearly distinguished between anatomical subsites within the oesophagus and stomach. In a prospective study of people aged 27-75 years, we directly measured fat mass and fat-free mass (using bioelectrical impedance analysis), height, weight and waist and hip circumferences. Among 41,295 people followed on average for 11.3 years, 30 cases with cancers in the gastric cardia or lower third of the oesophagus and 68 cases with noncardia gastric adenocarcinomas were ascertained via the population cancer registry. The risk of adenocarcinoma of the lower oesophagus and gastric cardia was positively associated with BMI with a hazards ratio (HR) and (95% confidence interval) for people with BMI>or=30 kg/m2 compared with those<25 kg/m2, of 3.7 (1.1-12.4), an HR per 10 cm increase in waist circumference of 1.46 (1.05-2.04), and a HR per 10 kg increase on fat-free mass of 2.06 (1.15-3.69). Noncardia gastric adenocarcinoma showed little relationship with body size. We observed an increased risk of adenocarcinoma of the lower oesophagus and gastric cardia associated with increased BMI, central adiposity and the nonfat component of weight, but found no association with noncardia gastric adenocarcinoma. An increasing prevalence of obesity may be associated with the increasing incidence of gastro-oesophageal cancer observed in many populations.
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PMID:Body size and composition and the risk of gastric and oesophageal adenocarcinoma. 1635 51

The aim of our study was to evaluate the association between the expression of E-cadherin and clinical prognostic factors in uterine endometrioid adenocarcinoma of different histological grade. We have studied 104 postmenopausal women with diagnosis of endometrioid adenocarcinoma. We evaluated the presence of obesity and vaginal bleeding. Surgical specimens were fixed in 10% neutral buffered formalin solution and embedded in paraffin. 4 mm sections were stained by hematoxylin-eosin, von Gieson, and histological type of cancer, metastatic involvement of lymph nodes and depth of myometrial invasion were evaluated. Histological grade of cancer was assessed by FIGO grading system. All samples were analyzed by immunohistochemistry for E-cadherin (Dakocytomation). We assessed the number of E-cadherin-positive and negative tumor cells and degree of positivity (low, moderate, high). Histological study by hematoxylin-eosin has showed grade 1 endometrioid carcinoma in 35 cases (33.7%, group I), grade 2 adenocarcinoma in 44 cases (42.3%, group II), and grade 3 adenocarcinoma in 25 cases (24%, group III). Our results suggest that the loss of E-cadherin expression is associated with a higher histological grade of uterine endometrioid adenocarcinoma, depth of myometrial invasion, lymph node positivity, coexistence of obesity and vaginal bleeding. It seems that local invasion and metastatic spread of tumor should be preceded by the loss of E-cadherin expression in tumor cells, which progressively occurs in carcinogenesis. Therefore, E-cadherin negativity can be used as a poor prognostic factor and more aggressive chemotherapy regimen should be used.
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PMID:The expression of cadherin e and clinical prognostic factors in uterine endometrioid adenocarcinoma. 1636 55

Patients with ovarian cancer with clear cell histology often have venous thromboembolism (VTE) even before surgery. In view of the possible association between clear cell histology and VTE in endometrial cancer, we measured the plasma levels of thrombin-antithrombin III complex (TAT) and D-dimer (DD) in the preoperative examinations of a patient with clear cell adenocarcinoma of the endometrium. Plasma TAT and DD were both highly elevated, though the patient had no symptoms of VTE or risk factors such as obesity or diabetes mellitus. Ultrasound Doppler examination and lung perfusion scintigraphy just before surgery revealed a thrombosis in the left popliteal vein and a pulmonary embolism. After implanting an inferior vena cava filter to prevent a fatal embolism of the lung, we performed abdominal total hysterectomy, bilateral salpingo-oophorectomy, and sampling of the pelvic lymph nodes. The VTE gradually disappeared and the plasma levels of TAT and DD returned to normal after surgery. Possibly, the VTE in this patient may have been associated with the clear cell histology.
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PMID:Successful diagnosis of thromboembolism before surgery in a woman with clear cell adenocarcinoma of the endometrium. 1636 52

The incidence of esophageal cancer has increased dramatically in the Western population in the last 2 decades. In 1975, about three fourths of the esophageal neoplasms were squamous cell carcinomas and the remainder were adenocarcinomas. During the last 2 to 3 decades, this pattern has changed dramatically and the incidence of squamous cell carcinomas has declined while the incidence of adenocarcinomas has increased. The reason for this dramatic increase is not clear, but gastro esophageal reflux disease, obesity and Barrett's esophagus have been identified as risk factors. High grade dysplasia in Barrett's esophagus is a premalignant condition which can progress to invasive adenocarcinoma. In this article, we discuss the natural history of high grade dysplasia (HGD), difficulties in the diagnosis, the incidence of adenocarcinoma in resected specimens and the surgical aspects in the treatment of HGD, including minimally invasive esophagectomy.
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PMID:Surgical aspects of the patient with high-grade dysplasia. 1642 39

At first the association between body mass, reflux, and oesophageal adenocarcinoma might seem easily interpreted, but a more thorough assessment of the published work shows that several factors are missing. Reflux and obesity are established risk factors for oesophageal adenocarcinoma, particularly when they occur in combination. However, the interplay between these and other factors with regard to oesophageal adenocarcinoma is uncertain. Moreover, the contribution of these risk factors in explaining the increasing incidence of oesophageal adenocarcinoma is unclear, because the trends in prevalence of reflux and obesity do not match those of incidence of oesophageal adenocarcinoma. Moreover, none of these factors contribute strongly to the striking predominance of oesophageal adenocarcinoma in men. Thus, several factors that can explain the development of oesophageal adenocarcinoma need to be addressed.
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PMID:Controversies surrounding body mass, reflux, and risk of oesophageal adenocarcinoma. 1657 50

Adenocarcinoma of the exocrine pancreas is the fourth leading cause of cancer-related death in men and women in the U.S. Cytokines and other proinflammatory mediators have been implicated in inflammatory pancreatic diseases including pancreatitis and cancer. We analyzed cytokine gene polymorphisms as risk factors for pancreatic cancer using questionnaire data obtained by in-person interviews and germ line DNA collected in a population-based case-control study of pancreatic cancer (532 cases and 1,701 controls) conducted in the San Francisco Bay Area. We used mass spectrometry and gel-based methods to genotype 308 cases and 964 population-based controls. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using logistic regression analysis and included adjustment for age, sex, and smoking. We assessed potential interactions between these polymorphisms, proinflammatory conditions (e.g., pancreatitis, ulcer, and obesity), and smoking as risk factors for pancreatic cancer. There was no overall association between pancreatic cancer risk and tumor necrosis factor-alpha (TNF-A -308G/A), regulated upon activation, normally T cell-expressed, and presumably secreted (RANTES -403G/A), and CC chemokine receptor 5 (CCR5-Delta32) polymorphisms. There was a nearly 7-fold increased relative risk estimate for pancreatic cancer in individuals with a history of pancreatitis (adjusted OR, 6.9; 95% CI, 3.4-14.1). Among patients with pancreatic cancer, pancreatitis was significantly associated with TNF-A -308 GA + AA (OR, 3.1; 95% CI, 1.3-7.4) and with RANTES -403 GA + AA (OR, 2.3; 95% CI, 1.0-5.4). There was evidence for a possible interaction between current active smoking and CCR5-32del. Our results lend support for the hypothesis that proinflammatory gene polymorphisms, in combination with proinflammatory conditions, may influence the development of pancreatic cancer.
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PMID:Inflammation, genetic polymorphisms in proinflammatory genes TNF-A, RANTES, and CCR5, and risk of pancreatic adenocarcinoma. 1661 15

Recent evidence links obesity with the rising incidence of oesophageal adenocarcinoma. In Ireland between 1995 and 2004 the incidence of oesophageal adenocarcinoma increased by 38%, and this coincided with a 67% increase in the prevalence of obesity. In this study, a prospective case-control study was undertaken in 760 patients presenting to a tertiary centre between 1994 and 2004 diagnosed with cancer of the oesophagus, gastric cardia or stomach. Data were compared with 893 healthy controls. Multivariate logistic regression models were used to calculate the odds ratio (OR) of developing either cancer type according to quartiles of body mass index (BMI). Based on pre-illness BMI, 82% of patients who developed adenocarcinoma of the oesophagus were either overweight or obese compared with 59% of the healthy control population (P<0.001). A dose-dependent relationship existed between BMI and oesophageal adenocarcinoma in males. The adjusted odds ratio was 4.3 (95% CI: 2.3-7.9) among males in the highest BMI quartile compared with males in the lowest quartile (P<0.001 for trend). Using common cut-off points for BMI, the OR of adenocarcinoma of the lower oesophagus was 11.3 times higher (95% CI: 3.5-36.4) for individuals with a BMI >30 kg/m2 versus individuals with a BMI <22 kg/m2 (P<0.001 for trend). For adenocarcinoma of the gastric cardia, males in the top quartile of BMI had an OR of 3.5 (95% CI: 1.3-9.4) compared with the lowest quartile (P=0.03 for trend). A significant (P<0.001) inverse relationship between BMI and oesophageal SCC was observed. The odds ratio for adenocarcinoma of the oesophagus, the oesophago-gastric junction and gastric cardia rose significantly with increasing BMI. For tumours of the lower oesophagus, obesity increased the risk 10.9-fold. The increased risk is significant in males only.
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PMID:Adenocarcinoma of the oesophagus and gastric cardia: male preponderance in association with obesity. 1663 Jul 14

The aim of this study was to compare clinical characteristics of prognostic factors in uterine endometrioid adenocarcinoma of various grades. We have studied 104 postmenopausal women with a histological diagnosis of uterine endometrioid adenocarcinoma. Staging and grading of primary tumor were done according to FIGO system. The following factors were examined: family history of cancer, presence of obesity and vaginal bleeding, recurrence rate within the two years of the study (disease-free periods), vessel permeation, muscle invasion (<1/3, 2/3, >2/3), cervical involvement, lymph node metastasis, ascites cell analysis, parametrium invasion, adnexal metastasis, CA125 pre-surgery values. Histological examination has showed grade 1 endometrioid adenocarcinoma in 35 cases (33,7%, group 1), grade 2 adenocarcinoma in 44 cases (42,3%, group 2), and grade 3 adenocarcinoma in 25 cases (24%, group 3). Most of the factors we have examined seem to be associated with histological grade of uterine endometrioid carcinoma. The analysis of clinicopathological prognostic factors in G1 endometrioid adenocarcinoma cases has showed that about half of these patients are obese, vaginal bleeding is not common, no cervical involvement, parametrium invasion, adnexal metastasis and vessel permeation at the time of diagnosis, no recurrence within two years, pre-surgery value of CA125 is normal, and myometrial invasion is less than 1/3. G3 endometrioid adenocarcinoma cases have showed family history of endometrial cancer, more than half of the patients were obese, with uncommon vaginal bleeding and positive peritoneal cytology, but cervical involvement, parametrium invasion, adnexal metastasis and vessel permeation are present at the time of diagnosis, pre-surgery value of CA125 is high, and myometrial invasion is 2/3 or more than 2/3 in majority of cases, furthermore, in some cases recurrent tumors were developed within two years. G2 endometrioid adenocarcinoma can be considered as an intermediary form which should be managed according to the clinical stage. The results lead to conclude that the histological grade of uterine endometrioid adeno carcinoma seems to be an important independent prognostic indicetor as it is strongly associated with other clinical pathological prognostic factors.
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PMID:Clinical characteristics of prognostic factors in uterine endometrioid adenocarcinoma of various grade. 1663 72

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.
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PMID: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. 1674 Sep 77

Although significant advancements have been made in the treatment of esophageal cancer, this aggressive malignancy commonly presents as locally advanced disease with a poor prognosis. Despite improvements in the detection of premalignant pathology, newer preventative strategies, and the development of more effective combination therapies, the overall incidence of esophageal carcinomas has risen. A clear association has been established between the development of esophageal cancer and Helicobacter pylori infection, gastroesophageal reflux disease, smoking, and heavy alcohol use. However, the growing number of newly diagnosed esophageal adenocarcinomas, despite widespread treatments with proton pump inhibitors and the eradication of H. pylori, leaves the medical community searching for more answers. There is a potential link between esophageal adenocarcinoma and obesity. Common presenting symptoms of esophageal cancer are dysphagia, odynophagia, and progressive weight loss. The initial assessment for patients with these symptoms is made with double-contrast barium esophagraphy. Treatment modalities include surgery, chemotherapy, radiation therapy, or a combination of modalities. Prevention strategies include smoking and alcohol cessation.
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PMID:Esophageal cancer: a review and update. 1683 35


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