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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pancreatic cancer (PC) is the most fatal of all gastrointestinal cancers, wherein its mortality compares strikingly with its incidence. Unfortunately, 80-90% of PCs are diagnosed in the nonresectable stage. While the lifetime risk of PC in developed countries is approximately 1-3%, it is the fifth most common cause of cancer deaths among both males and females in Western countries. It occurs in excess in Jews. Approximately 5-10% of PC shows familial clustering. Examination of such familial clusters must take into consideration cancers of diverse anatomic sites, such as malignant melanoma in the familial atypical multiple melanoma (FAMMM) syndrome due to the CDKN2A (p16) germline mutation, and combinations of colorectal and endometrial carcinoma, ovarian carcinoma, and several other cancers in hereditary nonpolyposis colorectal cancer (HNPCC), which are due to mismatch repair germline mutations, the most common of which are MSH2 and MLH1 . Other hereditary disorders predisposing to PC include Peutz-Jeghers syndrome, due to the STK11 mutation, familial pancreatitis due to the cationic trypsinogen gene, site-specific familial pancreatic cancer which may be due to the 4q32-34 mutation, hereditary breast-ovarian cancer (HBOC) syndrome that is due to BRCA2 and possibly some families with HBOC that is due to BRCA1 , familial adenomatous polyposis due to the ATP gene, and ataxia telangiectasia due to the ATM germline mutation. This extant heterogeneity mandates that the physician be knowledgeable about these PC-prone syndromes which play such an important role when considering the differential diagnosis of hereditary PC. Unfortunately, there are no PC screening programs with acceptable sensitivity and specificity. However, the gold standard for screening at this time is endoscopic ultrasound. Clearly, there is a great need for the development of novel screening approaches with acceptable sensitivity and specificity. Further research is needed to elucidate those etiologic factors that contribute to the apparent excess of PC in Ashkenazi Jews. Attention should also be given to the search for mutations predisposing to PC in Jews so that opportunities to learn more about the disease's pathogenesis, as well as screening and control, may take place.
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PMID:Familial pancreatic carcinoma in Jews. 1551 47

The objective of this study was to determine the site-specific cancer incidence of hypertensive patients and examine the effect of blood pressure-related variables on the risk of cancers with elevated incidence among the hypertensive patients. A record linkage study of Hypertension Register of the North Karelia Project and the Finnish Cancer Registry was conducted. The mean follow-up time was 16 years. A total of 20 529 hypertensive patients were studied. Main outcome measures were standardised incidence ratios and hazard ratios. The overall cancer incidence was close to that of the general population for both men and women. The incidence rate for the kidney cancer was significantly increased in hypertensive patients (standardised incidence ratio 1.34, 95% confidence interval (CI) 1.11-1.60), as well as incidence rates for cancers of pancreas (1.26, 1.02-1.54), and endometrium (1.22, 1.01-1.44) in hypertensive women. The incidence of lung cancer was significantly decreased (0.86, 0.77-0.95). The incidence of liver cancer was elevated with borderline significance (1.36, 0.99-1.82). In Cox regression models, the use of antihypertensive drugs at baseline was a significant predictor of kidney (hazard ratio for use of antihypertensive drugs 1.89, 95% CI 0.96-3.75) and pancreatic cancer (1.78, 0.99-3.22) in women but not in men. The incidence of endometrial cancer or liver cancer was not related to blood pressure levels or the use of antihypertensive drugs. In women, obesity was a significant predictor of cancers of the endometrium, kidney and liver. In conclusion, increased occurrence of some cancer types among hypertensive patients seem to be partly explained by obesity and the use of antihypertensive drugs.
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PMID:Cancer pattern among hypertensive patients in North Karelia, Finland. 1570 72

The purpose was to evaluate the safety and efficacy of high-dose-rate (HDR) CT-guided interstitial brachytherapy in the treatment of extrahepatic, extrapulmonary, secondary malignancies. Nineteen patients were included in this prospective study. The median age was 66 years (49-77). Underlying primaries comprised colorectal carcinomas in six, renal cell carcinoma in three, pancreatic carcinoma in three, cervical cancer in two, endometrial cancer in two and NSCLC, breast cancer and sarcoma in one patient each. All patients had undergone extensive pretreatments. CT-guided HDR brachytherapy employed a 192Iridium source. Dose planning for brachytherapy was performed using 3D CT data acquired after CT-guided percutaneous applicator positioning. MRI follow-up was performed 6 weeks and every 3 months post intervention. Primary endpoints were complications, local tumor control and progression-free survival. The median tumor diameter was 6 cm (2-15 cm). Tumor locations included the hepatoduodenal ligament, mesentery, adrenal gland, mesogastrium and local recurrences after rectal or pancreatic cancer. The minimal median dose in the target volume was 11 Gy (4-18 Gy). Minor complications comprised pain and fever (n=6, 32%). Major complications included one hospital death of unknown causes (n=1; 5%). Median follow-up was 7 months (1-16). Four patients (21%) died during the follow-up period. Local tumor control was 76.5% after 6 months and progression-free survival 47% after 6 months. Minimally invasive CT-guided HDR brachytherapy is safe and effective in the palliative treatment of extrahepatic, extrapulmonary secondary malignancies.
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PMID:CT-guided interstitial brachytherapy in the local treatment of extrahepatic, extrapulmonary secondary malignancies. 1662 47

Several studies have reported an inverse association between tomato and/or lycopene intake and the risk of some types of cancer. In 2004, the U.S. Food and Drug Administration (FDA) received two petitions for qualified health claims regarding tomatoes, lycopene, and the risk reduction for some forms of cancer. Health claims that characterize the relationship between a food or food component and a disease or health-related condition require premarket approval by FDA to be included on the labels of conventional foods and dietary supplements. Here we describe FDA's review of the scientific data for tomato and/or lycopene intake with respect to risk reduction for certain forms of cancer. The FDA found no credible evidence to support an association between lycopene intake and a reduced risk of prostate, lung, colorectal, gastric, breast, ovarian, endometrial, or pancreatic cancer. The FDA also found no credible evidence for an association between tomato consumption and a reduced risk of lung, colorectal, breast, cervical, or endometrial cancer. The FDA found very limited evidence to support an association between tomato consumption and reduced risks of prostate, ovarian, gastric, and pancreatic cancers.
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PMID:The U.S. Food and Drug Administration's evidence-based review for qualified health claims: tomatoes, lycopene, and cancer. 1762 95

Interleukin-6 (IL-6) is proinflammatory cytokine that produces multifunctional effects. It is also involved in the regulation of immune reactions, hematopoiesis and inflammatory state. Interleukin-6 has been shown to be associated with tumor progression including inhibition of cancer cells apoptosis and stimulation of angiogenesis. Anti-IL-6 therapy is a new strategy in the inflammatory autoimmune diseases and cancer. Clinical studies have shown elevated serum IL-6 concentrations in patients with endometrial cancer, non-small cell lung carcinoma, colorectal cancer, renal cell carcinoma, breast and ovarian cancer. Serum IL-6 levels correlate with tumor stage, and survival of patients. In this article we have focused on a role of IL-6 as a prognostic factor in several malignancies such as colorectal cancer, breast cancer, gastric cancer and pancreatic cancer.
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PMID:[Clinical significance of interleukin-6 (IL-6) as a prognostic factor of cancer disease]. 1803 Aug 75

The prevalence of overweight (body mass index, BMI, between 25 and 30 kg/m2) and obesity (BMI of 30 kg/m2 or higher) is increasing rapidly worldwide, especially in developing countries and countries undergoing economic transition to a market economy. One consequence of obesity is an increased risk of developing type II diabetes. Overall, there is considerable evidence that overweight and obesity are associated with risk for some of the most common cancers. There is convincing evidence of a positive association between overweight/obesity and risk for adenocarcinoma of the oesophagus and the gastric cardia, colorectal cancer, postmenopausal breast cancer, endometrial cancer and kidney cancer (renal-cell). Premenopausal breast cancer seems to be inversely related to obesity. For all other cancer sites the evidence of an association between overweight/obesity and cancer is inadequate, although there are studies suggesting an increased risk of cancers of the liver, gallbladder, pancreas, thyroid gland and in lymphoid and haematopoietic tissue. Far less is known about the association between diabetes mellitus type I (also called insulin dependent diabetes mellitus or juvenile diabetes), type II diabetes (called non-insulin dependent diabetes mellitus or adult onset diabetes mellitus) and cancer risk. The most common type of diabetes mellitus, type II, seems to be associated with liver and pancreas cancer and probably with colorectal cancer. Some studies suggest an association with endometrial and postmenopausal breast cancer. Studies reporting on the association between type I diabetes mellitus, which is relatively rare in most populations and cancer risk are scanty, but suggest a possible association with endometrial cancer. Overweight and obesity, as well as type II diabetes mellitus are largely preventable through changes in lifestyle. The fundamental causes of the obesity epidemic-and consequently the diabetes type II epidemic-are societal, resulting from an environment that promotes sedentary lifestyles and over-consumption of energy. The health consequences and economic costs of the overweight, obesity and type II diabetes epidemics are enormous. Avoiding overweight and obesity, as well as preventing type II diabetes mellitus, is an important purpose to prevent cancer and other diseases. Prevention of obesity and type II diabetes should begin early in life and be based on the life-long health eating and physical activity patterns. Substantial public investments in preventing overweight, obesity and type II diabetes mellitus are both appropriate and necessary in order to have a major impact on their adverse health effects including cancer.
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PMID:Obesity and diabetes epidemics: cancer repercussions. 1863 86

Hereditary non-polyposis colorectal cancer is a cancer predisposition syndrome known to be caused by heterozygous germline mutations in DNA mismatch repair genes (MMR) most commonly hMLH1, hMSH2, hMSH6. Heterozygous mutations in one of these genes confer an increased risk, mainly for colon and endometrial cancer. Recently, several publications identified that biallelic mutations in the MMR genes are associated with a more severe phenotype, including childhood malignancies and signs of neurofibromatosis type I (NF1). We report on a non-consanguineous Ashkenazi Jewish family with two affected siblings with features of NF1, colon cancer and astrocytoma at age 13 and 14. Their mother developed endometrial cancer at age 54. Their father had leukoplakia of the vocal cords with a family history of pancreatic cancer. Molecular and pathology studies were done on the tumor tissue and on genomic DNA of family members. Tumor testing demonstrated a high degree of microsatellite instability (MSI analysis), expression of MLH1 and absence of expression of both MSH2 and MSH6 proteins. A biallelic c.1906G > C (p.A636P) mutation in the hMSH2 gene was detected in the blood of one affected child. Parental genetic testing showed that each parent was heterozygote for the mutation. The c.1906G > C mutation is a founder mutation in the Ashkenazi Jewish population. To our knowledge this is the first report of homozygosity for this founder mutation.
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PMID:Homozygosity of MSH2 c.1906G-->C germline mutation is associated with childhood colon cancer, astrocytoma and signs of Neurofibromatosis type I. 1910 24

The genes TSC1 and TSC2, encoding hamartin and tuberin, respectively, have been shown to be involved in the development of the autosomal dominantly inherited tumor syndrome tuberous sclerosis (TSC). However, inactivation of these genes has also been demonstrated to be associated with sporadic bladder cancer, ovarian and gall bladder carcinoma, non-small-cell carcinoma of the lung, breast cancer, pancreatic cancer, astrocytoma, xanthoastrocytoma, ependymomas, oral squamous cell carcinoma and endometrial cancer. The hamartin/tuberin protein complex plays a central role in the regulation of the mammalian target of rapamycin (mTOR) signalling network. A wide variety of components of the mTOR cascade have been demonstrated to be involved in many different human cancers. Mutations in several mTOR pathway component genes are known to cause specific monogenic human genetic diseases and this signalling cascade has been shown to be of relevance for Alzheimer's disease, type 2 diabetes, obesity and hypertrophy. Consequently, e.g. clinical trials for the treatment with rapamycin, a negative regulator of mTOR, of hamartomas in TSC have already been initiated. Now the first evidence is provided for an involvement of the TSC genes in acute leukemia.
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PMID:New insights into the role of the tuberous sclerosis genes in leukemia. 1925 Jun 71

Pancreatic cancer is the fourth leading cause of cancer-related death in men and women in the United States. Reproductive factors and steroid hormones have been suspected risk factors for many years, but the results from epidemiologic studies to date have been inconclusive. CYP17A1 encodes cytochrome P450c17alpha, an enzyme with 17alpha-hydroxylase and 17,20-lyase activities in estradiol biosynthesis. A polymorphism in the 5'UTR promoter region of CYP17A1-34T/C(A1/A2) has been associated with circulating estrogens in premenopausal women and with susceptibility to breast, prostate, and endometrial cancer. Questionnaire data and germline DNA collected in a San Francisco Bay Area population-based case-control study of pancreatic cancer (cases = 532, controls = 1701) were used to conduct analyses of pancreatic cancer susceptibility related to the CYP17A1 polymorphism and whether effects associated with smoking and reproductive risk factors were modified by this polymorphism. Mass spectrometry- and TaqMan-based methods were used to determine CYP17A1 genotypes in DNA samples from 308 cases and 964 controls. Results showed that carriers of the A2 allele (vs. A1/A1) were significantly less likely to have been diagnosed with pancreatic cancer (A1/A2, adjusted odds ratio (OR) = 0.77, 95% confidence interval (CI) = 0.58-1.0; A2/A2, OR = 0.63, 95%CI = 0.42-0.93; p-trend = 0.01). ORs for CYP17A1 genotypes did not differ by sex, but the observed inverse association was stronger in postmenopausal women. ORs for smoking and pancreatic cancer were not modified by CYP17A1 genotype. Our results suggest that the CYP17A1 A2 allele may be associated with a lower risk of pancreatic cancer in both men and women.
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PMID:Genetic variation in CYP17A1 and pancreatic cancer in a population-based case-control study in the San Francisco Bay Area, California. 1964 97

Epidemiological findings have shown up to two-fold increases in the risks of cancers of the colorectum, breast, endometrium, kidney (renal cell tumours), liver and pancreas among diabetes patients. In the present review, we address the question whether, on the basis of these epidemiological observations, type 2 diabetes should be considered a specific and independent risk factor for these various forms of cancer, due to its particular metabolic characteristics of glucose intolerance and hyperinsulinemia. On the basis of further epidemiological evidence among non-diabetic individuals, as well as recent studies examining the effects of different types of diabetes treatment on cancer risks, we conclude that chronic elevations in fasting and non-fasting blood levels of glucose and/or insulin are plausible independent risk factors for cancer, but that much of the increase in cancer risks associated with these two metabolic factors may occur within the normoglycaemic and insulinemic (non-diabetic) ranges. Furthermore, for some tumour types (e. g. cancer of the endometrium) the associations of risk with type 2 diabetes may to a large extent be due to, and at least partially confounded by, other obesity-related alterations in (e. g. sex steroid) metabolism that in part are independent of glucose and/or insulin metabolism. Specifically for pancreatic cancer, a major question, addressed in detail by other reviews, is whether associations of risk with plasma glucose, insulin or overt type 2 diabetes could be either a cause, or possibly also a consequence of tumour development (or both).
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PMID:Diabetes mellitus type 2 - an independent risk factor for cancer? 2012 70


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