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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A mathematical model incorporating the processes of both cancer induction and subsequent tumor growth has been developed. The model was applied to incidence data of stomach classified into histologic subtypes: papillary adenocarcinoma (PAP), well and moderately differentiated tubular adenocarcinomas (WEL and MOD), poorly differentiated adenocarcinoma (POR), mucinous adenocarcinoma (MUC) and signet-ring cell carcinoma (SIG). The multistage theory was assumed for cancer induction as in the Armitage-Doll model. For the period of growth, exponential growth was assumed and clinical surfacing was formulated as a stochastic process related to tumor diameter. The number of stages in cancer induction and the tumor growth rate were simultaneously estimated for each histologic subtype using the maximum likelihood procedure. The present model showed better fits than the Armitage-Doll model in most histologic subtypes except WEL, PAP, WEL and MOD, which are characterized as differentiated subtypes with less mucous production, showed different features from POR, MUC and SIG: 1) the number of stages was estimated to be larger, 2) the differences in incidence rates between males and females were more marked, and 3) males tended to have larger growth rates in PAP and MOD, while in POR, MUC and SIG, females had larger values. The present study showed that an analysis by histologic subtypes is of importance in stomach cancer and that the period of tumor growth should not be ignored when formulating a model of the natural history of stomach cancer.
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PMID:Analysis of stomach cancer incidence by histologic subtypes based on a mathematical model of multistage cancer induction and exponential growth. 217 1

To evaluate beta-cell function in patients with pancreatic cancer, the glucagon stimulation test was performed in seven patients with pancreatic adenocarcinoma, seven patients with type I diabetes mellitus, seven patients with type II diabetes mellitus, and in seven healthy controls. C-peptide serum levels were determined before and after a 1-mg i.v. glucagon injection. Basal C-peptide values were normal or slightly increased in pancreatic cancer and type II diabetic patients and low in type I diabetic patients. Following glucagon stimulation, no significant increase was observed in C-peptide values of type I diabetics and pancreatic cancer patients, whereas significant increases occurred in controls and type II diabetics. It is concluded that the altered beta-cell function found in pancreatic cancer patients may lead to hyperglycemia, which is frequently associated with this tumor type.
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PMID:Beta-cell function in pancreatic adenocarcinoma. 802 55

By an indirect immunofluorescence method with In-111 cells (hamster insulinoma cell line), circulating islet cell surface antibodies (ICSA) were detected in 7 (20%) out of 36 patients with non-insulin dependent diabetes mellitus (NIDDM), 9% of 68 chronic thyroiditis (CT) patients, or 16% of 19 NIDDM patients associated with CT, but not in 18 normal subjects. Sera from five out of nine ICSA-positive patients examined further also showed cell-surface immunofluorescence on TPC-1 cells (human thyroid papillary adenocarcinoma cell line), and prior absorption of the sera with In-111 cells abolished the immunofluorescence. The 64 kDa protein from In-111 cells or human thyroid follicular cells was immunoprecipitated with ICSA-positive sera. In one case of NIDDM associated with CT, 64 kDa protein was detected in both cells. The results indicate that some ICSA in NIDDM patients recognize the same or a very closely-related autoantigen(s) in both islet beta-cells and thyroid follicular cells, suggesting an explanation, at least in part, for the autoimmune mechanism(s) in clinical association of NIDDM and CT.
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PMID:A possible common cell surface autoantigen in islet beta-cells and thyroid follicular cells in patients with non-insulin dependent diabetes mellitus and chronic thyroiditis. 888 24

Metastases of breast cancer are a major cause of treatment failure. To evaluate the therapeutic efficacy of suicide gene therapy in metastatic breast cancer, we used the herpes simplex virus thymidine kinase (HSV-tk) gene followed by ganciclovir (GCV) administration to treat breast cancer, generated by an adenocarcinoma cell line MOD in syngeneic mice. The bystander effect of HSV-tk + GCV on tumor cell killing was illustrated by demonstrating complete regression of subcutaneous tumors consisting of 90% parental tumor cells and 10% HSV-tk transformed tumor cells. To establish a model of breast cancer metastases in the liver, tumors were generated by intra-hepatic implantation of MOD cells in syngeneic animals. Two weeks after tumor cell implantation, replication defective adenoviral vectors expressing HSV-tk (ADV.tk), or beta-galactosidease (ADV. beta-Gal) were injected intratumorally, followed by buffer or GCV administration. Treatment with ADV.tk + GCV resulted in significant regression of tumor (P < .001), as assessed by computerized morphometric analysis of residual tumor. This was reflected as a significant prolongation of survival in treated animals (P < .001). These results demonstrate that ADV-mediated suicide gene therapy in vivo can be incorporated in a comprehensive treatment strategy for liver metastases of breast cancer.
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PMID:Adenoviral-mediated suicide gene therapy for hepatic metastases of breast cancer. 889 53

The incidence of diabetes is increased in patients with pancreatic cancer, but the mechanisms underlying this association are not clear. Alterations in beta-cell function, such as formation of amyloid from excessive production of amylin and reduced expression of GLUT2, have been suggested to be possible mechanisms. We compared in vivo secretory responses of amylin and insulin (n = 37) and expression of GLUT2 in pancreata (n = 10) obtained at surgery between diabetic and nondiabetic patients with and without pancreatic tumors. Fourteen had pancreatic adenocarcinoma, 7 had diabetes (duration 6 +/- 3 years) and a pancreatic tumor, 8 had type 2 diabetes (duration 6 +/- 2 years), and 8 were normal subjects. First (0 to 10 minutes) and second (10 to 120 minutes) phase insulin and amylin secretion were characterized using the hyperglycemic clamp technique. Both amylin and insulin concentrations followed a biphasic pattern in nondiabetic subjects. In nondiabetic patients with pancreatic cancer, total, as well as nonglycosylated amylin concentrations, were increased compared with nondiabetic subjects without pancreatic cancer. Both first- and second-phase plasma amylin and serum immunoreactive insulin concentrations were low in all patients with diabetes, ie, both in type 2 diabetes and in those patients with diabetes and pancreatic tumors. At surgery, specimens were obtained for characterization of GLUT2 expression in beta cells, which was unaltered in nondiabetic (n = 7) and diabetic (n = 3) patients. Amyloid staining was similarly negative in diabetic and nondiabetic pancreata independent of pancreatic carcinoma. In conclusion, plasma amylin, but not insulin concentrations, are increased in nondiabetic patients with pancreatic cancer, but low in all patients with diabetes. These data support the potential of using an increase in the ratio of circulating amylin to insulin as a marker for pancreatic cancer in nondiabetic patients.
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PMID:In vivo glucose-stimulated amylin secretion is increased in nondiabetic patients with pancreatic cancer. 1155 35

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

We present a case of a 40-year-old man with strong family history of diabetes. His pancreatic ultrasonography was normal at the discovery of his diabetes. Anti-pancreatic antibodies were negative. The patient was treated by insulin and continued to loose weight. His diabetes remained unstable during the follow-up. Three years later, a pancreatic adenocarcinoma was diagnosed which was locally advanced and could not be removed surgically. This observation argues among several mechanisms explaining diabetes in subjects with pancreatic cancer, in favor of tumor-derived diabetogenic substance and suggests that diabetes mellitus could reveal pancreatic cancer even in the presence of conventional risk factors of type 2 diabetes.
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PMID:Diabetes mellitus as an early symptom of pancreatic cancer diagnosed three years later. 1899 44

Since hyperinsulinaemia may promote obesity-linked cancers, we compared type 2 diabetes prevalence among oesophageal adenocarcinoma (OAC) patients and population controls. Diabetes increased the risk of OAC (adjusted odds ratio 1.59, 95% confidence interval (CI) 1.04-2.43), although the risk was attenuated after further adjusting for body mass index (1.32, 95% CI 0.85-2.05).
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PMID:Does type 2 diabetes influence the risk of oesophageal adenocarcinoma? 1919 Jun 30

Esophageal adenocarcinoma and its precursor Barrett's esophagus are increasing in incidence in western populations. Gastroesophageal reflux and high body mass index (BMI) are known risk factors. Studies about Barrett's esophagus in obese patients have emphasised the role of central adiposity as a stronger risk factor than BMI in the development of specialized intestinal metaplasia and subsequently esophagus adenocarcinoma. The proinflammatory impact of adipocytokines of the abdominal fat associated with the metabolic syndrome is also relevant. Except cardiovascular diseases, type 2 diabetes and non alcoholic steatohepatitis, abdominal obesity and metabolic syndrome are responsible of an increase of prevalence of esophageal adenocarcinoma, but also other cancer sites. In this review, we study the up to date main epidemiologic and physiopathologic data concerning this association that could be important in future for a preventive action in obese patients, especially when metabolic syndrome is present.
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PMID:[Review of the association between obesity and gastroesophageal reflux and its complications]. 1925 Jul 82

The etiology of idiopathic pulmonary fibrosis (IPF) remains poorly understood, but some studies have suggested that cigarette smoking or other occupational or environmental exposures, diabetes mellitus, or gastroesophageal reflux may play a role. In this study we evaluated the clinical records of a group of 97 consecutive patients with IPF, and 560 patients suffering 5 different respiratory disorders that were examined as controls: asthma (n=111), chronic obstructive pulmonary disease (n=132), squamous cell lung carcinoma (n=118), lung adenocarcinoma (n=101) and patients with otorhinolaryngology problems but without lung disease (n=98). In bivariate analyses male sex, diabetes mellitus and being former cigarette smoker were associated with IPF. After adjusting by these variables, multivariate analysis revealed that type 2 diabetes mellitus [11.3% in IPF patients vs 2.9% in controls, OR=4.3 (95% CI: 1.9-9.8), p<0.0001] was an independent risk factor associated to IPF. Our results provide additional evidence of a putative relationship between DM2 and idiopathic pulmonary fibrosis. Experimental research is necessary for thorough assessment of the pathogenic mechanisms involved in this association.
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PMID:Risk factors for idiopathic pulmonary fibrosis in a Mexican population. A case-control study. 1978 52


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