Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic mastopathy is an uncommon tumor-like proliferation of fibrous tissue of the breast that usually occurs in a patient who has suffered from type I diabetes mellitus of long duration. Here we report a rare case of diabetic mastopathy that occurred in type II non-insulin dependent diabetes mellitus. This patient was a 63-year-old postmenopausal woman. Mammography, ultrasonography and MR imaging could not distinguish it from breast cancer. Although the core needle biopsy specimen showed fibrosis without evidence of malignancy, excisional biopsy was performed. Histological findings demonstrated typical diabetic mastopathy with keloid-like fibrosis, perivascular lymphocytic infiltration, and lymphocytic lobulitis without evidence of malignancy. These lymphocytes were composed predominantly of B-cells. Five months after surgical biopsy, a nodular formation approximately 4 cm in diameter recurred adjacent to the resected end of the biopsy.
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PMID:An uncommon case of diabetic mastopathy in type II non-insulin dependent diabetes mellitus. 1675 19

The objective of this study was to assess the frequency of micrometastatic disease (MID) in pelvic lymph nodes (PLNs) in carcinoma of the uterine cervix (CUC) and to determine the risk of recurrence. The PLNs from 289 patients with CUC (IB and IIA) were studied. Each PLN was assessed via immunohistochemistry using a single histologic section (AE1/AE3). Metastatic deposits were measured and the disease status was classified into three groups: 1) absence of metastatic disease (MOD); 2) MID, one or more metastatic PLN with only isolated tumor cells and/or micrometastases (up to 2 mm); and 3) macrometastatic disease (MAD), presence of one or more metastatic PLN with macrometastases (more than 2 mm). Eleven patients (3.8%) were classified as having MID and 37 (12.8%) as having MAD. The 5-year disease-free survival (DFS) rates for MOD, MAD, and MID were 88.7%, 80.4%, and 50.0%, respectively (P < 0.001). The Cox proportional hazards model showed that MID was an independent variable for recurrence when adjusted for MAD, depth of tumor invasion, severity of inflammatory reaction, and use of adjuvant radiotherapy. We conclude that the frequency of MID in PLN was low. However, patients with MID presented a high risk of recurrence and reduced DFS.
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PMID:Assessment of pelvic lymph node micrometastatic disease in stages IB and IIA of carcinoma of the uterine cervix. 1680 5

Up to now, the studies involving diabetes mellitus and malignancies show controversial results: Many of them have found incidences of malignancies that were comparable or even lower than those in nondiabetic subjects; others conclude that diabetes mellitus is linked to a higher incidence of malignancies and/or a predictor of mortality from cancer. Insulin and its precursors, pro- and pre-proinsulin, have been shown to have some homology to the insulin-like growth factors, but, moreover they have some affinity to bind at receptors of the tumor growth factor and some hybrids too. Hence, an association between diabetes mellitus, insulin, hyperinsulinaemia, and carcinogenesis appears plausible. On the other hand, diabetes mellitus can influence different hormone levels. In some tumor entities, such as prostate carcinoma, this effect can somewhat counterbalance the direct mitogene effect of insulin and its precursors. All in all, as a result of the complexity of these mechanisms and the differences between the tumor entities, the question whether diabetes mellitus is associated with an increased or a reduced risk for the development and in respect of the prognosis of cancer cannot be answered. The only way to give some answer is to focus on specific tumor entities: It seems that diabetes mellitus and/or hyperglycaemia are independent risk factors and/or predictors at least in respect of cancer of the colon, pancreas, female breast, endometrium, and, in men, of the liver and bladder. However, most of these data were assessed in patients with type 2 diabetes mellitus. This makes it highly questionable whether the data can easily be transferred to patients with type 1 diabetes. Moreover, additional potential limitations are that most of the studies do not focus on the treatment modality or the race of participants. In conclusion, up to the present, we have an increased risk for some and a reduced risk for other tumor entities, but still, we cannot give the general answer.
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PMID:Diabetes, insulin, and risk of cancer. 1681 Mar 43

Pituitary metastasis and sarcoidosis are two causes of pituitary stalk thickening. Their association has been described ago three decades. In this setting, we report a case of panhypopituitarism revealing pituitary metastasis from a small-cell lung carcinoma associated with sarcoidosis. A 49 year-old smoking patient with type 2 diabetes was admitted for acute adrenal failure with polyuria polydipsia syndrome and a pituitary tumor syndrome. Hormone explorations confirmed anterior pituitary insufficiency. Water restriction revealed central diabetes insipidus. The hypothalamic-pituitary MRI revealed a 1-cm sellar mass with nodular thickening of the stalk. The chest radiograph showed a heterogeneous opacity in the left lung. The thoraco-abdominal scan demonstrated a mass in the left lung highly suggestive of malignancy and many enlarged mediastinal nodes, hepatic nodules, and hypertrophy of the left adrenal. Bronchoscopy was performed three times and showed infiltration of the left bronchial tree but histological examination of the bronchial biopsies was negative for all samples. Ultrasound-guided biopsy of the liver was achieved and histology demonstrated sarcoidosis. The diagnosis of sarcoidosis was incompatible with the deterioration of the patient's general status. Subsequent radiographic explorations showed an increase in the size of the tumor mass and histological evaluation of a scan-guided trans-thoracic biopsy demonstrated small-cell carcinoma. Small-cell lung carcinoma is the most common cancer with pituitary metastasis. The proposed link between sarcoidosis and malignancy has remained controversial but has not been proven false.
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PMID:[Panhypopituitarism revealing metastasis of small-cell lung carcinoma associated with sarcoidosis]. 1684 Sep 19

Insulin resistance is a worldwide risk factor for the two most dangerous human disease groups; namely, for cardiovascular lesions and malignancies. The insulin resistance syndrome have five basic criteria: hyperglycemia, visceral obesity, elevated serum triglyceride level, low HDL-cholesterol level (dyslipidemia) and hypertension. Each of these criteria alone are risk factors for cancer, and they mean together a multiple risk. Insulin resistance of the liver, skeletal muscles, and fatty tissue leads to a reactive hyperinsulinemia by the increased secretory activity of the beta-cells. Insulin has diverse metabolic effects, and at the same time is a growth factor. It enhances the production and mitogenic activity of other, insulin-like growth factors, and leads to pathological cell proliferation. In the uncompensated phase of insulin resistance hyperglycemia appears, which promotes tumor genesis by several pathways. The elevated serum glucose level is advantageous for the increased DNA synthesis of the tumor cells. It provokes deliberation of free radicals, which will cause derangement of both the DNA and the enzymes having a role in the repair mechanisms. Hyperglycemia leads to a nonenzymatic glycation of protein structures, and the glycated products enhance the deliberation of free radicals, cytokines and growth factors. Insulin resistance means an enhanced risk for breast, pancreas, liver, colon, bladder, prostate and oral cavity cancers. The moderately increased fasting glucose level is also a risk factor for breast, stomach and colon cancers, even without manifestation of type 2 diabetes. Insulin resistance promotes tumor progression as well. In cancer patients with hyperglycemia or type 2 diabetes, the rate of tumor recurrence, metastatic spread and fatal outcome is higher as compared with the tumor patients without metabolic disease. The correlation between insulin resistance and tumor promotion reveals new possibilities in the prevention and treatment of cancer. The healthy diet, physical activity and weight loss increase insulin sensitivity, and decrease the risk for both cardiovascular diseases and malignancies.
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PMID:[Correlations of insulin resistance and neoplasms]. 1688 76

A 54-year-old man with type 2 diabetes was referred to our hospital for endocrine evaluation of acromegaly. Physical examination showed typical acromegalic features without Cushingoid features. Magnetic resonance imaging of the brain revealed the presence of a pituitary macroadenoma. Basal plasma levels of GH and insulin-like growth factor-I under fasting hyperglycemia (202 mg/dl) were markedly elevated. Plasma GH levels paradoxically increased after stimulation with TRH and LH-RH, and decreased after bromocriptine and octreotide administration. Endocrine examination of the hypothalamo-pituitary-adrenal (HPA) axis showed a lack of circadian rhythm of ACTH and cortisol, non-suppressibility to low-dose (1 mg), but suppressibility to high-dose (8 mg) dexamethasone, and normal response to CRH stimulation. The tumor resected by transsphenoidal surgery was histopathologically consistent with the diagnosis of eosinophilic adenoma: positive immunoreactivities of GH, PRL and ACTH were demonstrated, but negative immunoreactivities of prohormone convertase (PC) 1/3 by immunohistochemical method. After surgery, plasma GH and IGF-I levels decreased along with normalization of HPA axis. Metabolic co-morbidities such as diabetes and hypertension disappeared after removal of the pituitary tumor. This is a very rare case of GH-producing pituitary adenoma causing typical acromegaly with concomitant production of ACTH causing subclinical Cushing's disease.
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PMID:A Case of acromegaly associated with subclinical Cushing's disease. 1692 23

A left adrenal incidentaloma was found by abdominal ultrasound and computed tomography (CT) in a 53-year-old woman who had a history of non-insulin dependent diabetes mellitus. Abdominal CT showed a well-circumscribed adrenal mass (5.5 x 4.5 x 3.5 cm) with low density (32HU) on precontrast scan and heterogeneous enhancement on postcontrast scan. Laboratory examinations revealed a nonfunctional adrenal tumor. As the malignant potential of the tumor could not be ruled out, the patient underwent hand-assisted laparoscopic adrenalectomy. Postoperative recovery was uneventful, and pathologic examination revealed leiomyoma.
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PMID:Adrenal leiomyoma treated by hand-assisted laparoscopic adrenalectomy: a case report. 1711 Mar 47

Evidence is accumulating that individual risk of neoplasia depends on complex interactions among genetic inheritance, a range of exposures both in utero and in postnatal life, and the play of chance. Knowledge of the portfolio of genetic variants that confer susceptibility or resistance to cancer is limited, and there is potential for genome-wide scans and hypothesis-driven studies to reveal novel polymorphisms and haplotypes that modify risk. There is only fragmentary evidence of the scale and nature of diet-gene interactions that modulate risk of neoplasia, but it seems probable that such interactions will play a significant role as they do in other complex diseases including cardiovascular disease and type 2 diabetes. All existing evidence about diet-gene interactions and cancer risk comes from observational studies, and it will be necessary to undertake intervention studies to test the hypotheses generated by epidemiologic investigations. Because it is very unlikely that primary cancer will be an endpoint in dietary intervention studies in the foreseeable future, development of robust surrogate endpoints is a high priority. Emerging biological science using epigenomics, proteomics, and other molecular technologies appears to offer novel approaches to the discovery and validation of surrogate endpoints.
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PMID:The biological revolution: understanding the impact of SNPs on diet-cancer interrelationships. 1718 36

The AMP-activated protein kinase (AMPK) system acts as a sensor of cellular energy status that is conserved in all eukaryotic cells. It is activated by increases in the cellular AMP:ATP ratio caused by metabolic stresses that either interfere with ATP production (eg, deprivation for glucose or oxygen) or that accelerate ATP consumption (eg, muscle contraction). Activation in response to increases in AMP involves phosphorylation by an upstream kinase, the tumor suppressor LKB1. In certain cells (eg, neurones, endothelial cells, and lymphocytes), AMPK can also be activated by a Ca(2+)-dependent and AMP-independent process involving phosphorylation by an alternate upstream kinase, CaMKKbeta. Once activated, AMPK switches on catabolic pathways that generate ATP, while switching off ATP-consuming processes such as biosynthesis and cell growth and proliferation. The AMPK complex contains 3 subunits, with the alpha subunit being catalytic, the beta subunit containing a glycogen-sensing domain, and the gamma subunits containing 2 regulatory sites that bind the activating and inhibitory nucleotides AMP and ATP. Although it may have evolved to respond to metabolic stress at the cellular level, hormones and cytokines such as insulin, leptin, and adiponectin can interact with the system, and it now appears to play a key role in maintaining energy balance at the whole body level. The AMPK system may be partly responsible for the health benefits of exercise and is the target for the antidiabetic drug metformin. It is a key player in the development of new treatments for obesity, type 2 diabetes, and the metabolic syndrome.
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PMID:AMP-activated protein kinase in metabolic control and insulin signaling. 1730 71

Thiazolidinediones, also known as glitazones, represent a relatively new class of medication used for glycemic control in patients with type II diabetes mellitus. These drugs interact with the peroxisome proliferator-activated receptor gamma, a member of the nuclear receptor superfamily, which in turn heterodimerizes with retinoid X receptors to stimulate gene transcription. At a physiologic level, glitazones stimulate adipocyte differentiation, enhance insulin-sensitive glucose uptake by muscle and fat cells, suppress angiogenesis, inhibit tumor cell growth, and normalize keratinocyte differentiation. They have also demonstrated the capacity to diminish inflammatory cytokine production, most notably, that of tumor necrosis factor alpha. Patients with such disparate conditions as psoriasis, hirsutism, melanoma, angiosarcoma, lipodystrophy, and necrobiosis lipoidica have benefited from the administration of thiazolidinediones. Clinicians should become familiar with glitazones as they are experiencing a burgeoning use among patients with non-insulin-dependent diabetes mellitus and have demonstrated clinical efficacy in treating certain skin conditions.
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PMID:Thiazolidinediones in dermatology. 1755 May 51


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