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retinoblastoma/pretilost
Veza se sprema u međuspremnik
Stranica 1 iz 38 rezultatima
Haploinsufficiency of the retinoblastoma protein gene reduces diet-induced obesity, insulin resistance, and hepatosteatosis in mice.
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Brown adipose tissue activity dissipates energy as heat, and there is evidence that lack of the retinoblastoma protein (pRb) may favor the development of the brown adipocyte phenotype in adipose cells. In this work we assessed the impact of germ line haploinsufficiency of the pRb gene (Rb) on the
[Establishment of human retinoblastoma model in human immune reconstruction non-obese diabetic-severe combine immunodeficient mice].
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OBJECTIVE
To develop a novel immunotherapy model of retinoblastoma (RB) in human PBL non-obese diabetic-severe combined immunodeficient (NOD-SCID) mice, and to investigate its biological features.
METHODS
Twenty NOD-SCID mice were randomly divided into 4 groups: group A, subcutaneous injection of
Molecular connections of obesity and aging: a focus on adipose protein 53 and retinoblastoma protein.
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Obesity is an induced health problem that human beings have been facing with non-optimal treatment so far. Humans are on average getting fatter with age, and obesity and aging interact each other to shorten lifetime and decrease life quality. Obesity also causes several aging related-disorders such
The LXCXE Retinoblastoma Protein-Binding Motif of FOG-2 Regulates Adipogenesis.
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GATA transcription factors and their FOG cofactors play a key role in tissue-specific development and differentiation, from worms to humans. Mammals have six GATA and two FOG factors. We recently demonstrated that interactions between retinoblastoma protein (pRb) and GATA-1 are crucial for erythroid
Interaction between HMGA1 and retinoblastoma protein is required for adipocyte differentiation.
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It is generally accepted that the regulation of adipogenesis prevents obesity. However, the mechanisms controlling adipogenesis have not been completely defined. We have previously demonstrated that HMGA1 proteins play a critical role in adipogenesis. In fact, suppression of HMGA1 protein synthesis
Inhibition of STAT3 activity delays obesity-induced thyroid carcinogenesis in a mouse model.
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Compelling epidemiologic studies indicate that obesity is a risk factor for many human cancers, including thyroid cancer. In recent decades, the incidence of thyroid cancer has dramatically increased along with a marked rise in obesity prevalence. We previously demonstrated that a high fat diet
Obesity increases tumor aggressiveness in a genetically engineered mouse model of serous ovarian cancer.
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OBJECTIVE
Obesity is associated with increased risk and worse outcomes for ovarian cancer. Thus, we examined the effects of obesity on ovarian cancer progression in a genetically engineered mouse model of serous ovarian cancer.
METHODS
We utilized a unique serous ovarian cancer mouse model that
Hepatic cellular senescence pathway genes are induced through histone modifications in a diet-induced obese rat model.
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Overnutrition, such as a high-fat (HF) diet, is a feature followed by some in developed nations that leads to obesity and fatty liver disease. In rats, when fed a fat-high diet, some develop obesity (obesity prone, OP) while others display an obesity-resistant (OR) phenotype. The present study
Reduction of both number and proliferative activity of human endothelial progenitor cells in obesity.
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OBJECTIVE
Circulating endothelial progenitor cells (EPCs), responsible for neoangiogenesis and vascular repair, negatively correlate with vascular dysfunction and atherosclerotic risk factors. Because obesity may have a crucial role in the development of endothelial dysfunction, this study evaluated
Decreased RB1 mRNA, protein, and activity reflect obesity-induced altered adipogenic capacity in human adipose tissue.
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Retinoblastoma (Rb1) has been described as an essential player in white adipocyte differentiation in mice. No studies have been reported thus far in human adipose tissue or human adipocytes. We aimed to investigate the possible role and regulation of RB1 in adipose tissue in obesity using human
Increased expression of FGF1-mediated signaling molecules in adipose tissue of obese mice.
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Fibroblast growth factors (FGFs) are pleiotropic growth factors that control cell proliferation, migration, and differentiation. Herein, we evaluated whether visceral adiposity of mice is accompanied by the alteration of signaling molecules mediated by fibroblast growth factor receptor 1 (FGFR1)
Diet-induced obesity increases tumor growth and promotes anaplastic change in thyroid cancer in a mouse model.
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Recent epidemiological studies provide strong evidence suggesting obesity is a risk factor in several cancers, including thyroid cancer. However, the molecular mechanisms by which obesity increases the risk of thyroid cancer are poorly understood. In this study, we evaluated the effect of
Irisin is expressed and produced by human muscle and adipose tissue in association with obesity and insulin resistance.
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BACKGROUND
Recently irisin (encoded by Fndc5 gene) has been reported to stimulate browning and uncoupling protein 1 expression in sc adipose tissue of mice.
OBJECTIVE
The objective of the study was to investigate FNDC5 gene expression in human muscle and adipose tissue and circulating irisin
Neuronal Cell Cycle Events Link Caloric Intake to Obesity.
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Obesity is a neurological disorder that operates by favoring energy storage within adipose depots and increased caloric intake. Most cases of human obesity are acquired without any underlying genetic basis. Here, we suggest that obesity can impair the function of some hypothalamic neurons critical
Genotype-phenotype correlations in patients with retinoblastoma and interstitial 13q deletions.
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Patients with an interstitial 13q deletion that contains the RB1 gene show retinoblastoma and variable clinical features. Relationship between phenotypic expression and loss of specific neighboring genes are unresolved, yet. We obtained clinical, cytogenetic and molecular data in 63 patients with an
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