4 edition of Increased Lipogenesis in Human Tumors found in the catalog.
December 31, 2004
by Leuven Univ Pr
Written in English
|The Physical Object|
|Number of Pages||138|
Activated mTORC1 phosphorylates lipin1, which resides in the cytoplasm and allows nuclear SREBP binding to lipogenic target genes resulting in increased lipogenesis. (B) Inactivation of mTORC1 results in nuclear entry of lipin 1, which disrupts SREBP binding to target genes, thus suppressing lipogenesis (modified according to Peterson et al For example, increased expression of FAS and SCD1 in the adipose tissue of FABP4/5-deficient mice significantly increases de novo production of the monounsaturated fatty acid palmitoleate. In turn, palmitoleate increases insulin sensitivity in muscle and suppresses lipogenesis and steatosis in the liver.
To investigate how antioxidants might affect cancer progression, Martin Bergö, Ph.D., of the University of Gothenburg in Sweden, led a study in mouse models of human lung cancer. The researchers found that adding the antioxidants N-acetylcysteine (NAC) or vitamin E to the diet of mice with small lung tumors substantially increased the. To determine whether increased lipogenesis contributes to human obesity, we measured (postabsorptive state), in lean and obese subjects, lipid synthesis (deuterated water method) and the mRNA concentration (RT-competitive PCR) in subcutaneous adipose tissue of fatty acid synthase (FAS) and sterol regulatory element-binding protein (SREBP)-1c.
Sebum, an oily material secreted by glands in the skin, has a physiological role, but abnormally high secretion of sebum can be associated with acne. Through a detailed investigation of sebum production in human skin samples and volunteer individuals, Esler et al. determined that most of the sebum in human skin is generated through de novo lipogenesis rather than recycled from . Major conclusions The deregulation of DNL in the major lipogenic tissues of the human body is often observed in various metabolic anomalies - including obesity, non-alcoholic fatty liver disease and metabolic syndrome. In addition to that de novo lipogenesis is reported to be exacerbated in cancer tissues, virus infected cells etc.
Strategic management and competitive advantage
Skeletons in the closet
Complex Analysis, Microlocal Calculus, and Relativistic Quantum Theory
Hearing on (H.R. 10259) for the Relief of Charles W. Eaton
legend of Delaware Valley
catalog of books represented by Library of Congress printed cards issued to July 31, 1942.
Desert gold and total prospecting
London wall by St. Alphages churchyard
Elements of botany
Paul Meggitts delusion
revision of Macrocarpaea
The relevance of aberrant lipogenesis in cancer is underscored by a recent body of data showing that suppression of the main lipogenic enzymes is able to both strongly restrain the in vitro growth of cell lines from various tumor types and to reduce tumorigenesis in vivo.
4 – 6, 11, 12 In human HCC, reports on de novo lipogenesis are by: The underling mechanisms need further investigation. On the contrary, several studies also reported the oncogenic effect of PDK4 in tumors.
For example, PDK4 was increased in normal mucosa of colorectal cancer (CRC) due to the decreased methylation of its CpGs, and played oncogenic role in human colon cancer ce Cited by: 2.
Lipogenesis de novo has been demonstrated in human fetal subcutaneous adipose tissue during the initial stages of lipid accumulation (Dunlop and Court, ). It was shown that lipogenic capacity, as measured by incorporation of acetate into neutral lipids, increased with gestational age.
Consistent with an increased demand for lipid synthesis, diverse human cancer cells express high levels of lipogenic enzymes, such as fatty acid synthase (FASN) and stearoyl-CoA desaturase 1 (SCD1).
Results. In human liver samples, de novo lipogenesis was progressively induced from nontumorous liver tissue toward the HCC. Extent of aberrant lipogenesis correlated with clinical aggressiveness, activation of the AKT−mammalian target of rapamycin signaling pathway, and suppression of adenosine monophosphate−activated protein by: 1.
Introduction. Solid tumors require high levels of energy for growth and membrane synthesis. Lipids provide this energy. In normal tissues lipids come from circulating lipids, while cancer cells mainly use de novo synthesized lipids ().As a result, the rate of lipogenesis is highly induced ().Lipogenesis occurs both in liver and adipose tissues resulting in the synthesis of de novo fatty.
Calvisi, D. et al. Increased lipogenesis, induced by AKT-mTORC1-RPS6 signaling, promotes development of human hepatocellular carcinoma. Gastroenterology. Prostate cancer is one of the most common tumors in men. Although characterized by slow growth rate, preventing prostate cancer progression to an aggressive stage is a major challenge.
Watt et al. focused on cancer metabolism and showed increased fatty acid uptake in human malignant prostate cancer tissue. The increased uptake was mediated by up-regulation of the fatty acid translocase CD Tumors reprogram pathways of nutrient acquisition and metabolism to meet the bioenergetic, biosynthetic, and redox demands of malignant cells.
These reprogrammed activities are now recognized as hallmarks of cancer, and recent work has uncovered remarkable flexibility in the specific pathways activated by tumor cells to support these key functions.
Prostate cancer (PCa) is the leading malignancy among men in United States. Recent studies have focused on the identification of novel metabolic characteristics of PCa, aimed at devising better preventive and therapeutic approaches.
PCa cells have revealed unique metabolic features such as higher expression of several enzymes associated with de novo lipogenesis, fatty acid up-take and β. Liver cancer incidence is rising faster than that for any other cancer .In the global cancer statistic report, liver cancer was the sixth most commonly diagnosed cancer and the fourth leading cause of cancer death .Hepatocellular carcinoma (HCC) is the most common primary malignant liver tumor, comprising 10–15% of cases .Although much progress has been made in the clinical.
Elevated level of lipogenic enzymes and overall lipogenesis have been reported in a wide variety of cancers and blocking the lipogenic pathway by chemical inhibitors or RNA interference causes tumor cell death by apoptosis which provides a strong rationale for targeting lipogenic pathway for the treatment and prevention of cancer however the exact role of lipogenesis as a cause, facilitator or.
Aberrant lipid and cholesterol anabolism is strongly linked with prostate cancer [36,37]. Up-regulation of lipogenesis and cholesterogenesis in cancer cells is associated with increased need for. Increased lipogenesis involves modulation of multiple lipogenic enzymes at both transcriptional and posttranscriptional level and is linked to other cancer-associated metabolic changes.
Not only fatty acid synthase, but in fact all key enzymes involved in fatty acid synthesis as well as key metabolic regulators are potential targets for. Increased lipid rafts in tumors. Cell membranes contain different classes of lipids, some of which, in particular cholesterol and sphingolipids, form specific planar microdomains known as lipid.
The relevance of aberrant lipogenesis in cancer is un-derscored by a recent body of data showing that suppres-sion of the main lipogenic enzymes is able to both strongly restrain the in vitro growth of cell lines from various tumor types and to reduce tumorigenesis in vivo.4–6,11,12 In human HCC, reports on de novo lipogen-esis are scanty.
A family history of certain cancers can be a sign of a possible inherited cancer syndrome. (See the Hereditary Cancer Syndromes section for more information about inherited genetic mutations that can cause cancer.) Most cancer risk (and protective) factors are initially identified in epidemiology studies.
INTRODUCTION. Hepatic de novo lipogenesis (DNL) is a fundamental biosynthetic pathway within the liver, contributing to the lipids that are stored and secreted by hepatocytes (Jensen‐Urstad & Semenkovich, ).This process is an extension of the complex metabolic networks at play within the liver, and is provided with substrate primarily through glycolysis and the metabolism of.
Download PDF: Sorry, we are unable to provide the full text but you may find it at the following location(s): (external link). Abstract. Lipolysis is an important process determining fuel metabolism, and insulin regulates this process in adipose tissue.
The aim of this study was to investigate the long-term effects of insulin, an insulin enhancer (rosiglitazone [RSG]), and insulin in combination with RSG on the regulation of lipolysis and lipogenesis in human abdominal subcutaneous fat. Lipogenesis in prostate cancer. Though increased lipogenesis is accepted as a hallmark for cancers29, our live cell imaging study revealed that different cancer types might use distinct lipogenic pathways.
With glucose-d 7 and SRS imaging, we measured the lipogenesis in multiple types of cancer cells, including breast cancer MCF7, lung cancer.
Familial multiple lipomatosis (FML) is a rare condition that is characterized by multiple lipomas on the trunk and extremities.
As the name suggests, FML is diagnosed when multiple lipomatosis occurs in more than one family member, often over several generations.The most recent findings on the role of lipogenesis in cancer progression and metastatic process are presented.
2. Lipogenesis, tumor growth and apoptosis An elevated FAS expression induces progression of cancer cells into S phase (12). In contrast, inhibition of FAS expression decreases tumor growth and it induces apoptosis of cancer cells (8,13).