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Relevant bibliographies by topics / Cancer cachexia, metabolism, pyruvate

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Journal articles

Academic literature on the topic 'Cancer cachexia, metabolism, pyruvate'

Author: Grafiati

Published: 14 March 2023

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Journal articles on the topic "Cancer cachexia, metabolism, pyruvate"

1

Khamoui, Andy V., Dorota Tokmina-Roszyk, Harry B. Rossiter, Gregg B. Fields, and Nishant P. Visavadiya. "Hepatic proteome analysis reveals altered mitochondrial metabolism and suppressed acyl-CoA synthetase-1 in colon-26 tumor-induced cachexia." Physiological Genomics 52, no. 5 (2020): 203–16. http://dx.doi.org/10.1152/physiolgenomics.00124.2019.

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Cachexia is a life-threatening complication of cancer traditionally characterized by weight loss and muscle dysfunction. Cachexia, however, is a systemic disease that also involves remodeling of nonmuscle organs. The liver exerts major control over systemic metabolism, yet its role in cancer cachexia is not well understood. To advance the understanding of how the liver contributes to cancer cachexia, we used quantitative proteomics and bioinformatics to identify hepatic pathways and cellular processes dysregulated in mice with moderate and severe colon-26 tumor-induced cachexia; ~300 different

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2

Mannelli, Michele, Tania Gamberi, Francesca Magherini, and Tania Fiaschi. "A Metabolic Change towards Fermentation Drives Cancer Cachexia in Myotubes." Biomedicines 9, no. 6 (2021): 698. http://dx.doi.org/10.3390/biomedicines9060698.

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Cachexia is a disorder associated with several pathologies, including cancer. In this paper, we describe how cachexia is induced in myotubes by a metabolic shift towards fermentation, and the block of this metabolic modification prevents the onset of the cachectic phenotype. Cachectic myotubes, obtained by the treatment with conditioned medium from murine colon carcinoma cells CT26, show increased glucose uptake, decreased oxygen consumption, altered mitochondria, and increased lactate production. Interestingly, the block of glycolysis by 2-deoxy-glucose or lactate dehydrogenase inhibition by

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3

Archid, Solass, Tempfer, et al. "Cachexia Anorexia Syndrome and Associated Metabolic Dysfunction in Peritoneal Metastasis." International Journal of Molecular Sciences 20, no. 21 (2019): 5444. http://dx.doi.org/10.3390/ijms20215444.

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: Patients with peritoneal metastasis (PM) of gastrointestinal and gynecological origin present with a nutritional deficit characterized by increased resting energy expenditure (REE), loss of muscle mass, and protein catabolism. Progression of peritoneal metastasis, as with other advanced malignancies, is associated with cancer cachexia anorexia syndrome (CAS), involving poor appetite (anorexia), involuntary weight loss, and chronic inflammation. Eventual causes of mortality include dysfunctional metabolism and energy store exhaustion. Etiology of CAS in PM patients is multifactorial including

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4

Michalak, Krzysztof Piotr, Agnieszka Maćkowska-Kędziora, Bogusław Sobolewski, and Piotr Woźniak. "Key Roles of Glutamine Pathways in Reprogramming the Cancer Metabolism." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–14. http://dx.doi.org/10.1155/2015/964321.

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Glutamine (GLN) is commonly known as an important metabolite used for the growth of cancer cells but the effects of its intake in cancer patients are still not clear. However, GLN is the main substrate for DNA and fatty acid synthesis. On the other hand, it reduces the oxidative stress by glutathione synthesis stimulation, stops the process of cancer cachexia, and nourishes the immunological system and the intestine epithelium, as well. The current paper deals with possible positive effects of GLN supplementation and conditions that should be fulfilled to obtain these effects. The analysis of

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5

Sharma, Raj Kumar, Santosh Kumar Bharti, Balaji Krishnamachary, et al. "Abstract 6353: Metabolic changes in the spleen and pancreas induced by PDAC xenografts with or without glutamine transporter downregulation." Cancer Research 82, no. 12_Supplement (2022): 6353. http://dx.doi.org/10.1158/1538-7445.am2022-6353.

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Abstract Introduction: Our ongoing studies are focused on characterizing metabolic changes induced in the organs of mice with cachexia-inducing Pa04C human pancreatic cancer xenografts. Because pancreatic cancer cells are glutamine dependent [1], we downregulated the glutamine transporter SLC1A5 in Pa04C cells to determine if metabolic changes induced in the spleen and pancreas by Pa04C tumors were normalized when SLC1A5 was downregulated in these tumors. Metabolic patterns were characterized using high-resolution quantitative 1H magnetic resonance spectroscopy (MRS) of spleen and pancreas tis

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6

Muranaka, Hayato, Natalie Moshayedi, Andrew Eugene Hendifar, et al. "Plasma metabolomics to predict chemotherapy (CTX) response in advanced pancreatic cancer (PC) patients (pts) on enteral feeding for cachexia." Journal of Clinical Oncology 40, no. 4_suppl (2022): 600. http://dx.doi.org/10.1200/jco.2022.40.4_suppl.600.

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600 Background: We evaluated the potential of plasma metabolites as predictors of response to CTX in a prospective cohort of pts who received enteral feeding for cachexia and advanced PC. Methods: The PANCAX-1 (NCT02400398) prospective trial enrolled 31 cachectic advanced PC pts to receive jejunal tube peptide-based diet for 12 weeks (wks) who were planned for palliative CTX. Out of 16 evaluable pts, 62.5% receiving enteral feeding met the primary endpoint of weight stability at 12 wks. As part of an exploratory analysis of the PANCAX-1 trial, serial blood samples were collected at 3 predefine

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7

Dalal, Shalini. "Lipid metabolism in cancer cachexia." Annals of Palliative Medicine 8, no. 1 (2019): 13–23. http://dx.doi.org/10.21037/apm.2018.10.01.

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8

Mulligan, HD, SA Beck, and MJ Tisdale. "Lipid metabolism in cancer cachexia." British Journal of Cancer 66, no. 1 (1992): 57–61. http://dx.doi.org/10.1038/bjc.1992.216.

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9

Penna, Fabio, Riccardo Ballarò, Marc Beltrá, Serena De Lucia, and Paola Costelli. "Modulating Metabolism to Improve Cancer-Induced Muscle Wasting." Oxidative Medicine and Cellular Longevity 2018 (2018): 1–11. http://dx.doi.org/10.1155/2018/7153610.

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Muscle wasting is one of the main features of cancer cachexia, a multifactorial syndrome frequently occurring in oncologic patients. The onset of cachexia is associated with reduced tolerance and response to antineoplastic treatments, eventually leading to clinical conditions that are not compatible with survival. Among the mechanisms underlying cachexia, protein and energy dysmetabolism play a major role. In this regard, several potential treatments have been proposed, mainly on the basis of promising results obtained in preclinical models. However, at present, no treatment yet reached valida

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10

Dave, Dhwani T., and Bhoomika M. Patel. "Mitochondrial Metabolism in Cancer Cachexia: Novel Drug Target." Current Drug Metabolism 20, no. 14 (2020): 1141–53. http://dx.doi.org/10.2174/1389200220666190816162658.

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Background: Cancer cachexia is a metabolic syndrome prevalent in the majority of the advanced cancers and is associated with complications such as anorexia, early satiety, weakness, anaemia, and edema, thereby reducing performance and impairing quality of life. Skeletal muscle wasting is a characteristic feature of cancer-cachexia and mitochondria is responsible for regulating total protein turnover in skeletal muscle tissue. Methods: We carried out exhaustive search for cancer cachexia and role of mitochondria in the same in various databases. All the relevant articles were gathered and the p

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