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

Author: Grafiati

Published: 14 March 2023

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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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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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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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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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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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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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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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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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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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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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Zhong, Xiaoling, and Teresa A. Zimmers. "Sex Differences in Cancer Cachexia." Current Osteoporosis Reports 18, no. 6 (2020): 646–54. http://dx.doi.org/10.1007/s11914-020-00628-w.

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Abstract Purpose of Review Cachexia, a feature of cancer and other chronic diseases, is marked by progressive weight loss and skeletal muscle wasting. This review aims to highlight the sex differences in manifestations of cancer cachexia in patients, rodent models, and our current understanding of the potential mechanisms accounting for these differences. Recent Findings Male cancer patients generally have higher prevalence of cachexia, greater weight loss or muscle wasting, and worse outcomes compared with female cancer patients. Knowledge is increasing about sex differences in muscle fiber t

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Pisters, Peter W. T., and Murray F. Brennan. "Amino Acid Metabolism in Human Cancer Cachexia." Annual Review of Nutrition 10, no. 1 (1990): 107–32. http://dx.doi.org/10.1146/annurev.nu.10.070190.000543.

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13

Porporato, P. E. "Understanding cachexia as a cancer metabolism syndrome." Oncogenesis 5, no. 2 (2016): e200-e200. http://dx.doi.org/10.1038/oncsis.2016.3.

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Tisdale, Michael J. "Cancer anorexia and cachexia." Nutrition 17, no. 5 (2001): 438–42. http://dx.doi.org/10.1016/s0899-9007(01)00506-8.

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Lai, Shaoqing. "Review: The Commonality of Energy Metabolism of Starvation, Disorders of Glucose-Lipid Metabolism, Diabetes Mellitus and Cachexia." Journal of Biomedical Research & Environmental Sciences 3, no. 5 (2022): 552–55. http://dx.doi.org/10.37871/jbres1478.

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Diabetes mellitus, pathoglycemia, dyslipidemia, non-alcoholic fatty liver, overweight, hypertension, and atherosclerosis are common diseases endangering human health. Cachexia is a life-threatening disease condition. Cachexia is associated with increased mortality. Cancer patients with cachexia are less tolerant and have a decreased response to chemotherapy and radiation. Do these diseases have a common pathogenesis? We will discuss the commonality of energy metabolism in starvation, disorders of glucose-lipid metabolism, diabetes mellitus and cachexia, and how the stress response alters the p

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Iwagaki, Hiromi, Akio Hizuta, Yasuki Nitta, and Noriaki Tanaka. "Altered Tryptophan and Neopterin Metabolism In Cancer Patients." Pteridines 9, no. 1 (1998): 29–32. http://dx.doi.org/10.1515/pteridines.1998.9.1.29.

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Summary Plasma 5-hydroxytryptamine (serotonin), tryptophan and neopterin levels were measured in patients with depressive cancer cachexia and in healthy controls during the same time period. Patients with advanced cancers had significantly raised neopterin, a marker of endogenous gamma-interferon (IFN-γ) production, but decreased serotonin and tryptophan levels. IFN-γ induces a high level of indoleamine dioxvgenase (IDO), a tryptophan degrading enzyme, which in turn increases metabolism along the tryptophan- nicotinic acid pathway, resulting in decreased synthesis of serotonin. These results s

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Bing, Chen, and Paul Trayhurn. "Regulation of adipose tissue metabolism in cancer cachexia." Current Opinion in Clinical Nutrition and Metabolic Care 11, no. 3 (2008): 201–7. http://dx.doi.org/10.1097/mco.0b013e3282f948e2.

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Tijerina, Amanda J. "The Biochemical Basis of Metabolism in Cancer Cachexia." Dimensions of Critical Care Nursing 23, no. 6 (2004): 237–43. http://dx.doi.org/10.1097/00003465-200411000-00001.

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NORTON, JEFFREY A. "Protein and Amino Acid Metabolism in Cancer Cachexia." Annals of Surgery 226, no. 1 (1997): 102–3. http://dx.doi.org/10.1097/00000658-199707000-00019.

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Camargo, Rodolfo Gonzalez, Henrique Quintas Teixeira Ribeiro, Murilo Vieira Geraldo, et al. "Cancer Cachexia and MicroRNAs." Mediators of Inflammation 2015 (2015): 1–5. http://dx.doi.org/10.1155/2015/367561.

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Cancer cachexia is a paraneoplastic syndrome compromising quality of life and survival, mainly characterized by involuntary weight loss, fatigue, and systemic inflammation. The syndrome is described as a result of tumor-host interactions characterized by an inflammatory response by the host to the presence of the tumor. Indeed, systemic inflammation is considered a pivotal feature in cachexia progression and maintenance. Cytokines are intimately related to chronic systemic inflammation and the mechanisms underlying the release of these factors are not totally elucidated, the etiology of cachex

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Luan, Yi, Mikyoung You, Pauline C. Xu, Tom Thompson, and So-Youn Kim. "Activin A Plays a Critical Role in Adipose Tissue Wasting in the Progression of Cancer Cachexia." Journal of the Endocrine Society 5, Supplement_1 (2021): A40. http://dx.doi.org/10.1210/jendso/bvab048.078.

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Abstract Background: Nearly 50% of cancer patients suffer from cancer cachexia, a wasting syndrome with atrophy of white adipose tissue (WAT) and skeletal muscle. Cachexia leads to negative energy balance, limits cancer therapies, and reduces survival rate. It is characterized by body weight loss due to negative nutrients and energy balance from involuntary reduced food intake and abnormal metabolic conditions such as insulin resistance and hypertriglyceridemia. Cancer-driven factors such as activin A and IL-6 (interlukein-6) contribute to the occurrence of cachexia symptoms during cancer prog

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Rauckhorst, Adam J., and Eric B. Taylor. "Mitochondrial pyruvate carrier function and cancer metabolism." Current Opinion in Genetics & Development 38 (June 2016): 102–9. http://dx.doi.org/10.1016/j.gde.2016.05.003.

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23

Sørensen, Jonas. "Lung Cancer Cachexia: Can Molecular Understanding Guide Clinical Management?" Integrative Cancer Therapies 17, no. 3 (2018): 1000–1008. http://dx.doi.org/10.1177/1534735418781743.

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Cachexia has been recognized for a long time as an adverse effect of cancer. It is associated with reduced physical function, reduced tolerance to anticancer therapy, and reduced survival. This wasting syndrome is mainly known for an ongoing loss of skeletal muscle leading to progressive functional impairment and is driven by a variable combination of reduced food intake and abnormal metabolism. Cytokines derived from host immune system or the tumor itself is believed to play a role in promoting cancer cachexia. Circulating levels of cytokines, including IL-1α, IL-6, and TNFα have been identif

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Argilés, Josep M., Britta Stemmler, Francisco J. López-Soriano, and Silvia Busquets. "Inter-tissue communication in cancer cachexia." Nature Reviews Endocrinology 15, no. 1 (2018): 9–20. http://dx.doi.org/10.1038/s41574-018-0123-0.

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Rosa-Caldwell, Megan E., Jacob L. Brown, David E. Lee, et al. "Hepatic alterations during the development and progression of cancer cachexia." Applied Physiology, Nutrition, and Metabolism 45, no. 5 (2020): 500–512. http://dx.doi.org/10.1139/apnm-2019-0407.

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Cancer-associated bodyweight loss (cachexia) is a hallmark of many cancers and is associated with decreased quality of life and increased mortality. Hepatic function can dramatically influence whole-body energy expenditure and may therefore significantly influence whole-body health during cancer progression. The purpose of this study was to examine alterations in markers of hepatic metabolism and physiology during cachexia progression. Male C57BL/6J mice were injected with 1 × 106 Lewis Lung Carcinoma cells dissolved in 100 μL PBS and cancer was allowed to develop for 1, 2, 3, or 4 weeks. Cont

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Miyaguti, Natália Angelo da Silva, Gabriela de Matuoka e. Chiocchetti, Carla de Moraes Salgado, et al. "Walker-256 Tumour-Induced Cachexia Altered Liver Metabolomic Profile and Function in Weanling and Adult Rats." Metabolites 11, no. 12 (2021): 831. http://dx.doi.org/10.3390/metabo11120831.

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Cancer cachexia occurs in up to 85% of advanced cancer patients, affecting different tissues and organs, mainly the liver, which plays a central role in body metabolism control. However, liver responses to cancer cachexia progression are still poorly understood. Considering the possible different challenges provided by the rodent’s phase of life and the cachexia progression, we evaluated the liver metabolic alterations affected by Walker-256 tumour growth in weanling and young-adult rats. For this, we applied a metabolomics approach associated with protein and gene expression analyses. Higher

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Durham, William J., Edgar Lichar Dillon, and Melinda Sheffield-Moore. "Inflammatory burden and amino acid metabolism in cancer cachexia." Current Opinion in Clinical Nutrition and Metabolic Care 12, no. 1 (2009): 72–77. http://dx.doi.org/10.1097/mco.0b013e32831cef61.

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Reiter, Russel J. "Melatonin Reprograms Glucose Metabolism in Cancer Cell Mitochondria." Series of Endocrinology, Diabetes and Metabolism 1, no. 3 (2019): 52–61. http://dx.doi.org/10.54178/jsedmv1i3001.

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Melatonin has a long history of studies which confirm its ability to inhibit cancer growth. Melatonin is present in high concentrations in the mitochondria of normal cells but is likely absent from the mitochondria of cancer cells, at least when isolated from tumors harvested during the day. Herein, we hypothesize that melatonin’s absence from cancer cell mitochondria prevents these organelles from metabolizing pyruvate to acetyl coenzyme A (acetyl-CoA) due to suppression of the activity of the enzyme pyruvate dehydrogenase complex (PDC), the enzyme that catalyzes the conversion of pyruvate to

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Mitchell, Toni, Lewis Clarke, Alexandra Goldberg, and Karen S. Bishop. "Pancreatic Cancer Cachexia: The Role of Nutritional Interventions." Healthcare 7, no. 3 (2019): 89. http://dx.doi.org/10.3390/healthcare7030089.

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Pancreatic cancer is a cancer with one of the highest mortality rates and many pancreatic cancer patients present with cachexia at diagnosis. The definition of cancer cachexia is not consistently applied in the clinic or across studies. In general, it is “defined as a multifactorial syndrome characterised by an ongoing loss of skeletal muscle mass with or without loss of fat mass that cannot be fully reversed by conventional nutritional support and leads to progressive functional impairment.” Many regard cancer cachexia as being resistant to dietary interventions. Cachexia is associated with a

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Argilés, Josep M., Francisco J. López-Soriano, and Silvia Busquets. "Mediators of cachexia in cancer patients." Nutrition 66 (October 2019): 11–15. http://dx.doi.org/10.1016/j.nut.2019.03.012.

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Madeddu, Clelia, Giulia Gramignano, Luciana Tanca, Maria Cristina Cherchi, Carlo Aurelio Floris, and Antonio Macciò. "A combined treatment approach for cachexia and cancer-related anemia in advanced cancer patients: A randomized placebo-controlled trial." Journal of Clinical Oncology 32, no. 31_suppl (2014): 189. http://dx.doi.org/10.1200/jco.2014.32.31_suppl.189.

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189 Background: Cancer progression is characterized by specific energy metabolism alterations and by symptoms including fatigue, anorexia, nausea, depression, which results in cachexia syndrome and compromised quality of life (QL). This condition is often associated to anemia (cancer-related anemia, CRA), which negatively impacts patient QL and disease outcome. Methods: Adult advanced cancer patients with cachexia (i.e., weight loss > 5% in the previous 6 months) and CRA were randomly assigned (1:1 by computer generated list) to receive 3 months of a combined approach consisting of celecoxi

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Dalise, Stefania, Peppino Tropea, Luca Galli, Andrea Sbrana, and Carmelo Chisari. "Muscle function impairment in cancer patients in pre-cachexia stage." European Journal of Translational Myology 30, no. 2 (2020): 258–67. http://dx.doi.org/10.4081/ejtm.2020.8931.

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Cancer cachexia has been reported to be directly responsible for at least 20% of cancer deaths. Management of muscle wasting in cancer-associated cachexia appears to be of pivotal importance for survival of patients. In this regard, it would be interesting to identify before its patent appearance eventual functional markers of muscle damage, to plan specific exercise protocols to counteract cachexia. The muscle function of 13 oncologic patients and 15 controls was analyzed through: i) analysis of the oxidative metabolism, indirectly evaluated trough dosage of blood lactate levels before and af

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Giacosa, Attilio, and Mariangela Rondanelli. "Fish oil and treatment of cancer cachexia." Genes & Nutrition 3, no. 1 (2008): 25–28. http://dx.doi.org/10.1007/s12263-008-0078-1.

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van de Haterd, Britt, Kenneth Verboven, Frank Vandenabeele, and Anouk Agten. "The Role of Skeletal Muscle Mitochondria in Colorectal Cancer Related Cachexia: Friends or Foes?" International Journal of Molecular Sciences 23, no. 23 (2022): 14833. http://dx.doi.org/10.3390/ijms232314833.

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Up to 60% of colorectal cancer (CRC) patients develop cachexia. The presence of CRC related cachexia is associated with more adverse events during systemic therapy, leading to a high mortality rate. The main manifestation in CRC related cachexia is the loss of skeletal muscle mass, resulting from an imbalance between skeletal muscle protein synthesis and protein degradation. In CRC related cachexia, systemic inflammation, oxidative stress, and proteolytic systems lead to mitochondrial dysfunction, resulting in an imbalanced skeletal muscle metabolism. Mitochondria fulfill an important function

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Donohoe, Claire L., Aoife M. Ryan, and John V. Reynolds. "Cancer Cachexia: Mechanisms and Clinical Implications." Gastroenterology Research and Practice 2011 (2011): 1–13. http://dx.doi.org/10.1155/2011/601434.

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Cachexia is a multifactorial process of skeletal muscle and adipose tissue atrophy resulting in progressive weight loss. It is associated with poor quality of life, poor physical function, and poor prognosis in cancer patients. It involves multiple pathways: procachectic and proinflammatory signals from tumour cells, systemic inflammation in the host, and widespread metabolic changes (increased resting energy expenditure and alterations in metabolism of protein, fat, and carbohydrate). Whether it is primarily driven by the tumour or as a result of the host response to the tumour has yet to be

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Petruzzelli, Michele, Miriam Ferrer, Martijn J. Schuijs, et al. "Early Neutrophilia Marked by Aerobic Glycolysis Sustains Host Metabolism and Delays Cancer Cachexia." Cancers 14, no. 4 (2022): 963. http://dx.doi.org/10.3390/cancers14040963.

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An elevated neutrophil–lymphocyte ratio negatively predicts the outcome of patients with cancer and is associated with cachexia, the terminal wasting syndrome. Here, using murine model systems of colorectal and pancreatic cancer we show that neutrophilia in the circulation and multiple organs, accompanied by extramedullary hematopoiesis, is an early event during cancer progression. Transcriptomic and metabolic assessment reveals that neutrophils in tumor-bearing animals utilize aerobic glycolysis, similar to cancer cells. Although pharmacological inhibition of aerobic glycolysis slows down tum

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Ragni, Maurizio, Claudia Fornelli, Enzo Nisoli, and Fabio Penna. "Amino Acids in Cancer and Cachexia: An Integrated View." Cancers 14, no. 22 (2022): 5691. http://dx.doi.org/10.3390/cancers14225691.

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Rapid tumor growth requires elevated biosynthetic activity, supported by metabolic rewiring occurring both intrinsically in cancer cells and extrinsically in the cancer host. The Warburg effect is one such example, burning glucose to produce a continuous flux of biomass substrates in cancer cells at the cost of energy wasting metabolic cycles in the host to maintain stable glycemia. Amino acid (AA) metabolism is profoundly altered in cancer cells, which use AAs for energy production and for supporting cell proliferation. The peculiarities in cancer AA metabolism allow the identification of spe

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Zangari, Joséphine, Francesco Petrelli, Benoît Maillot, and Jean-Claude Martinou. "The Multifaceted Pyruvate Metabolism: Role of the Mitochondrial Pyruvate Carrier." Biomolecules 10, no. 7 (2020): 1068. http://dx.doi.org/10.3390/biom10071068.

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Pyruvate, the end product of glycolysis, plays a major role in cell metabolism. Produced in the cytosol, it is oxidized in the mitochondria where it fuels the citric acid cycle and boosts oxidative phosphorylation. Its sole entry point into mitochondria is through the recently identified mitochondrial pyruvate carrier (MPC). In this review, we report the latest findings on the physiology of the MPC and we discuss how a dysfunctional MPC can lead to diverse pathologies, including neurodegenerative diseases, metabolic disorders, and cancer.

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Fonseca, Guilherme Wesley Peixoto da, Jerneja Farkas, Eva Dora, Stephan von Haehling, and Mitja Lainscak. "Cancer Cachexia and Related Metabolic Dysfunction." International Journal of Molecular Sciences 21, no. 7 (2020): 2321. http://dx.doi.org/10.3390/ijms21072321.

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Cancer cachexia is a complex multifactorial syndrome marked by a continuous depletion of skeletal muscle mass associated, in some cases, with a reduction in fat mass. It is irreversible by nutritional support alone and affects up to 74% of patients with cancer—dependent on the underlying type of cancer—and is associated with physical function impairment, reduced response to cancer-related therapy, and higher mortality. Organs, like muscle, adipose tissue, and liver, play an important role in the progression of cancer cachexia by exacerbating the pro- and anti-inflammatory response initially ac

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Nixon, Daniel W. "Cancer, cancer cachexia, and diet: lessons from clinical research." Nutrition 12, no. 1 (1996): S52—S56. http://dx.doi.org/10.1016/0899-9007(95)00077-1.

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NIXON, D. "Cancer, cancer cachexia, and diet: Lessons from clinical research." Nutrition 12 (January 1996): S52—S56. http://dx.doi.org/10.1016/0899-9007(96)90020-9.

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Hardee, Justin P., Brittany R. Counts, and James A. Carson. "Understanding the Role of Exercise in Cancer Cachexia Therapy." American Journal of Lifestyle Medicine 13, no. 1 (2017): 46–60. http://dx.doi.org/10.1177/1559827617725283.

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Cachexia, the unintentional loss of body weight, is prevalent in many cancer types, and the associated skeletal muscle mass depletion increases patient morbidity and mortality. While anorexia can be present, cachexia is not reversible with nutritional therapies alone. Pharmacological agents have been proposed to treat this condition, but there are currently no approved treatments. Nonetheless, the hallmark characteristics associated with cancer cachexia remain viable foundations for future therapies. Regular physical activity holds a promising future as a nonpharmacological alternative to impr

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Pitzer, Christopher R., Hector G. Paez, and Stephen E. Alway. "The Contribution of Tumor Derived Exosomes to Cancer Cachexia." Cells 12, no. 2 (2023): 292. http://dx.doi.org/10.3390/cells12020292.

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Cancer cachexia is defined as unintentional weight loss secondary to neoplasia and is associated with poor prognosis and outcomes. Cancer cachexia associated weight loss affects both lean tissue (i.e., skeletal muscle) and adipose tissue. Exosomes are extracellular vesicles that originate from multivesicular bodies that contain intentionally loaded biomolecular cargo. Exosome cargo includes proteins, lipids, mitochondrial components, and nucleic acids. The cargo carried in exosomes is thought to alter cell signaling when it enters into recipient cells. Virtually every cell type secretes exosom

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Kulyté, Agné, Silvia Lorente-Cebrián, Hui Gao, et al. "MicroRNA profiling links miR-378 to enhanced adipocyte lipolysis in human cancer cachexia." American Journal of Physiology-Endocrinology and Metabolism 306, no. 3 (2014): E267—E274. http://dx.doi.org/10.1152/ajpendo.00249.2013.

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Cancer cachexia is associated with pronounced adipose tissue loss due to, at least in part, increased fat cell lipolysis. MicroRNAs (miRNAs) have recently been implicated in controlling several aspects of adipocyte function. To gain insight into the possible impact of miRNAs on adipose lipolysis in cancer cachexia, global miRNA expression was explored in abdominal subcutaneous adipose tissue from gastrointestinal cancer patients with ( n = 10) or without ( n = 11) cachexia. Effects of miRNA overexpression or inhibition on lipolysis were determined in human in vitro differentiated adipocytes. O

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Tisdale, Michael J. "Newly identified factors that alter host metabolism in cancer cachexia." Trends in Pharmacological Sciences 11, no. 11 (1990): 473–75. http://dx.doi.org/10.1016/0165-6147(90)90134-t.

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Bartosch-Härlid, A., and R. Andersson. "Cachexia in pancreatic cancer – Mechanisms and potential intervention." e-SPEN, the European e-Journal of Clinical Nutrition and Metabolism 4, no. 6 (2009): e337-e343. http://dx.doi.org/10.1016/j.eclnm.2009.10.002.

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Lira, Fábio Santos, José Cesar Rosa Neto, and Marília Seelaender. "Exercise training as treatment in cancer cachexia." Applied Physiology, Nutrition, and Metabolism 39, no. 6 (2014): 679–86. http://dx.doi.org/10.1139/apnm-2013-0554.

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Abstract:

Cachexia is a wasting syndrome that may accompany a plethora of diseases, including cancer, chronic obstructive pulmonary disease, aids, and rheumatoid arthritis. It is associated with central and systemic increases of pro-inflammatory factors, and with decreased quality of life, response to pharmacological treatment, and survival. At the moment, there is no single therapy able to reverse cachexia many symptoms, which include disruption of intermediary metabolism, endocrine dysfunction, compromised hypothalamic appetite control, and impaired immune function, among other. Growing evidence, neve

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Heo, Ji-Won, and Sung-Eun Kim. "Comparative Transcriptomic Profiling of Organs Associated With Metabolic Dysfunction in Cancer-Induced Cachexia." Current Developments in Nutrition 5, Supplement_2 (2021): 501. http://dx.doi.org/10.1093/cdn/nzab041_016.

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Abstract Objectives Approximately 50–80% of cancer patients suffer from cachexia represented by weight loss mainly due to loss of skeletal muscle. Cancer-induced cachexia is a complex metabolic syndrome associated with not only systemic inflammation but also perturbations to energy metabolism. In this study, we profiled gene expression patterns of different organs in CT-26 tumor bearing mice in order to understand metabolic dysfunction in cancer cachexia. Methods The transcriptomic profiles of skeletal muscle, adipose tissue, and liver of CT26-tumor bearing mice were generated using SurePrint

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Izquierdo-Garcia, Jose L., Pavithra Viswanath, Pia Eriksson, et al. "IDH1 Mutation Induces Reprogramming of Pyruvate Metabolism." Cancer Research 75, no. 15 (2015): 2999–3009. http://dx.doi.org/10.1158/0008-5472.can-15-0840.

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Tisdale, Michael J. "Cancer cachexia: Metabolic alterations and clinical manifestations." Nutrition 13, no. 1 (1997): 1–7. http://dx.doi.org/10.1016/s0899-9007(96)00313-9.

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