• Journal of Digestive Cancer Research
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• v.3 no.2
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• pp.61-69
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• 2015

About 80% of all pancreatic cancer patients suffer from a wasting syndrome defined as the cancer cachexia characterized by abnormally low weight, weakness, and loss of skeletal muscle mass, which directly impacts physical activity, quality of life and overall survival. Over the past decades, we have gained new insights into the underlying mechanism of cachexia associated with pancreatic cancer. The aim of this review was to explore recent findings about cancer cachexia pathophysiology and describe the current pharmacologic approach. Pancreatic cancer cachexia is a multifactorial syndrome mediated by mechanical factors, inflammatory cytokines, neuropeptides, hormones and tumor-derived factors. The treatment of cancer cachexia remains controversial but is currently an active area of research. Several new targeted drugs are under investigation, and we hope to open a new prospect in the management of cancer cachexia in the future.

• Asian Oncology Nursing
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• v.11 no.1
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• pp.20-25
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• 2011

Purpose: The study was aimed to review and understand the meaning of cancer cachexia. Methods: Using the keywords "cachexia" and "cancer cachexia" 30 oncology research published from 1974 to 2009 were selected for the review. Results: The mechanism of cancer cachexia has not been fully understood, but various pathogenesis appears to be involved in the development cachexia including altered metabolism of carbohydrate, lipid, and protein associated with cytokines and hormone. As a result, muscle strength, food intake and resting energy expenditure (REE) are reduced. Most medications for the treatment of cachexia show debating results except some drugs such as megace. Supportive care including nutritional education, nursing care, and social support are found another effective treatment options. Conclusion: The results of this study would help oncology nurses to understand the mechanism of cancer cachexia and its management.

• Journal of Applied Biological Chemistry
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• v.65 no.4
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• pp.387-396
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• 2022

Skeletal muscle accounts for about 40-50% of body weight and is an important tissue that performs various functions, such as maintaining posture, supporting soft tissues, maintaining body temperature, and respiration. Cancer, which occurs widely around the world, causes cancer cachexia accompanied by muscular atrophy, which reduces the effectiveness of anticancer drugs and greatly reduces the quality of life and survival rate of cancer patients. Therefore, research to improve cancer cachexia is ongoing. However, there are few studies on the link between cancer and muscle atrophy. Cancer cells exhibit distinct microenvironment and metabolism from tumor cells, including tumor-associated macrophages (TAM), tumor-associated neutrophils (TAN), and insulin resistance due to the Warburg effect. Therefore, we summarize the microenvironment and metabolic characteristics of cancer cells, and the molecular mechanisms of muscle atrophy that can be affected by cytokine and insulin resistance. In addition, this suggests the possibility of improving cancer cachexia of substances affecting TAM, TAN, and Warburg effect. We also summarize the mechanisms identified so far through single agents and the signaling pathways mediated by them that may ameliorate cancer cachexia.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.sup3
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• pp.119-123
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• 2016

Thyroid cancer, the most common endocrine neoplasia, consists of four main types of carcinomas: papillary, follicular, and anaplastic, all with thyroid follicular origin, and medullary thyroid cancer (MTC) related to para-follicular cells. Cronic diseases such as diverse cancers may be associated with cachexia, especially at advanced stage. Cancer-induced cachexia is associated with diminished quality of life, functional performance, reduced response to antitumor therapy, and increased morbidity and mortality. Myostatin (Mst) is one of the outstanding molecules in the skeletal muscle loss process in cancer and it may be released by both skeletal muscle and cachexia-inducing tumors. Recently changes in serum levels of Mst have been identified as an important factor of cancer-induced cachexia. The goal of this study was to assessserum Mst levels in MTC patients. In this descriptive and case-control study, 90 participants were selected, comprising 45 MTC patients (20 males, $29{\pm}13.9years$, 25 females, $29{\pm}14.5years$) and 45 control individuals (25 males, $23.1{\pm}11.6years$, 20 females, $31.5{\pm}14.4years$). Serum Mst was determined using an ELISA kit and body mass index (BMI) was calculated by weight and height measurements. The Kolmogorov Simonov test showed a normal distribution for log transformed Mst serum levels in both case and control groups. Geometric means were 5.9 and 8.2 ng/ml respectively, and a significant difference was found according to the independent t-test results (P<0.01). There was also a significant difference mean of Mst between females in control and MTC groups, but not for the males. Pearson correlation test showed no correlation between age and BMI with Mst serum levels. The findings of this study support the hypothesis that Mst serum levels may have a potential ability for early diagnosis of cachexia in MTC patients, especially in females.

• Journal of Korean Biological Nursing Science
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• v.14 no.2
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• pp.129-138
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• 2012

Purpose: Cachexia is a complex metabolic syndrome associated with wasting of skeletal muscle which contributes to nearly one-third of all cancer deaths. Cachexia lowers the frequency of response to chemotherapy and radiation and ultimately can impact survival as well as quality of life during treatment. NF-kappa B is one of the most important molecular mediators of cachexia. In this study, therefore, possible candidates for inhibitors of NF-kappa B were searched. Methods: Amino acids that regulate cellular redox potential by adjusting the level of NAD/NADH ratio, such as aspartate, pyruvate, and isocitrate were selected. Results: Pyruvate effectively inhibited luciferase activity in TNF-stimulated 293T cells transfect with an NF-kB dependent luciferase reporter vector. Pyruvate also showed protective effect on muscle atrophy of differentiated C2C12 myocyte induced by TNF/IFN. Conclusion: We might be able to develop the nutritional management strategy for cancer cachexia patients with pyruvate supplementation.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.18
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• pp.8075-8077
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• 2016

Sarcopenia, characterized by a decline of skeletal muscle plus low muscle strength and/or physical performance, has emerged to be an important prognostic factor for advanced cancer patients. It is associated with poor performance status, toxicity from chemotherapy, and shorter time of tumor control. There is limited data about sarcopenia in cancer patients and associated factors. Moreover, the knowledge about the changes of muscle mass during chemotherapy and its impact to response and toxicity to chemotherapy is still lacking. This review aimed to provide understanding about sarcopenia and to emphasize its importance to cancer treatment.

• BMB Reports
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• v.56 no.7
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• pp.365-373
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• 2023

Loss of skeletal muscle mass is a primary feature of sarcopenia and cancer cachexia. In cancer patients, tumor-derived inflammatory factors promote muscle atrophy via tumor-to-muscle effects, which is closely associated with poor prognosis. During the past decade, skeletal muscle has been considered to function as an autocrine, paracrine, and endocrine organ by releasing numerous myokines. The circulating myokines can modulate pathophysiology in the other organs, as well as in the tumor microenvironment, suggesting myokines function as muscle-to-tumor signaling molecules. Here, we highlight the roles of myokines in tumorigenesis, particularly in terms of crosstalk between skeletal muscle and tumor. Better understanding of tumor-to-muscle and muscle-to-tumor effects will shed light on novel strategies for the diagnosis and treatment of cancer.

• BMB Reports
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• v.57 no.4
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• pp.167-175
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• 2024

Cancer progression is driven by genetic mutations, environmental factors, and intricate interactions within the tumor microenvironment (TME). The TME comprises of diverse cell types, such as cancer cells, immune cells, stromal cells, and neuronal cells. These cells mutually influence each other through various factors, including cytokines, vascular perfusion, and matrix stiffness. In the initial or developmental stage of cancer, neurotrophic factors such as nerve growth factor, brain-derived neurotrophic factor, and glial cell line-derived neurotrophic factor are associated with poor prognosis of various cancers by communicating with cancer cells, immune cells, and peripheral nerves within the TME. Over the past decade, research has been conducted to prevent cancer growth by controlling the activation of neurotrophic factors within tumors, exhibiting a novel attemt in cancer treatment with promising results. More recently, research focusing on controlling cancer growth through regulation of the autonomic nervous system, including the sympathetic and parasympathetic nervous systems, has gained significant attention. Sympathetic signaling predominantly promotes tumor progression, while the role of parasympathetic signaling varies among different cancer types. Neurotransmitters released from these signalings can directly or indirectly affect tumor cells or immune cells within the TME. Additionally, sensory nerve significantly promotes cancer progression. In the advanced stage of cancer, cancer-associated cachexia occurs, characterized by tissue wasting and reduced quality of life. This process involves the pathways via brainstem growth and differentiation factor 15-glial cell line-derived neurotrophic factor receptor alpha-like signaling and hypothalamic proopiomelanocortin neurons. Our review highlights the critical role of neurotrophic factors as well as central nervous system on the progression of cancer, offering promising avenues for targeted therapeutic strategies.

• Journal of Korean Traditional Oncology
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• v.17 no.1
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• pp.1-7
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• 2012

Objective : The association of cancer survival and components of the systemic inflammatory response, combined to form inflammation-based prognostic scores (modified Glasgow Prognostic Score (GPS), Neutrophil Lymphocyte Ratio, Platelet Lymphocyte Ratio) is reviewed in this article. Methods and Results : With extensive research of papers in the PubMed, there is good evidence that preoperative measures of the systemic inflammatory response predict cancer survival, independent of tumor stage, in primary operable cancer. GPS also shows its prognostic value as a predictor of survival, independent of tumor stage, performance status and treatment in a variety of advanced cancer. GPS is associated with chemotherapy related toxicities as well as response to treatment and C-reactive protein shows its clinical value as a monitor of chemotherapy response. The systemic inflammatory response is closely related to cachexia and may be suitable measure for the clinical definition of cancer cachexia. Conclusion : Anticipated survival using the inflammation-based prognostic score is a major factor to be taken into consideration when deciding whether active intervention including surgery and chemotherapy or palliation therapy including acupuncture and herb medication is appropriate.

• Clinical Nutrition Research
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• v.5 no.2
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• pp.126-136
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• 2016

Due to poor nutrition and abnormal energy metabolism, cancer patients typically experience the loss of muscle mass. Although the diabetic conditions or dyslipidemia have been reported as a causal link of cancer but the consequence of such conditions in relation to gain or loss of skeletal muscle mass in cancer patients has not been well documented. The purpose of this study was to investigate the relationship of lean body mass and systemic parameters related to lipid metabolism in non-diabetic cancer patients using data from the Korean National Health and Nutrition Examination Survey (KNHANES) 2008-2011. As results the level of serum total cholesterol (total-C) was negatively associated with both total lean body mass and appendicular lean body mass in cancer patients after adjustment for sex, physical activity, energy intake and comorbidity. The associations between consumption of dietary factors (energy, carbohydrate, protein and fat) and lean body mass were disappeared after adjusting comorbidities of cancer patients. Multivariate-adjusted linear regression analysis by quartiles of serum total-C showed that higher quartile group of total-C had significantly lower percent of lean body mass than reference group in cancer patients. The data indicate that serum lipid status can be the potential estimate of loss of skeletal muscle mass in cancer patients and be referenced in nutrition care of cancer patients under the onset of cachexia or parenteral/enteral nutrition. This data need to be confirmed with large pool of subjects and should be specified by stage of cancer or the site of cancer in future studies.