scholarly journals P3.05-018 Assessment of Skeletal Muscle Mass as a Predictive Factor for Chemotherapy Toxicity and TTP in Advanced NSCLC Patients with Cancer Cachexia

2017 ◽  
Vol 12 (1) ◽  
pp. S1422-S1423
Author(s):  
Drazena Srdic ◽  
Sanja Plestina ◽  
Ana Sverko-Peternac ◽  
Nora Nikolac ◽  
Ana Bacelic Gabelica ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Predictive Factor ◽  
Skeletal Muscle Mass ◽  
Cancer Cachexia ◽  
Advanced Nsclc ◽  
Chemotherapy Toxicity ◽  
Patients With Cancer ◽  
Nsclc Patients

scholarly journals The pathogenesis and treatment of cardiac atrophy in cancer cachexia

2016 ◽  
Vol 310 (4) ◽  
pp. H466-H477 ◽  
Author(s):  
Kate T. Murphy
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Cancer Cachexia ◽  
Cardiac Cachexia ◽  
Patients With Cancer ◽  
Cardiac Atrophy ◽  
Lack Of Information ◽  
And Function ◽  
Made In

Cancer cachexia is a multifactorial syndrome characterized by a progressive loss of skeletal muscle mass associated with significant functional impairment. In addition to a loss of skeletal muscle mass and function, many patients with cancer cachexia also experience cardiac atrophy, remodeling, and dysfunction, which in the field of cancer cachexia is described as cardiac cachexia. The cardiac alterations may be due to underlying heart disease, the cancer itself, or problems initiated by the cancer treatment and, unfortunately, remains largely underappreciated by clinicians and basic scientists. Despite recent major advances in the treatment of cancer, little progress has been made in the treatment of cardiac cachexia in cancer, and much of this is due to lack of information regarding the mechanisms. This review focuses on the cardiac atrophy associated with cancer cachexia, describing some of the known mechanisms and discussing the current and future therapeutic strategies to treat this condition. Above all else, improved awareness of the condition and an increased focus on identification of mechanisms and therapeutic targets will facilitate the eventual development of an effective treatment for cardiac atrophy in cancer cachexia.

scholarly journals Impact of Sarcopenia as a Prognostic Biomarker of Bladder Cancer

2018 ◽  
Vol 19 (10) ◽  
pp. 2999 ◽  
Author(s):  
Hiroshi Fukushima ◽  
Kosuke Takemura ◽  
Hiroaki Suzuki ◽  
Fumitaka Koga
Keyword(s):  
Skeletal Muscle ◽  
Bladder Cancer ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Cancer Cachexia ◽  
Prognostic Biomarker ◽  
Inflammatory Diseases ◽  
Patients With Cancer ◽  
Poor Nutritional Status ◽  
The Impact

Sarcopenia, the degenerative and systemic loss of skeletal muscle mass, indicates patient frailty and impaired physical function. Sarcopenia can be caused by multiple factors, including advanced age, lack of exercise, poor nutritional status, inflammatory diseases, endocrine diseases, and malignancies. In patients with cancer cachexia, anorexia, poor nutrition and systemic inflammation make the metabolic state more catabolic, resulting in sarcopenia. Thus, sarcopenia is considered as one of manifestations of cancer cachexia. Recently, growing evidence has indicated the importance of sarcopenia in the management of patients with various cancers. Sarcopenia is associated with not only higher rates of treatment-related complications but also worse prognosis in cancer-bearing patients. In this article, we summarized metabolic backgrounds of cancer cachexia and sarcopenia and definitions of sarcopenia based on computed tomography (CT) images. We conducted a systematic literature review regarding the significance of sarcopenia as a prognostic biomarker of bladder cancer. We also reviewed recent studies focusing on the prognostic role of changes in skeletal muscle mass during the course of treatment in bladder cancer patients. Lastly, we discussed the impact of nutritional support, medication, and exercise on sarcopenia in cancer-bearing patients.

scholarly journals Higher skeletal muscle protein synthesis and lower breakdown after chemotherapy in cachectic mice

2001 ◽  
Vol 281 (1) ◽  
pp. R133-R139 ◽  
Author(s):  
S. E. Samuels ◽  
A. L. Knowles ◽  
T. Tilignac ◽  
E. Debiton ◽  
J. C. Madelmont ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Cancer Cachexia ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Human Condition ◽  
Skeletal Muscle Protein ◽  
Tumor Bearing

The influence of cancer cachexia and chemotherapy and subsequent recovery of skeletal muscle protein mass and turnover was investigated in mice. Cancer cachexia was induced using colon 26 adenocarcinoma, which is characteristic of the human condition, and can be cured with 100% efficacy using an experimental nitrosourea, cystemustine (C6H12CIN3O4S). Reduced food intake was not a factor in these studies. Three days after cachexia began, healthy and tumor-bearing mice were given a single intraperitoneal injection of cystemustine (20 mg/kg). Skeletal muscle mass in tumor-bearing mice was 41% lower ( P < 0.05) than in healthy mice 2 wk after cachexia began. Skeletal muscle wasting was mediated initially by decreased protein synthesis (−38%; P < 0.05) and increased degradation (+131%; P < 0.05); later wasting resulted solely from decreased synthesis (∼−54 to −69%; P < 0.05). Acute cytotoxicity of chemotherapy did not appear to have an important effect on skeletal muscle protein metabolism in either healthy or tumor-bearing mice. Recovery began 2 days after treatment; skeletal muscle mass was only 11% lower than in healthy mice 11 days after chemotherapy. Recovery of skeletal muscle mass was affected initially by decreased protein degradation (−80%; P < 0.05) and later by increased protein synthesis (+46 to +73%; P < 0.05) in cured compared with healthy mice. This study showed that skeletal muscle wasted from cancer cachexia and after chemotherapeutic treatment is able to generate a strong anabolic response by making powerful changes to protein synthesis and degradation.

scholarly journals Molecular pathways leading to loss of skeletal muscle mass in cancer cachexia – can findings from animal models be translated to humans?

BMC Cancer ◽  
2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Tara C. Mueller ◽  
Jeannine Bachmann ◽  
Olga Prokopchuk ◽  
Helmut Friess ◽  
Marc E. Martignoni
Keyword(s):  
Skeletal Muscle ◽  
Animal Models ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Cancer Cachexia ◽  
Molecular Pathways

Growth differentiation factor 15 (GDF-15) inhibition to increase muscle mass and function in cancer cachexia.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e15633-e15633
Author(s):  
Matthew Peloquin ◽  
Brianna LaCarubba ◽  
Stephanie Joaqium ◽  
Gregory Weber ◽  
John Stansfield ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Weight ◽  
Muscle Mass ◽  
Muscle Function ◽  
Skeletal Muscle Mass ◽  
Cancer Cachexia ◽  
Tumor Model ◽  
Growth Differentiation Factor 15 ◽  
Myostatin Inhibition ◽  
And Function

e15633 Background: Almost half of cancer deaths are attributed to cancers most frequently associated with cachexia. Cachexia is a complex metabolic disease characterized by anorexia and unintentional weight loss. Skeletal muscle depletion has been recognized as a key feature of the disease, however muscle anabolic therapies have not been successful, suggesting that treatments that target multiple aspects of the disease will be most effective. Growth differentiation factor 15 (GDF-15) is a cytokine that induces anorexia and weight loss and is associated with cachexia in cancer patients. In preclinical cancer cachexia models, GDF-15 inhibition is sufficient to normalize food intake and body weight, including skeletal muscle mass. However, it remains to be determined whether the increased skeletal muscle mass also results in restoration of muscle function. Therefore, we examined the effect of GDF-15 inhibition on muscle mass and function in mouse models of cancer cachexia in comparison with myostatin inhibition, an established muscle anabolic pathway. Methods: Cachectic mouse tumor models were established with subcutaneous implantation of tumor cell lines reported to be GDF-15-dependent; mouse renal cell carcinoma (RENCA) and human ovarian cancer (TOV-21G) cell lines. Mice were treated with anti-GDF-15 (mAB2) or anti-myostatin (RK35) monoclonal antibodies and skeletal muscle function was assessed in vivo via maximum force, maximum rate of contraction and half relax time. In the RENCA tumor model, GDF-15 inhibition fully restored body weight and skeletal muscle mass whereas myostatin inhibition showed only a modest effect. Results: Consistent with the muscle mass improvement, GDF-15 inhibition dramatically increased functional muscle endpoints compared to the partial effect of myostatin inhibition. Interestingly, in the TOV-21G tumor model GDF-15 inhibition only partially restored body weight, however skeletal muscle mass and muscle function were completely normalized. Consistent with the functional assessment, GDF-15 inhibition in the RENCA tumor model decreased the expression of several catabolic genes (i.e. Trim63, Fbxo32, Myh7 and Myh2). The GDF-15 effect is likely to be secondary to the reversal of anorexia since wildtype mice pair-fed to Fc-GDF-15-treated mice demonstrated equivalent muscle mass loss. Conclusions: Taken together these data suggest that GDF-15 inhibition holds potential as an effective therapeutic approach to alleviate multiple aspects of cachexia.

scholarly journals Aerobic Exercise Training and In Vivo Akt Activation Counteract Cancer Cachexia by Inducing a Hypertrophic Profile through eIF-2α Modulation

Cancers ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 28
Author(s):  
Marcelo G. Pereira ◽  
Vanessa A. Voltarelli ◽  
Gabriel C. Tobias ◽  
Lara de Souza ◽  
Gabriela S. Borges ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Cancer Cachexia ◽  
Aerobic Exercise Training ◽  
Akt Activation ◽  
The Impact

Cancer cachexia is a multifactorial and devastating syndrome characterized by severe skeletal muscle mass loss and dysfunction. As cachexia still has neither a cure nor an effective treatment, better understanding of skeletal muscle plasticity in the context of cancer is of great importance. Although aerobic exercise training (AET) has been shown as an important complementary therapy for chronic diseases and associated comorbidities, the impact of AET on skeletal muscle mass maintenance during cancer progression has not been well documented yet. Here, we show that previous AET induced a protective mechanism against tumor-induced muscle wasting by modulating the Akt/mTORC1 signaling and eukaryotic initiation factors, specifically eIF2-α. Thereafter, it was determined whether the in vivo Akt activation would induce a hypertrophic profile in cachectic muscles. As observed for the first time, Akt-induced hypertrophy was able and sufficient to either prevent or revert cancer cachexia by modulating both Akt/mTORC1 pathway and the eIF-2α activation, and induced a better muscle functionality. These findings provide evidence that skeletal muscle tissue still preserves hypertrophic potential to be stimulated by either AET or gene therapy to counteract cancer cachexia.

scholarly journals Metabolic and Molecular Basis of Sarcopenia: Implications in the Management of Urothelial Carcinoma

2019 ◽  
Vol 20 (3) ◽  
pp. 760 ◽  
Author(s):  
Hiroshi Fukushima ◽  
Yasuhisa Fujii ◽  
Fumitaka Koga
Keyword(s):  
Skeletal Muscle ◽  
Urothelial Carcinoma ◽  
Muscle Mass ◽  
Molecular Basis ◽  
Skeletal Muscle Mass ◽  
Cancer Cachexia ◽  
Poor General Health ◽  
Advanced Urothelial Carcinoma ◽  
Muscle Invasive ◽  
Clinical Conditions

Sarcopenia, which represents the degenerative and systemic loss of skeletal muscle mass, is a multifactorial syndrome caused by various clinical conditions. Sarcopenia reflects not only frailty and poor general health status, but also the possible presence of advanced or progressive cancer or cancer cachexia. Therefore, sarcopenia affects the management of cancer-bearing patients, including those with urothelial carcinoma. Recently, growing evidence has shown that sarcopenia is significantly associated with higher rates of treatment-related complications and worse prognosis in patients with urothelial carcinoma, including muscle-invasive bladder cancer, upper tract urothelial carcinoma, and advanced urothelial carcinoma. Moreover, several studies reported that a post-therapeutic increase in skeletal muscle mass predicts favorable prognosis in urothelial carcinoma patients. To further explore the role of sarcopenia in the management of urothelial carcinoma patients, comprehensive understanding of its pathophysiology is vital. In this article, we reviewed the metabolic and molecular basis of cancer cachexia and sarcopenia. From this viewpoint, we discussed the possible mechanism of changes in skeletal muscle mass during the course of treatment.

The use of alternate vertebral levels to L3 in computed tomography scans for skeletal muscle mass evaluation and sarcopenia assessment in patients with cancer: a systematic review

2021 ◽  
pp. 1-49
Author(s):  
Belinda Vangelov ◽  
Judy Bauer ◽  
Damian Kotevski ◽  
Robert I. Smee
Keyword(s):  
Computed Tomography ◽  
Skeletal Muscle ◽  
Ct Scan ◽  
Cancer Patients ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Whole Body ◽  
Ct Scans ◽  
Cross Sectional ◽  
Patients With Cancer

ABSTRACT Body composition measurement using diagnostic computed tomography (CT) scans has emerged as a method to assess sarcopenia (low muscle mass) in oncology patients. Assessment of skeletal muscle mass (SMM) using the cross-sectional area (CSA) of a single vertebral slice (at lumbar L3) in a CT scan is correlated to whole body skeletal muscle volume. This method is used to assess CT-defined sarcopenia in patients with cancer, with low SMM effecting outcomes. However, as diagnostic scans are based on tumour location, not all include L3. We evaluated the evidence for the use of alternate vertebral CT slices for SMM evaluation when L3 is not available. Five electronic databases were searched from Jan 1996-April 2020 for studies using CT scan vertebral slices above L3 for SM measurement in adults with cancer (solid tumours). Validation with whole body SMM, rationale for the chosen slice, and sarcopenia cut-off values were investigated. Thirty-two studies were included, all retrospective and cross-sectional in design. Cervical, thoracic, and lumbar slices were used (from C3-L1), with no validation of whole body SMM using CT scans. Alternate slices were used in lung, and head and neck cancer patients. Sarcopenia cut-off values were reported in 75% of studies, with differing methods, with or without sex-specific values, and a lack of consensus. Current evidence is inadequate to provide definitive recommendations for alternate vertebral slice use for SMM evaluation in cancer patients. Variation in sarcopenia cut-offs warrants more robust investigation, in order for risk stratification to be applied to all patients with cancer.

Sign in / Sign up

Export Citation Format

Share Document