Practical multimodal care for cancer cachexia

Maddocks, Matthew; Hopkinson, Jane B.; Conibear, John; Reeves, Annie; Shaw, Clare; Fearon, K.C.H.

doi:10.1097/spc.0000000000000241

Cited by 48 publications

(43 citation statements)

References 71 publications

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“…Multimodal care has been recommended as a treatment approach for advanced cancer patients with cachexia [4,6,[53][54][55][56]. A systemic review demonstrated that multimodal rehabilitation program incorporating exercise and nutritional support improved many outcomes, e.g., improvements in physical endurance and depression, in patients with incurable cancer.…”

Section: Integration Of Palliative Supportive and Nutritional Carementioning

confidence: 99%

Integration of palliative, supportive, and nutritional care to alleviate eating-related distress among advanced cancer patients with cachexia and their family members

Amano

Baracos

Hopkinson

2019

Critical Reviews in Oncology/Hematology

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Advanced cancer patients with cachexia and their families can suffer from eating-related distress. This complex entity encompasses patients' struggle to nourish themselves, emotional and social consequences of their inability to maintain food intake, and profound disturbance in family relationships. With evidencebased nutritional care, as well as symptom management to enable food intake, cachexia can be mitigated to some degree. In addition, patients and families require psychosocial support and education to understand and cope with this condition. Only by taking an integrated approach can health care teams alleviate eatingrelated distress, improve quality of life (QOL), reduce interpersonal conflicts, and alter perceptions of nutritional neglect for patients and families. However, few studies have investigated eating-related distress among patients and families. The aim of this narrative review is to describe what is known about eating-related distress and the roles of integrated palliative, supportive, and nutritional care in improving QOL of patients and families.

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Section: Integration Of Palliative Supportive and Nutritional Carementioning

confidence: 99%

Integration of palliative, supportive, and nutritional care to alleviate eating-related distress among advanced cancer patients with cachexia and their family members

Amano

Baracos

Hopkinson

2019

Critical Reviews in Oncology/Hematology

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show abstract

“…In humans, therapeutic intervention with a single agent targeting exclusively systemic inflammation, low food intake, or catabolic pathways regulating muscle mass has proven ineffective to counteract cachexia 1 , 7 . A combinatorial approach is advocated for successful management of cachexia, in order to concurrently address different facets of the syndrome, such as inflammation and muscle atrophy 8 . IL6, the ubiquitin proteasome system, and autophagy have been individually investigated for potential therapeutic intervention, with limited success 9 – 12 .…”

Section: Introductionmentioning

confidence: 99%

Epigenetic targeting of bromodomain protein BRD4 counteracts cancer cachexia and prolongs survival

Segatto

Fittipaldi

et al. 2017

Nat Commun

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Cancer cachexia is a devastating metabolic syndrome characterized by systemic inflammation and massive muscle and adipose tissue wasting. Although it is responsible for approximately one-third of cancer deaths, no effective therapies are available and the underlying mechanisms have not been fully elucidated. We previously identified the bromodomain and extra-terminal domain (BET) protein BRD4 as an epigenetic regulator of muscle mass. Here we show that the pan-BET inhibitor (+)-JQ1 protects tumor-bearing mice from body weight loss and muscle and adipose tissue wasting. Remarkably, in C26-tumor-bearing mice (+)-JQ1 administration dramatically prolongs survival, without directly affecting tumor growth. By ChIP-seq and ChIP analyses, we unveil that BET proteins directly promote the muscle atrophy program during cachexia. In addition, BET proteins are required to coordinate an IL6-dependent AMPK nuclear signaling pathway converging on FoxO3 transcription factor. Overall, these findings indicate that BET proteins may represent a promising therapeutic target in the management of cancer cachexia.

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“…To address the numerous defects of cancer cachexia, a multi-modal therapeutic approach consisting of pharmaceutical agents, nutritional support, and programmed exercise training has been proposed [2,13]. In an effort to improve our understanding of therapeutic exercise applications, we recently investigated the impact of aerobic and resistance training on skeletal muscle plasticity in the colon-26 (C26) mouse model of cancer cachexia [14].…”

Section: Introductionmentioning

confidence: 99%

Bone mineral density and content are differentially impacted by aerobic and resistance training in the colon-26 mouse model of cancer cachexia

et al. 2017

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Background: Cancer cachexia is a debilitating paraneoplastic syndrome featuring unintended weight loss and skeletal muscle atrophy. Evidence suggests that bone health may also be compromised, further limiting mobility and quality of life. Aerobic and resistance training was recently reported to differentially affect skeletal muscle adaptations in cancer cachectic mice. The purpose of this investigation was to assess the effects of aerobic and resistance training on bone mineral density (BMD) and bone mineral content (BMC) in mice with colon-26 (C26) tumor-induced cachexia. Methods: Twelve-month old Balb/c mice were aerobic-trained (wheel running 5 days/week) or resistance-trained (weighted ladder climbing 3days/week) for 8 weeks prior to C26 cell injection, followed by an additional three weeks of exercise. BMD and BMC were assessed pre-and post-training by dual-energy x-ray absorptiometry. Results: Resistance-trained C26 mice lost total BMD by 7% (p = 0.06), which did not occur in aerobic-trained C26 mice. In terms of pelvic bone, both resistance-and aerobic-trained C26 mice had significantly lower BMD values (−12%, p = 0.01 and −6%, p = 0.04, respectively), albeit to a lesser degree in aerobic-trained C26 mice. Furthermore, resistance-trained C26 mice tended to lose total BMC (−12%), whereas aerobic-trained C26 mice maintained total BMC. In mice without C26 tumors, resistance training significantly increased total BMD (+13%, p = 0.001). Conclusions: Aerobic and resistance training may differentially affect bone status in C26 cancer cachexia, with high resistance loading possibly being detrimental to total and pelvis BMD, a region expected to bear significant loading stress and contribute substantially to overall mobility. Because resistance training improved BMD in tumor-free mice, the C26 tumor burden appeared to impair the beneficial effect of resistance training on bone mass.

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Practical multimodal care for cancer cachexia

Cited by 48 publications

References 71 publications

Integration of palliative, supportive, and nutritional care to alleviate eating-related distress among advanced cancer patients with cachexia and their family members

Integration of palliative, supportive, and nutritional care to alleviate eating-related distress among advanced cancer patients with cachexia and their family members

Epigenetic targeting of bromodomain protein BRD4 counteracts cancer cachexia and prolongs survival

Bone mineral density and content are differentially impacted by aerobic and resistance training in the colon-26 mouse model of cancer cachexia

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