scholarly journals Cancer-induced muscle wasting: latest findings in prevention and treatment

2017 ◽  
Vol 9 (5) ◽  
pp. 369-382 ◽  
Author(s):  
Zaira Aversa ◽  
Paola Costelli ◽  
Maurizio Muscaritoli
Keyword(s):  
Cancer Cachexia ◽  
Molecular Mechanisms ◽  
Muscle Wasting ◽  
Early Recognition ◽  
Poor Quality ◽  
Future Research ◽  
Pharmacological Interventions ◽  
Metabolic Alterations ◽  
Clinical Consequences

Cancer cachexia is a severe and disabling clinical condition that frequently accompanies the development of many types of cancer. Muscle wasting is the hallmark of cancer cachexia and is associated with serious clinical consequences such as physical impairment, poor quality of life, reduced tolerance to treatments and shorter survival. Cancer cachexia may evolve through different stages of clinical relevance, namely pre-cachexia, cachexia and refractory cachexia. Given its detrimental clinical consequences, it appears mandatory to prevent and/or delay the progression of cancer cachexia to its refractory stage by implementing the early recognition and treatment of the nutritional and metabolic alterations occurring during cancer. Research on the molecular mechanisms underlying muscle wasting during cancer cachexia has expanded in the last few years, allowing the identification of several potential therapeutic targets and the development of many promising drugs. Several of these agents have already reached the clinical evaluation, but it is becoming increasingly evident that a single therapy may not be completely successful in the treatment of cancer-related muscle wasting, given its multifactorial and complex pathogenesis. This suggests that early and structured multimodal interventions (including targeted nutritional supplementation, physical exercise and pharmacological interventions) are necessary to prevent and/or treat the devastating consequences of this cancer comorbidity, and future research should focus on this approach.

scholarly journals Amiloride ameliorates muscle wasting in cancer cachexia through inhibiting tumor-derived exosome release

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lin Zhou ◽  
Tong Zhang ◽  
Wei Shao ◽  
Ruohan Lu ◽  
Lin Wang ◽  
...  
Keyword(s):  
Muscle Atrophy ◽  
Cancer Cachexia ◽  
Molecular Mechanisms ◽  
Muscle Wasting ◽  
Drug Repositioning ◽  
Biochemical Analyses ◽  
Related Proteins ◽  
Metabolic Impairments

Abstract Background Cancer cachexia (CAC) reduces patient survival and quality of life. Developments of efficient therapeutic strategies are required for the CAC treatments. This long-term process could be shortened by the drug-repositioning approach which exploits old drugs approved for non-cachexia disease. Amiloride, a diuretic drug, is clinically used for treatments of hypertension and edema due to heart failure. Here, we explored the effects of the amiloride treatment for ameliorating muscle wasting in murine models of cancer cachexia. Methods The CT26 and LLC tumor cells were subcutaneously injected into mice to induce colon cancer cachexia and lung cancer cachexia, respectively. Amiloride was intraperitoneally injected daily once tumors were formed. Cachexia features of the CT26 model and the LLC model were separately characterized by phenotypic, histopathologic and biochemical analyses. Plasma exosomes and muscle atrophy-related proteins were quantitatively analyzed. Integrative NMR-based metabolomic and transcriptomic analyses were conducted to identify significantly altered metabolic pathways and distinctly changed metabolism-related biological processes in gastrocnemius. Results The CT26 and LLC cachexia models displayed prominent cachexia features including decreases in body weight, skeletal muscle, adipose tissue, and muscle strength. The amiloride treatment in tumor-bearing mice distinctly alleviated muscle atrophy and relieved cachexia-related features without affecting tumor growth. Both the CT26 and LLC cachexia mice showed increased plasma exosome densities which were largely derived from tumors. Significantly, the amiloride treatment inhibited tumor-derived exosome release, which did not obviously affect exosome secretion from non-neoplastic tissues or induce observable systemic toxicities in normal healthy mice. Integrative-omics revealed significant metabolic impairments in cachectic gastrocnemius, including promoted muscular catabolism, inhibited muscular protein synthesis, blocked glycolysis, and impeded ketone body oxidation. The amiloride treatment evidently improved the metabolic impairments in cachectic gastrocnemius. Conclusions Amiloride ameliorates cachectic muscle wasting and alleviates cancer cachexia progression through inhibiting tumor-derived exosome release. Our results are beneficial to understanding the underlying molecular mechanisms, shedding light on the potentials of amiloride in cachexia therapy.

scholarly journals Inflammation Based Regulation of Cancer Cachexia

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Jill K. Onesti ◽  
Denis C. Guttridge
Keyword(s):  
Quality Of Life ◽  
Skeletal Muscle ◽  
Cancer Cachexia ◽  
Molecular Mechanisms ◽  
Muscle Wasting ◽  
Nutritional Intake ◽  
Clinical Implications ◽  
Life Outcomes ◽  
Skeletal Muscle Wasting

Cancer cachexia, consisting of significant skeletal muscle wasting independent of nutritional intake, is a major concern for patients with solid tumors that affects surgical, therapeutic, and quality of life outcomes. This review summarizes the clinical implications, background of inflammatory cytokines, and the origin and sources of procachectic factors including TNF-α, IL-6, IL-1, INF-γ, and PIF. Molecular mechanisms and pathways are described to elucidate the link between the immune response caused by the presence of the tumor and the final result of skeletal muscle wasting.

Couples Facing Cancer

2021 ◽  
pp. 729-736
Author(s):  
Hoda Badr ◽  
Courtney Bitz
Keyword(s):  
Routine Care ◽  
Poor Quality ◽  
Psychosocial Adaptation ◽  
Future Research ◽  
Great Promise ◽  
Clinical Implications ◽  
Social Challenges ◽  
Healthcare Settings ◽  
Care And Support

Cancer survivors experience significant physical, psychological, and social challenges that contribute to poor quality of life. Intimate partners provide critical care and support across the cancer continuum, but they report psychological distress, lack basic healthcare knowledge and skills, and experience increased tension and conflict in their relationships with survivors. Couple-based interventions hold great promise in cancer because they can simultaneously address survivor, partner, and relationship concerns. However, they are seldom implemented in healthcare settings as part of routine care. This chapter will therefore integrate what research has taught us about couples and cancer and what we have learned from couples in the clinical setting. We begin with an overview of challenges faced by couples across the cancer continuum, including biopsychosocial stressors. Next, we describe different perspectives that have shaped descriptive and intervention research on couples’ psychosocial adaptation to cancer. We conclude with clinical implications and directions for future research.

scholarly journals Cancer Cachexia: Mechanisms and Clinical Implications

2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Claire L. Donohoe ◽  
Aoife M. Ryan ◽  
John V. Reynolds
Keyword(s):  
Host Response ◽  
Cancer Cachexia ◽  
Resting Energy Expenditure ◽  
Poor Quality ◽  
Therapeutic Agents ◽  
Progressive Weight Loss ◽  
Slow Progress ◽  
Definition Of ◽  
The Relationship

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 fully elucidated. Cachexia is compounded by anorexia and the relationship between these two entities has not been clarified fully. Inconsistencies in the definition of cachexia have limited the epidemiological characterisation of the condition and there has been slow progress in identifying therapeutic agents and trialling them in the clinical setting. Understanding the complex interplay of tumour and host factors will uncover new therapeutic targets.

scholarly journals MicroRNAs in Skeletal Muscle and Hints on Their Potential Role in Muscle Wasting During Cancer Cachexia

2020 ◽  
Vol 10 ◽  
Author(s):  
Gioacchino P. Marceca ◽  
Giovanni Nigita ◽  
Federica Calore ◽  
Carlo M. Croce
Keyword(s):  
Skeletal Muscle ◽  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Phenotypic Alteration ◽  
Specific Tumor ◽  
Non Coding Rnas

Cancer-associated cachexia is a heterogeneous, multifactorial syndrome characterized by systemic inflammation, unintentional weight loss, and profound alteration in body composition. The main feature of cancer cachexia is represented by the loss of skeletal muscle tissue, which may or may not be accompanied by significant adipose tissue wasting. Such phenotypic alteration occurs as the result of concomitant increased myofibril breakdown and reduced muscle protein synthesis, actively contributing to fatigue, worsening of quality of life, and refractoriness to chemotherapy. According to the classical view, this condition is primarily triggered by interactions between specific tumor-induced pro-inflammatory cytokines and their cognate receptors expressed on the myocyte membrane. This causes a shift in gene expression of muscle cells, eventually leading to a pronounced catabolic condition and cell death. More recent studies, however, have shown the involvement of regulatory non-coding RNAs in the outbreak of cancer cachexia. In particular, the role exerted by microRNAs is being widely addressed, and several mechanistic studies are in progress. In this review, we discuss the most recent findings concerning the role of microRNAs in triggering or exacerbating muscle wasting in cancer cachexia, while mentioning about possible roles played by long non-coding RNAs and ADAR-mediated miRNA modifications.

Cockroaches: Allergens, Component-Resolved Diagnosis (CRD) and Component-Resolved Immunotherapy

2020 ◽  
Vol 21 (2) ◽  
pp. 124-141 ◽  
Author(s):  
Nitat Sookrung ◽  
Anchalee Tungtrongchitr ◽  
Wanpen Chaicumpa
Keyword(s):  
Molecular Mechanisms ◽  
Allergic Diseases ◽  
Poor Quality ◽  
Allergen Specific Immunotherapy ◽  
Healthcare Facilities ◽  
Increasing Demand ◽  
Socio Economic Impact ◽  
Medical And Healthcare ◽  
Working Efficiency

Allergic diseases are assuming increasing trend of prevalence worldwide. The diseases confer increasing demand on medical and healthcare facilities. Patients with allergies have poor quality of life and impaired cognition. Adult patients have subpar working efficiency while afflicted children are less effective at school, often have school absenteeism and need more attention of their caregivers. All of them lead to negative socio-economic impact. This narrative review focuses on cockroach allergy including currently recognized cockroach allergens, pathogenic mechanisms of allergy, componentresolved diagnosis and allergen-specific immunotherapy, particularly the component-resolved immunotherapy and the molecular mechanisms that bring about resolution of the chronic airway inflammation.

scholarly journals Enriching limited information on rare diseases from heterogeneous networks for drug repositioning

2021 ◽  
Vol 21 (S9) ◽  
Author(s):  
Hongkui Cao ◽  
Liang Zhang ◽  
Bo Jin ◽  
Shicheng Cheng ◽  
Xiaopeng Wei ◽  
...  
Keyword(s):  
Rare Disease ◽  
Heterogeneous Networks ◽  
Drug Repositioning ◽  
Research Work ◽  
Protein Molecule ◽  
Poor Quality ◽  
Future Research ◽  
Limited Information ◽  
Biased Random Walk

Abstract Background The historical data of rare disease is very scarce in reality, so how to perform drug repositioning for the rare disease is a great challenge. Most existing methods of drug repositioning for the rare disease usually neglect father–son information, so it is extremely difficult to predict drugs for the rare disease. Method In this paper, we focus on father–son information mining for the rare disease. We propose GRU-Cooperation-Attention-Network (GCAN) to predict drugs for the rare disease. We construct two heterogeneous networks for information enhancement, one network contains the father-nodes of the rare disease and the other network contains the son-nodes information. To bridge two heterogeneous networks, we set a mapping to connect them. What’s more, we use the biased random walk mechanism to collect the information smoothly from two heterogeneous networks, and employ a cooperation attention mechanism to enhance repositioning ability of the network. Result Comparing with traditional methods, GCAN makes full use of father–son information. The experimental results on real drug data from hospitals show that GCAN outperforms state-of-the-art machine learning methods for drug repositioning. Conclusion The performance of GCAN for drug repositioning is mainly limited by the insufficient scale and poor quality of the data. In future research work, we will focus on how to utilize more data such as drug molecule information and protein molecule information for the drug repositioning of the rare disease.

scholarly journals Insight of Mechanism and Signaling Pathway in Pathogenesis of Diabetic Neuropathy: A Review

2021 ◽  
Vol 20 (4) ◽  
Author(s):  
Norhamidar Ab Hamid ◽  
Norsuhana Omar ◽  
Che Aishah Nazariah Ismail ◽  
Idris Long
Keyword(s):  
Quality Of Life ◽  
Diabetic Neuropathy ◽  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Poor Quality ◽  
Nerve Fibers ◽  
Drug Treatments ◽  
Underlying Causes ◽  
The Common

Diabetic neuropathy (DN) is a common chronic microvascular complication of diabetes mellitus. The features of DN include allodynia, hyperalgesia, abnormal or loss of sensation of nerve fibers. The clinical features will contribute to poor quality of life, disrupt sleep, lead to depression, and increases mortality. Current drug treatments have been shown to alleviate the symptoms of DN but failed to treat the underlying causes of DN. Therefore, a better understanding of the molecular mechanisms underlying the development and progression of DN is needed for early diagnosis and intervention and understanding the failure of existing treatments. Identification of potential mechanisms is critical for better prediction of progression and for designing preventive therapies. DN's exact pathogenesis is incomplete, although it is understood that its multifunctional dysfunction involving many signaling pathways. This review summarized the common deterioration of signaling pathways and mechanisms involved in DN pathogenesis. 

An Overview on Adult Acne, Its Pathogenesis, Clinical Presentation, Treatment and Scope in Homoeopathy

2021 ◽  
Vol 34 (04) ◽  
pp. 291-299
Author(s):  
Rashmi Sharma ◽  
Deepti Dewan
Keyword(s):  
Bacterial Resistance ◽  
Late Onset ◽  
Holistic Approach ◽  
Poor Quality ◽  
Future Research ◽  
Adult Women ◽  
Lactation Period ◽  
General Acceptance ◽  
High Prevalence

AbstractAdult acne is defined as a presence of acne beyond the age of 25 years. Two main subtypes can be identified: persistent acne and late-onset acne (beginning after the age of 25 years), which are responsible for 80 and 20% of cases, respectively. Women have a high prevalence and incidence when compared with men. Hyperandrogenism is the main aetiology associated with acne in this age group. Stress-related worsening of acne is a common complaint. Due to the visibility of acne, it is known to have psychosocial impact that can influence person's perceptions regarding their self-appearance, resulting in poor quality of life. Adult acne is often refractory to treatment as older skin presents increased irritancy to topical applications and has potential for bacterial resistance. Treatment failures with antibiotics occur in up to 80% of adult women. Antiandrogens are associated with the risk of feminisation of male foetus, hepatotoxicity, hyperkalaemia etc. Isotretinoin which is given in severe cases is proved to be potent teratogen. In this backdrop, there has been a need for gentle and effective way of treatment, and homoeopathy has the answer. Homoeopathy has a holistic approach having the general acceptance and compliance amongst masses; it has been considered safe in pregnancy and during lactation period. Further, no bacterial resistance develops after prolonged use of homoeopathic medicines. Earlier studies conducted signify the action of homoeopathic medicines in the treatment of adolescent acne with effective results. Not many studies have focused or conducted on the adult acne. This review suggests conducting the future research studies on adult acne through homoeopathic medicine.

scholarly journals Vitamin K Dependent Proteins in Kidney Disease

2019 ◽  
Vol 20 (7) ◽  
pp. 1571 ◽  
Author(s):  
Ciprian Silaghi ◽  
Tamás Ilyés ◽  
Vladimir Filip ◽  
Marius Farcaș ◽  
Adriana van Ballegooijen ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Vitamin K ◽  
Specific Protein ◽  
Poor Quality ◽  
Matrix Gla Protein ◽  
Future Research ◽  
Current State ◽  
Increased Risk ◽  
Calcification Inhibitors

Patients with chronic kidney disease (CKD) have an increased risk of developing vascular calcifications, as well as bone dynamics impairment, leading to a poor quality of life and increased mortality. Certain vitamin K dependent proteins (VKDPs) act mainly as calcification inhibitors, but their involvement in the onset and progression of CKD are not completely elucidated. This review is an update of the current state of knowledge about the relationship between CKD and four extrahepatic VKDPs: matrix Gla protein, osteocalcin, growth-arrest specific protein 6 and Gla-rich protein. Based on published literature in the last ten years, the purpose of this review is to address fundamental aspects about the link between CKD and circulating VKDPs levels as well as to raise new topics about how the interplay between molecular weight and charge could influence the modifications of circulating VKDPs at the glomerular level, or whether distinct renal etiologies have effect on VKDPs. This review is the output of a systematic literature search and may open future research avenues in this niche domain.

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