Patients with established cancer cachexia lack the motivation and self-efficacy to undertake regular structured exercise

Abstract

Objectives

Patients with advanced cancer frequently suffer a decline in activities associated with involuntary loss of weight and muscle mass (cachexia). This can profoundly affect function and quality of life. Although exercise participation can maintain physical and psychological function in patients with cancer, uptake is low in cachectic patients who are underrepresented in exercise studies. To understand how such patients' experiences are associated with exercise participation we investigated exercise history, self-confidence and exercise motivations in patients with established cancer cachexia, and relationships between relevant variables.

Methods

Lung and gastrointestinal cancer outpatients with established cancer cachexia (n=196) completed a questionnaire exploring exercise history and key constructs of the Theory of Planned Behaviour relating to perceived control, psychological adjustment and motivational attitudes.

Results

Patients reported low physical activity levels and few undertook regular structured exercise. Exercise self-efficacy was very low with concerns it could worsen symptoms and cause harm. Patients showed poor perceived control and a strong need for approval but received little advice from healthcare professionals. Preferences were for low intensity activities, on their own, in the home setting. Regression analysis revealed no significant factors related to the independent variables.

Conclusions

Frequently employed higher intensity, group exercise models do not address the motivational and behavioural concerns of cachectic cancer patients in this study. Developing exercise interventions which match perceived abilities and skills are required to address challenges of self-efficacy and perceived control identified. Greater engagement of health professionals with this group is required to explore potential benefits of exercise.

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KIAA1522 overexpression promotes tumorigenicity and metastasis of esophageal cancer cells through potentiating the ERK activity

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Volumetric modulated arc therapy for treatment of solid tumors: current insights

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Incidence and 5-year survival rate for head and neck cancers in Grenada compared to the African American population over the period 1991–2010

Abstract

Very little data exist on the incidence and burden of cancer in the individual Caribbean countries. Some data are available for larger areas, reported under a bigger geographical region; Latin America and the Caribbean, but many of the individual countries are not included. One of the main reasons is a lack of official cancer registries. Data are usually collected from hospital records or private physician records, and since it is not in an official registry, these data are not always accessible for inclusion in databases such as SEER and GLOBOCAN. Grenada is one of the countries that currently does not have a registry. Our aim is to report on the incidence for head and neck cancer with subcategories; hypopharynx, oropharynx, oral cavity, salivary glands, and larynx from data collected by the sole ear nose and throat specialist over a 20-year period. The age adjusted incidence per 100,000 for these cancers, whether combined or individually, is lower than that of similar populations. The incidence in males is only slightly higher than those reported in some parts of Africa. In females, only Eastern Africa is reported to have a lower incidence than that found in our study. While the incidence of oral cancers is lower than that of African Americans, the survival rate is comparable. Socioeconomic status, lack of infrastructure, and advanced stage at diagnosis appear to be closely related to the survival rate. Incidence reports suggest that incidence of head and neck cancers in individuals of African descent is lower than other populations. It is therefore not surprising that the incidence in Grenada is relatively low, although the incidence may be underestimated.

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Conception and Management of a Poorly Understood Spectrum of Dermatologic Neoplasms: Atypical Fibroxanthoma, Pleomorphic Dermal Sarcoma, and Undifferentiated Pleomorphic Sarcoma

Opinion Statement

Atypical fibroxanthoma (AFX) and pleomorphic dermal sarcoma (PDS) tumors share many clinical, etiologic, and histologic features and likely represent components of a tumor spectrum. In dermatologic oncology, differentiating between AFX and PDS is pivotal as tumors with histological features consistent with PDS are more likely to behave in a clinically aggressive manner. Importantly, the term "pleomorphic dermal sarcoma" (PDS) is a more appropriate designation than "undifferentiated pleomorphic sarcoma" (UPS) for describing deeper, more aggressive, histologically high-grade cutaneous tumors that otherwise resemble AFX. Surgery remains the gold standard for treatment. In the setting of AFX, excision with the Mohs micrographic technique appears to offer superior tumor control rates while maintaining greater tissue preservation over wide local excision and should be considered first line. In the setting of PDS, optimal management is less clear given the paucity of available data. However, due to its greater propensity to recur and metastasize, extirpation with complete tumor margin control appears paramount. The roles of imaging and SLNB in management and clinical outcomes of AFX and PDS are unclear given the lack of available data. In reality, these tools are unlikely to be helpful in most cases of AFX. However, in the setting of PDS, emerging literature indicates that these tumors are inherently higher risk, and thus, imaging and SLNB may be helpful in select cases. Additionally, radiation therapy may be of adjuvant benefit for these tumors when clear surgical margins cannot be obtained. While traditional chemotherapy has been largely ineffectual, the recent discovery of key oncogenetic mutations has allowed for the identification of several potential molecular drug targets that may have a therapeutic role with future study. In the unfortunate setting of metastatic disease, a multidisciplinary approach is optimal. Further studies are needed to establish definitive conclusions regarding risk stratification and best management practices.

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Targeted next-generation sequencing identifies clinically relevant mutations in patients with chronic neutrophilic leukemia at diagnosis and blast crisis

Abstract

Purpose

Chronic neutrophilic leukemia is a rare form of myeloproliferative neoplasm characterized by mature neutrophil hyperleukocytosis. The majority of patients harbor somatic mutations of CSF3R gene and are potentially amenable to targeted therapy with JAK inhibitors. The incidence and clinical significance of additional mutations requires clarification.

Materials and methods

A next-generation sequencing approach for myeloid malignancy-associated mutations was applied to diagnostic and matched blast crisis samples from four chronic neutrophilic leukemia patients.

Results

Next-generation sequencing confirmed the CSF3R T618I in all patients with identification of concurrent SRSF2, SETBP1, NRAS and CBL mutations at diagnosis. At blast crisis, clonal evolution was evidenced by an increased CSF3R T618I allele frequency and by loss or acquisition of CBL and NRAS mutations.

Conclusion

The diagnostic utility of a targeted next-generation sequencing approach was clearly demonstrated with the identification of additional mutations providing the potential for therapeutic stratification of chronic neutrophilic leukemia patients.

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MiR-15a/16 deficiency enhances anti-tumor immunity of glioma-infiltrating CD8+ T cells through targeting mTOR

Abstract

MiR-15a/16, a miRNA cluster located at chromosome 13q14, has been reported to act as an immune regulator in inflammatory disorders besides its aberrant expression in cancers. However, little is known about its regulation in tumor-infiltrating immune cells. In this study, using an orthotropic GL261 mouse glioma model, we found that miR-15a/16 deficiency in host inhibited tumor growth and prolonged mice survival, which might be associated with the accumulation of tumor-infiltrating CD8+ T cells. More importantly, tumor-infiltrating CD8+ T cells without miR-15a/16 showed lower expression of PD-1, Tim-3 and LAG-3, and stronger secretion of IFN-γ, IL-2 and TNF-α than WT tumor-infiltrating CD8+ T cells. Also, our in vitro experiments further confirmed that miR-15a/16^-/- CD8+ T displayed higher active phenotypes, more cytokines secretion and faster expansion, compared with WT CD8+ T cells. Mechanismly, mTOR was identified as a target gene of miR-15a/16 to negatively regulate the activation of CD8+ T cells. Taken together, these data suggest that miR-15a/16 deficiency resists the exhaustion and maintains the activation of glioma-infiltrating CD8+ T cells to alleviate glioma progression via targeting mTOR. Our findings provide evidence for the potential immunotherapy through targeting miR-15a/16 in tumor-infiltrating immune cells. This article is protected by copyright. All rights reserved.

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