Improving the quality of life in a breast cancer patient and caregiver: Protocol for the application of the integrative medical service model.

BACKGROUND: Patients with chronic diseases require ongoing treatment, and caregivers face financial burdens as well as psychological and physical difficulties. However, the current healthcare system does not provide adequate systems or services to address the difficulties that patients and caregivers face. PURPOSE: The purpose of this study was to conduct an observational case study in order to evaluate and improve the application of an integrative healthcare service model developed for distress management and improved quality of life in breast cancer (BC) patients and caregivers. METHOD: The integrative healthcare service model was intensively applied to a patient-caregiver pair in this observational study. This was followed by gathering feedback from participants and experts, as well as reflecting on the content of the feedback in order to improve the model further. RESULTS: This study will then modify and improve the program with feedback and provide integrative medical services to a BC patient and caregiver. CONCLUSION: This study used the BC patients' pain management and quality of life enhancement model, aiming to provide basic data for the establishment of a healthcare service system for patients suffering from chronic pain due to diseases such as BC by systematically integrating previously applied interventions into the current healthcare system and soliciting feedback from patients and caregivers.

Normal Physiologic and Benign Foci with F-18 FDG Avidity on PET/CT in Patients with Breast Cancer.

PURPOSE: The aim of this study was to evaluate the physiologic and benign F-18 fluorodeoxyglucose (FDG) avid foci in patients with breast cancer. METHODS: On 309 F-18 FDG PET/CT scans of 241 women with breast cancer, the hypermetabolic lesions compared with the surrounding normal region were evaluated retrospectively. Available reports of other relevant radiological imaging, medical records, and follow-up PET/CT were reviewed for explanations of the abnormal uptake. RESULTS: Among the 70 physiologic foci, muscular uptake of the lower neck following the surgical and/or radiation therapy of ipsilateral breast (29%), hypermetabolic ovaries (16%) and uterine (10%) uptake during the ovulatory and menstrual phases during the normal menstrual cycle were identified, and also hypermetabolic brown fat in cold-induced thermogenesis (7%), non-specific bowel uptake (35%) were observed. Among the 147 benign lesions, sequelae of the chest wall and breasts following surgical and/or radiation therapy, were often observed (27%). Hypermetabolic thyroid glands were noted as adenomas and chronic thyroiditis (18%). Reactive hyperplasia of cervical or mediastinal lymph nodes (32%), degenerative osteoarthritis and healed fractures (15%), hypermetabolic benign lung lesions (6%) were observed. CONCLUSION: Altered physiologic and benign F-18 FDG uptake in the lower cervical muscle and chest wall following ipsilateral breast surgery or radiotherapy were common, and also normal physiologic uptake in ovary and uterus, brown fat, thyroid were considered as predominant findings in women patients with breast cancer. Knowledge of these findings might aid in the interpretation of FDG PET/CT in patients with breast cancer.

KAI1/CD82 decreases Rac1 expression and cell proliferation through PI3K/Akt/mTOR pathway in H1299 lung carcinoma cells.

Although the KAI1/CD82 protein has been reported to inhibit cell metastasis in many studies, its mechanism of action has not yet been fully elucidated. In the present study, we investigated the possible effects of KAI1/CD82 on the metastatic phenotype in H1299 lung carcinoma cells. These studies were based on the pivotal role that the acquisition of motile phenotype plays on the initial steps of metastasis. KAI1/CD82-mediated morphological changes were observed using phase contrast microscopy. We report here, that a KAI1/CD82-induced phenotypic change was involved in the decrease of Rac1 expression and GTPase activity. However, we found that KAI1/CD82 did not regulate Rac1 mRNA levels. This suggests the existence of another regulatory mechanism of Rac1 protein maturation or activation. To identify the signaling pathway of Rac1 regulation, we investigated the PI3K/Akt/mTOR pathway, since the PI3K/Akt pathway regulates Rac1 activation and mTOR is known to play a regulatory role in protein translation. H1299/CD82-transfectants showed lower mTOR expression and cell growth than the control group. The data obtained from this study suggested that KAI1/CD82 decreased the metastatic phenotype of H1299 lung carcinoma cells by down-regulating Rac1 expression through the PI3K/Akt/mTOR pathway.