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1.
Br J Med Med Res ; 12(3)2016.
Artigo em Inglês | MEDLINE | ID: mdl-28217532

RESUMO

AIMS: In order to develop an application that addresses the most significant challenges facing IBD patients, this qualitative study explored the major hurdles of living with IBD, the information needs of IBD patients, and how application technology may be used to improve quality of life. METHODS: 15 IBD patients participated in two focus groups of 120 minutes each. Data collection was achieved by combining focus groups with surveys and direct observation of patients looking at a patient-engaged app (HealthPROMISE) screenshots. The survey elicited information on demographics, health literacy and quality of life through the Short IBD Questionnaire (SIBDQ). RESULTS: The needs of IBD patients center around communication as it relates to both patient information needs and navigating the social impacts of IBD on patients' lives: Communication Challenges regarding Information Needs: Patients cited a doctor-patient communication divide where there is a continued lack of goal setting when discussing treatments and a lack of objectivity in disease control. When objectively compared with the SIBDQ, nearly half of the patients in the focus groups wrongly estimated their IBD control.Communication Challenges regarding Social Impacts of IBD: Patients strongly felt that while IBD disrupts routines, adds significant stress, and contributes to a sense of isolation, the impact of these issues would be significantly alleviated through more conversation and better support.Implication for Mobile Health Solutions: Patients want a tool that improves tracking of symptoms, medication adherence and provides education. Physician feedback to patient input on an application is required for long-term sustainability. CONCLUSIONS: IBD patients need mobile health technologies that evaluate disease control and the goals of care. Patients feel an objective assessment of their disease control, goal setting and physician feedback will greatly enhance utilization of all mobile health applications.

2.
Oncotarget ; 2(12): 1109-26, 2011 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-22190384

RESUMO

Anaplastic thyroid carcinoma (ATC) is the most aggressive form of thyroid cancer, and often derives from pre-existing well-differentiated tumors. Despite a relatively low prevalence, it accounts for a disproportionate number of thyroid cancer-related deaths, due to its resistance to any therapeutic approach. Here we describe the first mouse model of ATC, obtained by combining in the mouse thyroid follicular cells two molecular hallmarks of human ATC: activation of PI3K (via Pten deletion) and inactivation of p53. By 9 months of age, over 75% of the compound mutant mice develop aggressive, undifferentiated thyroid tumors that evolve from pre-existing follicular hyperplasia and carcinoma. These tumors display all the features of their human counterpart, including pleomorphism, epithelial-mesenchymal transition, aneuploidy, local invasion, and distant metastases. Expression profiling of the murine ATCs reveals a significant overlap with genes found deregulated in human ATC, including genes involved in mitosis control. Furthermore, similar to the human tumors, [Pten, p53]thyr-/- tumors and cells are highly glycolytic and remarkably sensitive to glycolysis inhibitors, which synergize with standard chemotherapy. Taken together, our results show that combined PI3K activation and p53 loss faithfully reproduce the development of thyroid anaplastic carcinomas, and provide a compelling rationale for targeting glycolysis to increase chemotherapy response in ATC patients.


Assuntos
PTEN Fosfo-Hidrolase/metabolismo , Neoplasias da Glândula Tireoide/metabolismo , Neoplasias da Glândula Tireoide/patologia , Proteína Supressora de Tumor p53/metabolismo , Aneuploidia , Animais , Linhagem Celular Tumoral , Modelos Animais de Doenças , Transição Epitelial-Mesenquimal , Perfilação da Expressão Gênica , Glicólise , Humanos , Camundongos , Camundongos Transgênicos , Mitose/genética , Invasividade Neoplásica , Metástase Neoplásica , Fosfatidilinositol 3-Quinases/metabolismo , Carcinoma Anaplásico da Tireoide , Glândula Tireoide/metabolismo , Glândula Tireoide/patologia , Neoplasias da Glândula Tireoide/genética
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