RESUMO
Primary cardiac lymphoma (PCL) is among the rarest heart neoplasms. Its estimated incidence is about 1%-2% among primary cardiac tumor and 0.5% of extranodal lymphoma. It usually causes heart failure, pericardial effusion, tamponade, and arrhythmias. Prognosis is poor; treatment is combined medical and surgical. We described the case of a 62-year-old male with PLC that presented with syncope and cardiac tamponade, submitted to R-CHOP therapy because of failure of surgery. Clinical state is stable 3 months after diagnosis and first chemotherapy cycle.
RESUMO
AIM: We hypothesized that radiation-induced fibrosis was, in part, a result of altered signal transduction that directly modulates integrin expression and may indirectly affect the extracellular matrix (ECM). Major focus was given on protein kinase C (pKC). MATERIALS AND METHODS: Rat FRTL-5 and primary thyroid cells were exposed to proton radiation (5 and 10 Gy). Hours to days after exposure, a series of assays were performed. In addition, the neck region of Lewis rats was proton-irradiated to 40 Gy (5 Gy/day or 10 Gy/day). At 11 weeks after exposure, thyroid tissue was evaluated. RESULTS: Accumulation of ECM in irradiated FRTL-5 and primary thyroid cells was coincident with loss of tissue organization and follicularization at one or more doses and time points. Several pKC isoforms increased post-irradiation, which coincided with modulated integrin expression; fibronectin, laminin and collagen were also altered (p<0.05 vs. 0 Gy). Modulation of thyroid cells in culture with 12-O-tetradecanoylphorbol-13-acetate (TPA)±calphostin C supported a direct role of pKC in these altered properties. Thyroid tissue from irradiated rats had significantly more fibrotic lesions and increases in several pKC isoforms, integrins and fibronectin compared to 0-Gy (p<0.05). CONCLUSION: pKC is a likely contributor to alteration of key players associated with radiation-induced fibrosis.
Assuntos
Regulação da Expressão Gênica , Integrinas/genética , Proteína Quinase C/metabolismo , Glândula Tireoide/metabolismo , Glândula Tireoide/patologia , Animais , Moléculas de Adesão Celular/genética , Moléculas de Adesão Celular/metabolismo , Técnicas de Cultura de Células , Linhagem Celular , Ativação Enzimática/efeitos da radiação , Matriz Extracelular/metabolismo , Feminino , Fibrose , Regulação da Expressão Gênica/efeitos da radiação , Imuno-Histoquímica , Isoenzimas , Modelos Animais , Fótons/efeitos adversos , Proteína Quinase C/genética , Ratos , Glândula Tireoide/efeitos da radiaçãoRESUMO
PURPOSE: This work investigates the hypothesis that genetic background plays a significant role in the signalling mechanisms underlying induction and perpetuation of genomic instability following radiation exposure. MATERIALS AND METHODS: Bone marrow from two strains of mice (CBA and C57) were exposed to a range of X-ray doses (0, 0.01, 0.1, 1 and 3 Gy). Different cellular signalling endpoints: Apoptosis, cytokine levels and calcium flux, were evaluated at 2 h, 24 h and 7 d post-irradiation to assess immediate and delayed effects. RESULTS: In CBA (radiosensitive) elevated apoptosis levels were observed at 24 h post X-irradiation, and transforming growth factor-ß (TGF-ß) levels which increased with time and dose. C57 showed a higher background level of apoptosis, and sustained apoptotic levels 7 days after radiation exposure. Levels of tumor necrosis factor-α (TNF-α were increased in C57 at day 7 for higher X-ray doses. TGF-ß levels were higher in CBA, whilst C57 exhibited a greater TNF-α response. Calcium flux was induced in reporter cells on exposure to conditioned media from both strains. CONCLUSIONS: These results show genetic and dose specific differences in radiation-induced signalling in the initiation and perpetuation of the instability process, which have potential implications on evaluation of non-targeted effects in radiation risk assessment.