Neuronal apoptosis can be prevented by the combined therapy with melatonin and hypothermia in a neonatal rat model of hypoxic-ischemic encephalopathy.

Introduction: Birth hypoxia is a leading cause of perinatal mortality and neurological morbidity, resulting in central nervous system injury. Cerebral hypoxia and ischemia can produce a severe brain damage following a typical pattern, defined by selective vulnerability of the brain regions. The neonates are most prone to hypoxic-ischemic injuries due to the lack of efficient antioxidant defense.

Targeting TRAIL death receptor 4 with trivalent DR4 Atrimer complexes.

TRAIL is a trimeric protein that potently induces apoptosis in cancer cells by binding to the trimeric death receptors (DR4 or DR5). Death receptors are attractive therapeutic targets through both the recombinant TRAIL ligand as well as receptor agonist monoclonal antibodies. Although efficacy of the ligand is hampered by its short half-life, agonistic antibodies have a much longer half-life and have shown some clinical efficacy as antitumor agents.

Brain metastases secondary to breast cancer: symptoms, prognosis and evolution.

Aims And Background: Brain metastases confer a worse prognosis to breast cancer because they determine a severe increase in mortality. The aim of this study was to identify the early symptoms in patients with brain metastases after breast cancer treatment and to evaluate the median survival rate in women with single and operable brain lesions.

Patients And Methods: We examined 43 patients with brain metastases secondary to breast cancer treated in the Oncological Institute Prof I Chiricuţă, Cluj-Napoca, during the period 2000-2006.

Immune modulation by melanoma and ovarian tumor cells through expression of the immunosuppressive molecule CD200.

Background And Objective: Immune escape by tumors can occur by multiple mechanisms, each a significant barrier to immunotherapy. We previously demonstrated that upregulation of the immunosuppressive molecule CD200 on chronic lymphocytic leukemia cells inhibits Th1 cytokine production required for an effective cytotoxic T cell response. CD200 expression on human tumor cells in animal models prevents human lymphocytes from rejecting the tumor; treatment with an antagonistic anti-CD200 antibody restored lymphocyte-mediated tumor growth inhibition.