RESUMO
Stimulation of opioid receptors is widely used for relieving cancer pain in patients with advanced cancer. The expression of tissue opioid receptors varies depending on the types of cancer and it is regulated by several factors. This review provides a focused overview of the current evidence for the role of opioid receptors in modulating cancer progression, a discussion of the proposed underlying mechanisms and the pharmacological activity of opioid agonists and antagonists. Conflicting evidence from preclinical and clinical studies suggests the possible involvement of opioid receptor agonists in both the development and suppression of human cancer. Some retrospective clinical studies also show a possible detrimental effect on long-term patient outcomes. Among the opioid receptor agonists, morphine has been extensively studied in various cancer types. Moreover, various pathological processes of human cancer are affected by opioid receptor agonists, such as tumour growth, angiogenesis and immunosuppression. These findings highlight the functional value of opioid receptors in human cancer, and a potential double role of opioid receptor agonists and antagonists in human cancer treatment.
Assuntos
Analgésicos Opioides/uso terapêutico , Antineoplásicos/uso terapêutico , Dor do Câncer/tratamento farmacológico , Antagonistas de Entorpecentes/uso terapêutico , Neoplasias/tratamento farmacológico , Receptores Opioides/efeitos dos fármacos , Analgésicos Opioides/efeitos adversos , Animais , Antineoplásicos/efeitos adversos , Dor do Câncer/metabolismo , Dor do Câncer/fisiopatologia , Progressão da Doença , Humanos , Antagonistas de Entorpecentes/efeitos adversos , Neoplasias/metabolismo , Receptores Opioides/metabolismo , Transdução de SinaisRESUMO
Tumor heterogeneity strongly affects the molecular mechanisms driving resistance to hormonal therapies in castration-resistant prostate cancer. Since the current use of available treatments can be optimized on the basis of the molecular profile of tumor, the present review focuses on genetic biomarkers in prostate cancer and their application to a personalized treatment.
Assuntos
Biomarcadores Farmacológicos/análise , Biomarcadores Tumorais/análise , Resistencia a Medicamentos Antineoplásicos , Farmacogenética , Neoplasias de Próstata Resistentes à Castração/diagnóstico , Neoplasias de Próstata Resistentes à Castração/terapia , Androgênios/metabolismo , Androgênios/farmacologia , Antineoplásicos Hormonais/uso terapêutico , Resistencia a Medicamentos Antineoplásicos/efeitos dos fármacos , Resistencia a Medicamentos Antineoplásicos/genética , Humanos , Masculino , Prognóstico , Neoplasias de Próstata Resistentes à Castração/genética , Neoplasias de Próstata Resistentes à Castração/patologia , Receptores Androgênicos/genética , Receptores Androgênicos/metabolismo , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/genéticaRESUMO
Various procedures involving stimulations of facial regions are known to induce so-called trigemino-cardiac reflexes that entail a decrease of heart rate and blood pressure. We here report the effects of a specific stimulation that consists in a submaximal passive mandibular extension obtained by means of a dilatator applied for 10 minutes between the upper and lower incisor teeth, associated with partial active masticatory movements. Blood pressure and heart rate were determined in 18 young normal volunteers by Omron M4, before (20 minutes), during (10 minutes) and after mandibular extension (80 minutes) and under control conditions (same overall duration without stimulation). While control values remained stable, mandibular extension was followed by a progressive decline of both blood pressure (up to about 12/11 mmHg) and heart rate (up to about 13 bpm), statistically confirmed by ANOVA both on absolute values and on changes from basal values. The decline of systolic blood pressure and heart rate significantly correlated with basal values. The present findings indicate that submaximal opening of the mouth, associated to partial masticatory movements, induces a prolonged reduction of blood pressure and heart rate in normotensive volunteers.
