Hodgkinův lymfom (HL) je jedním z nejlépe léčitelných nádorových onemocnění. Moderními léčebnými strategiemi je vyléčeno 85–95 % pacientů. Do popředí začaly vystupovat pozdní následky léčby, především kardiotoxicita a sekundární malignity, na které 15 let po skončené terapii umírá více pacientů než na HL. Cílem výzkumu je najít takovou terapii, která by zajistila maximální kontrolu tumoru při minimalizaci akutní a dlouhodobé toxicity. German Hodgkin Study Group (GHSG) prokázala ve studii HD10 pro počáteční stadia HL možnost redukce chemoterapie i radioterapie, bez snížení účinnosti léčby. Studie pro pokročilá stadia HD9 prokázala výborné výsledky chemoterapie BEACOPP eskalovaný oproti konvenční terapii ABVD, ale s vyšší akutní a dlouhodobou toxicitou. Cílem dalších studií GHSG pro pokročilá stadia (HD12, HD15 a nyní aktivní studie HD18) je snížit intenzitu chemoterapie a posoudit, zda je nutná následná radioterapie. Pozitivní výsledky přináší hodnocení studie HD15, kde je testován význam FDG – PET při indikaci radioterapie. Současná studie HD18 sleduje pomocí FDG – PET i časnou odpověď tumoru po 2 cyklech chemoterapie. Další naděje jsou vkládány do nových biologických léků, které cílí přímo na receptory maligních buněk (monoklonální protilátky, inhibitory)., Hodgkin lymphoma (HL) is one of the best curable malignant diseases. Modern therapeutic strategies can cure 85–95 % of patients. Late effects have become increasingly important, especially cardiotoxicity and second tumors, that cause more deaths than HL 15 years after completion of treatment. The goal of the research is to find the therapy that maximizes tumor control and minimizes acute and longterm toxicity. German Hodgkin Study Group (GHSG) proved the possibility to reduce chemotherapy and radiotherapy without reducing the effectiveness of treatment in the HD10 study for early stages of HL. HD9 study for advanced stages demonstrated excellent results of BEACOPP escalated chemotherapy compared to the conventional therapy ABVD, but BEACOPP escalated induced higher acute and long-term toxicity. The goal of subsequent GHSG studies for advanced stages (HD12, HD15 and ongoing active HD18 study) is to reduce the intensity of chemotherapy and to evaluate the significance of subsequent radiotherapy. The HD15 study tests the significance of FDG-PET for indication of radiotherapy. Current HD18 study tests by FDG-PET the early response of tumor after 2 cycles of chemotherapy. New biological drugs that target receptors on malignant cells (monoclonal antibodies, inhibitors) are awaited., Jana Marková, and Lit.: 19
Perinatal hypoxic-ischemic insult (HII) is one of the main devastating causes of morbidity and mortality in newborns. HII induces brain injury which evolves to neurological sequelae later in life. Hypothermia is the only therapeutic approach available capable of diminishing brain impairment after HII. Finding a novel therapeutic method to reduce the severity of brain injury and its consequences is critical in neonatology. The present paper aimed to evaluate the effect of sulforaphane (SFN) pre-treatment on glucose metabolism, neurodegeneration, and functional outcome at the acute, sub-acute, and sub-chronic time intervals in the experimental model of perinatal hypoxic-ischemic insult in rats. To estimate the effect of SFN on brain glucose uptake we have performed 18F-deoxyglucose (FDG) μCT/PET. The activity of FDG was determined in the hippocampus and sensorimotor cortex. Neurodegeneration was assessed by histological analysis of Nissl-stained brain sections. To investigate functional outcomes a battery of behavioral tests was employed. We have shown that although SFN possesses a protective effect on glucose uptake in the ischemic hippocampus 24 h and 1 week after HII, no effect has been observed in the motor cortex. We have further shown that the ischemic hippocampal formation tends to be thinner in HIE and SFN treatment tends to reverse this pattern. We have observed subtle chronic movement deficit after HII detected by ladder rung walking test with no protective effect of SFN. SFN should be thus considered as a potent neuroprotective drug with the capability to interfere with pathophysiological processes triggered by perinatal hypoxicischemic insult.