Conferences archive > 2011 > SPEAKERS & ABSTRACTS

William Weiss

ENG. William A. Weiss, MD, PhD is Professor of Neurology, Pediatrics, and Neurological Surgery, interim director of Child Neurology at UCSF, and scientific director of the Pediatrics Malignancies Program in UCSF's Helen Diller Family Comprehensive Cancer Center.  His lab has developed mouse models for glioma, medulloblastoma and neuroblastoma, based on recapitulating cardinal genetic abnormalities in transgenic mice, and uses these animals to develop preclinical therapeutics focused on EGFR/PI3K/mTOR and myc pathways. His lab is actively studying and characterizing human cancer stem cells, and is deriving and treating new animal models for cancer based on implanting human cancer stem cells in mice.

ITA. William A. Weiss, titolare di una laurea e un dottorato in medicina, è Professore di Neurologia, Pediatria e Chirurgia Neurologica e direttore ad interim di neurologia infantile all'Università della California a San Francisco, e direttore scientifico del programma sui tumori maligni pediatrici nel Centro Onnicomprensivo per il Cancro della Famiglia Helen Diller presso la stessa università. Nel suo laboratorio sono stati sviluppati modelli su topi per i gliomi, i medulloblastomi e i neuroblastomi, basati sulla ricapitolazione di gravi anomalie genetiche nei topi transgenici, sui quali sono state sviluppate terapie precliniche focalizzate sulle vie EGFR/PI3K/mTOR e myc. Nel suo laboratorio si svolgono attivamente ricerche per studiare e caratterizzare le cellule staminali cancerose degli esseri umani e si sviluppano e curano modelli animali per il cancro impiantando nei topi cellule staminali cancerose di origine umana.

Anomalous brain development and stem cell involvement as potential contributors to cognitive decline in glioma Ã¢â‚¬â€œ AIRC LECTURE

Brain cancers are relatively rare, often lethal diseases, whose poor prognosis is mainly due to the localization in an organ, where surgery and therapies are frequently not an effective or feasible option. Among brain cancers, glioma is one of the most common diseases. All brain tumors, including gliomas, show profound effects on cognition, presumably affecting brain function through pressure on - or invasion of - normal structures. However, the cells that originate the diseases, and the mechanism that affect cognition, have not been identified yet. New data, obtained in my lab and labs of others, show that normal adult neural stem cells in mice are able to give rise to some types of gliomas. Surprisingly, while such stem cells normally give rise to both neurons and glial cells, we observed a progressive loss of normal neuronal development in the affected animals, accompanied by the expansion of a normally rare population of immature glial cells. These observations demonstrate that gliomas can arise from glial cells that acquire stem cell like features, and do so through disruption of normal development. Interestingly, these isolated glioma cells, which are similar to stem cells, were still sensitive to pharmacological intervention. The good news is that we were able to treat the mice and restore normal brain development, through the use of inhibitors of a prominent molecular pathway (the so called MAP kinase pathway), known to be involved in this pathological process. This is relevant to human glioma, as we showed that human glioma cells treated with the same inhibitors demonstrated an analogous reduction in proliferation and increased normal differentiation. These findings have broad relevance to both cancer research and stem cell biology, as they provide a model explaining how stem cells may give origin to cancer and at the same time disrupt normal brain development. That brain tumors disrupt normal neural development may in-part underlie the cognitive difficulties observed in patients with brain tumors.

torna top