Biomedical subjects

Ellsworth C Alvord

Publications and source records attributed to Ellsworth C Alvord.

6 recordsLinked to original sources

PubMed2007

The evolution of mathematical modeling of glioma proliferation and invasion.

Gliomas are well known for their potential for aggressive proliferation as well as their diffuse invasion of the normal-appearing parenchyma peripheral to the bulk lesion. This review presents a history of the use of mathematical modeling in the study of the proliferative-invasive growth of gliomas, illustrating the progress made in understanding the in vivo dynamics of invasion and proliferation of tumor cells. Mathematical modeling is based on a sequence of observation, speculation, development of hypotheses to be tested, and comparisons between theory and reality. These mathematical investigations, iteratively compared with experimental and clinical work, demonstrate the essential relationship between experimental and theoretical approaches. Together, these efforts have extended our knowledge and insight into in vivo brain tumor growth dynamics that should enhance current diagnoses and treatments.

Animals↗

PubMed2006

"Just look," he said.

Five personal examples are given illustrating the general principle that one can see if one looks or, conversely, that one cannot see anything that one believes not to exist.

Adamantinoma↗

PubMed2004

March 2004: a 24-year-old woman with bifrontal headaches.

A 24-year-old woman with bifrontal headaches was found to have a well-circumscribed lesion in the frontal lobe subcortical white matter. Microscopic examination showed clusters of small round cells separated by hypocellular neuropil-like areas, and a distinct border between tumor and surrounding white matter. Synaptophysin was diffusely positive in neuropil-like areas, and many tumor cells expressed NeuN. Based on these findings, a diagnosis of "extraventricular neurocytoma" was made. A double-label immunofluorescence stain was performed with NeuN and Ki-67 antibodies to determine if NeuN+ cells remained in the mitotic cycle. No colocalization of these markers was found, thus supporting the hypothesis that neuronal differentiation (as marked by NeuN expression) is incompatible with continued proliferation of tumor cells, as well as normal neurons.

Adult↗

PubMed2003

Virtual and real brain tumors: using mathematical modeling to quantify glioma growth and invasion.

Over the last 10 years increasingly complex mathematical models of cancerous growths have been developed, especially on solid tumors, in which growth primarily comes from cellular proliferation. The invasiveness of gliomas, however, requires a change in the concept to include cellular motility in addition to proliferative growth. In this article we review some of the recent developments in mathematical modeling of gliomas. We begin with a model of untreated gliomas and continue with models of polyclonal gliomas following chemotherapy or surgical resection. From relatively simple assumptions involving homogeneous brain tissue bounded by a few gross anatomical landmarks (ventricles and skull) the models have recently been expanded to include heterogeneous brain tissue with different motilities of glioma cells in grey and white matter on a geometrically complex brain domain, including sulcal boundaries, with a resolution of 1 mm(3) voxels. We conclude that the velocity of expansion is linear with time and varies about 10-fold, from about 4 mm/year for low-grade gliomas to about 3 mm/month for high-grade ones.

Brain Neoplasms↗

PubMed2003

Continuous growth of mean tumor diameter in a subset of grade II gliomas.

Serial magnetic resonance images of 27 patients with untreated World Health Organization grade II oligodendrogliomas or mixed gliomas were reviewed retrospectively to study the kinetics of tumor growth before anaplastic transformation. Analysis of the mean tumor diameters over time showed constant growth. Linear regression, using a mixed model, found an average slope of 4.1mm per year (95% confidence interval, 3.8-4.4mm/year). Untreated low-grade oligodendrogliomas or mixed gliomas grow continuously during their premalignant phase, and their pattern of growth can be predicted within a relatively narrow range. These findings could be of interest to optimize patients management and follow-up.

Adult↗

PubMed2002

Quantifying efficacy of chemotherapy of brain tumors with homogeneous and heterogeneous drug delivery.

Gliomas are diffuse and invasive brain tumors with the nefarious ability to evade even seemingly draconian treatment measures. Here we introduce a simple mathematical model for drug delivery of chemotherapeutic agents to treat such a tumor. The model predicts that heterogeneity in drug delivery related to variability in vascular density throughout the brain results in an apparent tumor reduction based on imaging studies despite continual spread beyond the resolution of the imaging modality. We discuss a clinical example for which the model-predicted scenario is relevant. The analysis and results suggest an explanation for the clinical problem of the long-standing confounding observation of shrinkage of the lesion in certain areas of the brain with continued growth in other areas.

Antineoplastic Agents↗