MIPS Molecular Imaging Program at Stanford

2013 MIPS Molecular Imaging Seminar Series

Calendars and Scheduling

Use the links below to view event calendars and the availability and schedules of rooms.

 
Seminar 5:30 − 6:15 pm
Discussion 6:15 − 6:30 pm
Reception 6:30 − 7:00 pm
Li Ka Shing Center, Rm. LK130
Stanford University Campus

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Current Molecular Imaging Seminar - 2013
Archived Molecular Imaging Seminars
2012 | 2011 | 2010 | 2009 | 2008 | 2007 | 2006 | 2005 | 2003-2004
Invited Speakers
January 10, 2013Cancelled
February 7, 2013Anna Wu, PhD - Webcast Not Available
March 7, 2013Henryk Barthel, MD, PhD - View Webcast
March 12, 2013Christropher McCurdy, Ph.D., R.Ph. - View Webcast
April 3, 2013Marion Hendriks-de Jong, PhD - View Webcast
April 4, 2013Robert J. Gillies, PhD - View Webcast
May 2, 2013Jamey Weichert, PhD - Webcast Not Available
June 2013 (no seminar)Summer Hiatus
July 2013 (no seminar)Summer Hiatus
August 2013 (no seminar)Summer Hiatus
September 5, 2013Jan Grimm, MD, PhD
October 3, 2013Anna Moore, PhD
November 7, 2013TBA
December 5, 2013David Sosnovik

 

Jan 5, 2013

Cancelled
Feb 7, 2013
Munzer

Photo of Anna Wu, PhD
Anna Wu, PhD
Prof. and Vice Chair, Mole & Med Pharm, UCLA
CNSI, UCLA
Engineered Antibodies for immunoPET imaging in Oncology and Beyond

Abstract
The accelerating shift to molecularly targeted therapeutics requires parallel advances in molecular diagnostics, in vivo as well as in vitro. Antibodies provide the basis of a class of molecular imaging agents for phenotypic assessment of cells and tissues in living organisms, including patients. Engineered antibody fragments (such as minibodies and cys-diabodies) preserve high affinity binding, maintain efficient targeting in vivo, and clear promptly from the circulation, making them ideal for rapid, same-day imaging. When labeled with positron-emitting radionuclides (such as I-124, Zr-89, Cu-64, F-18), engineered antibody fragments can be employed for high resolution, sensitive, quantitative imaging by PET (positron emission tomography). ImmunoPET can also be applied to detection of immune cell subsets (such as CD8 T cells or macrophages), for monitoring immune responses following cancer therapy. ImmunoPET provides a broad approach for imaging cell surface phenotype in vivo, and stands to play an expanding role in the detection and management of cancer and other diseases, for assessing key factors such as target expression, internalization and catabolism, and response to therapy and mechanism of response.
Mar 7, 2013
Munzer

Henryk Barthel, MD, PhD
Assistant Medical Director Neuro-PET and PET-MRI
Nuclear Medicine
University Hospital Leipzig, Germany
View Webcast
Strategies for PET-MR imaging of cell-based and other therapies in stroke and dementia

Abstract
With the recent introduction of integrated PET/MR imaging systems it is possible for the first time to investigate functional and morphological changes or different functional processes at the same time in the living human subject. This new opportunity provides a further stimulus to our ongoing imaging research program which is aimed at improving early diagnosis and therapy monitoring in Alzheimer's disease (AD) and acute ischemic stroke. With regard to AD, this talk will provide an insight into new techniques to image beta-amyloid and tau, the histopathological hallmarks to the disease. It will be discussed as to what extent these new opportunities help us to monitor the effect of cell-based and other therapies. Concerning acute ischemic stroke, our concepts to improve early diagnosis by means of simultaneous PET/MRI will be presented. Further, examples of our research to apply stroke imaging in the development of cell-based and other stroke therapies in a translational concept will be discussed. In summary, it will be concluded that cell-based therapies have a great potential to overcome the therapeutic dilemma in AD and stroke, and that PET/MRI plays an important role in the search for respective treatments.
Mar 12, 2013
Clark Auditorium

Christropher McCurdy, Ph.D., R.Ph.
DAC Distinguished Teaching Scholar
Associate Professor of Medicinal Chemistry and Pharmacology
Department of Medicinal Chemistry
School of Pharmacy
The University of Mississippi
View Webcast
The Role of Sigma-1 Receptors In Cocaine Self-Administration

Abstract
Sigma receptor antagonists have been demonstrated in the literature to attenuate many of the effects of cocaine. Recently the sigma receptor antagonist, rimcazole, was demonstrated to selectively block cocaine self-administration and attenuate cocaine-induced dopamine elevations in the shell of the nucleus accumbens. Interestingly, rimcazole also has effects on the dopamine system that appear critical for its effects on cocaine self-administration. Highly selective sigma receptor ligands alone are not able to attenuate cocaine self-administration. Standard dopamine uptake inhibitors dosedependently shift the cocaine dose-effect curve to the left. In contrast, combinations of dopamine uptake inhibitors and sigma receptor antagonists produced dose-related decreases in cocaine selfadministration without effects on food-maintained responding. Selective sigma receptor antagonists, developed in our lab, were utilized in these studies and will be discussed. Furthermore, the identification of a novel, dual acting sigma/DAT ligand will be discussed that blocks cocaine selfadministration without effecting food intake. This may indicate a potential avenue to develop PET imaging and therapeutic approaches to monitor and treat cocaine abuse respectively.
Apr 3, 2013
Alway M114

Marion Hendriks-de Jong, PhD
Prof. Nuclear Biology
Dept. Nuclear Medicine
Erasmus MC, Rotterdam
View Webcast
Radiopeptides for tumor imaging and radionuclide therapy

Abstract
Selective receptor-targeting radiopeptides have emerged as an important class of radiopharmaceuticals for molecular imaging and therapy of tumours that overexpress peptide receptors on the cell membrane. This presentation will give an overview of the research program of the preclinical and clinical groups of the department of Nuclear Medicin Erasmus MC, with a focus on peptide receptor-targeted imaging (PRI) and peptide receptor-targeted radionuclide therapy (PRRT) of receptor-positive cancers with radiolabelled peptides.

In the clinic we imaged over 5000 patients using radiolabelled somatostatin analogues, whereas over 1500 treatments were given. Our efforts now concentrate on widening the therapeutic window by increasing the tumour radiation dose and/or decreasing the dose to the normal, healthy, organs. To enlarge the panel of tumours to be imaged and treated, we also design and evaluate analogues of other peptides, including bombesin, CCK, and neurotensin analogues, that bind to their receptors in a variety of different tumours.
Apr 4, 2013
Munzer

Photo of Robert Gillies, PhD
Robert J. Gillies, PhD
Vice-chair of Rad & Dir, Experimental Imaging Program
View Webcast
Causes and Consequences of Tumor Heterogeneity

Abstract
Malignant cancers, whether inherited or sporadic, can be characterized by genetic instability within highly selective local microenvironments. This combination promotes somatic evolution. The existence of a harsh environment and genotypic heterogeneity can be formally combined in "evolutionary game theory", which is summarized in a basic equation governing evolutionary rate: ∂µ/∂t = σ2(∂G/∂µ) where ∂µ/∂t is the evolutionary rate at which the strategy (phenotype) (µ) of a population varies with time (t). σ represents the heritable phenotypic diversity. ∂G/∂µ is the fitness function, and a harsh environment generally produces a high slope, meaning that even small changes in phenotype can cause large variations in fitness. Hypoxia and acidosis are commonly encountered during the process of carcinogenesis. These microenvironmental forces are not only highly selective, but also induce genetic instability through increased genotoxicity, decreased repair and chromosomal rearrangements. As a result of these process that occur throughout carcinogenesis, malignant cancers contain dynamically evolving clades of cells living in distinct microhabitats that virtually ensure the emergence of therapy-resistant populations. Cytotoxic cancer therapies also impose intense evolutionary selection pressures on the surviving cells and thus, increase the evolutionary rate. Intratumoral hypoxia, acidosis and reactive oxygen species (ROS), are strong selective pressures, leading to common metabolic phenotypes of cancers. Hypoxia is observed in in-situ cancers and in later disease, as a consequence of poor perfusion. Hypoxia leads to genomic instability via multiple mechanisms. Acidosis in tumors is caused through a combination of increased metabolism and poor perfusion clastogenic. These microenvironmental forces can work alone, or in concert with heritable mutations, that either inhibit the DDR machinery directly, reduce apoptosis, or exacerbate the hostile microenvironment through promotion of hyperplasia.

Relevance to Imaging

Induction of genomic alterations and localized selection by heritable and/or environmental factors will result in phenotypic heterogeneity. Heterogeneity can be identified with imaging, by non-­-uniform patterns of enhancement with contrast, diffusion MRI, or CT attenuation and may be associated with poor outcome. Each tumor is an ecosystem inhabited by physical factors, physiological and metabolic factors, normal cells, inflammatory cells, and the actual populations of tumor cells. An important physiological factor is tumor perfusion, which is a measureable quantity with dynamic contrast enhanced (DCE) MRI. Quantified heterogeneity represents different "niches" within tumors and hence clades. It is also a powerfully negative prognostic factor. It is our hypothesis, then, that phenotypic heterogeneity of cancers presages emergence of resistant populations and that this may be observable through appropriate analyses of MR images. We further hypothesize that such analyses should be able to inform design of therapeutic approaches to better manage cancers.
May 2, 2013
Munzer

Jamey Weichert, PhD
Assoc Prof (Tenure)
Dir, Contrast Agent Laboratory
U Wisconsin
Molecular Diapeutics-Phospholipid Ether Based Targeting Approaches for Broad Spectrum Cancer Detection and Treatment

Abstract
It was reported by Snyder and colleagues in 1969 that tumor cells contained an overabundance of phospholipid ethers (PLE) relative to normal cells. This was thought to be due to under expression of an alkyl cleavage enzyme. In an attempt to exploit this difference we designed and synthesized a series of radioiodinated phospholipid ether analogs as tumor imaging agents in the early 1990's. Some of these showed tumor avidity in vivo and eventually over 30 analogs were synthesized, radioiodinated and evaluated for their tumor selectivity (Pinchuk et al, J Med Chem. 49:2155-2165 (2006)). One of these PLE analogs, NM404 (18-(4-iodophenyl)-octadecylphosphocholine), has displayed remarkable in vivo tumor avidity in over 60 in vivo human xenograft and spontaneous primary and metastatic rodent tumor models. Unlike, FDG, NM404 is not taken up by inflammatory or premalignant (mammary and colon adenomas) lesions. Recent cellular confocal microscopy studies with a fluorescent bodipy analog of NM404 have shown that the agent is taken up preferentially into cancer and cancer (glioma) stem cells over normal cells in co-cultured skin fibroblasts and melanoma cells. Tumor cell uptake occurs via surface membrane lipid rafts and once inside the cell enters the PIP3 kinase/AKT pathway. Lipid rafts are known to be more prevalent in malignant cells versus normal cells. A near infrared version of the agent (CLR1502), also exhibits similar tumor uptake and retention properties and is being evaluated in surgical tumor margin illumination studies. Due to its unique prolonged tumor cell retention properties, this agent is being evaluated in radiotherapy indications. Preclinical single dose survival studies conducted with 131I-NM404 in eight mouse xenograft models (renal cell, melanoma, lung, prostate, breast, glioma, pancreatic, and ovarian) showed significant prolongation of life ranging from 40-400 percent relative to saline treated control cohorts. Moreover, the therapy version (131I) of this agent is currently being clinical evaluated in a Phase 1b MTD safety trial in 8 human cancer types.
Sept 5, 2013
Munzer

Jan Grimm, MD, PhD
Sloan-Kettering Institute
TBA

Abstract
TBA
Oct 3, 2013
Munzer

Anna Moore, Ph.D.
Assoc Prof, Rad
Director, Molecular Imaging Laboratory, Mass Gen
Mass Gen
TBA

Abstract
TBA
Nov 1, 2013

TBA

Abstract
TBA
Dec 5, 2013
Munzer

David Sosnovik
Harvard University
Title TBA

Abstract
TBA

Sponsored by: Molecular Imaging Program at Stanford (MIPS) (mips.stanford.edu);
Host: Director, Sanjiv Sam Gambhir, MD, PhD (sgambhir@stanford.edu)

Current Seminar - 2013
Archived Molecular Seminar Series - 2012 | 2011 | 2010 | 2009 | 2008 | 2007 | 2006 | 2005 | 2003-2004

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