Walter M. Stadler

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A precise contrast agent (CA) arterial input function (AIF) is important for accurate quantitative analysis of dynamic contrast-enhanced (DCE)-MRI. This paper proposes a method to estimate the AIF using the dynamic data from multiple reference tissues, assuming that their AIFs have the same shape, with a possible difference in bolus arrival time. By(More)
PURPOSE Given their accessibility, surrogate tissues, such as peripheral blood mononuclear cells (PBMC), may provide potential predictive biomarkers in clinical pharmacogenomic studies. In leukemias and lymphomas, the prognostic value of peripheral blast expression profiles is clear; however, it is unclear whether circulating mononuclear cells of patients(More)
Expression profiling has demonstrated that transcriptomes of primary malignancies differ from those in normal tissue. It is unknown, however, whether there exist " surrogate " transcriptional markers in peripheral blood mononuclear cells (PBMCs) of patients with solid tumors. We identified transcripts expressed differentially between PBMCs from renal cell(More)
In dynamic contrast-enhanced MRI (DCE-MRI) studies, an accurate knowledge of the arterial contrast agent concentration as a function of time is crucial for the estimation of kinetic parameters. In this work, a novel method for estimating the arterial input function (AIF) based on the contrast agent concentration-vs.-time curves in two different reference(More)
OBJECTIVE Uncovering the dominant molecular deregulation among the multitude of pathways implicated in aggressive prostate cancer is essential to intelligently developing targeted therapies. Paradoxically, published prostate cancer gene expression signatures of poor prognosis share little overlap and thus do not reveal shared mechanisms. The authors(More)
MicroRNAs, small non-coding RNAs, may act as tumor suppressors or oncogenes, and each regulate their own transcription and that of hundreds of genes, often in a tissue-dependent manner. This creates a tightly interwoven network regulating and underlying oncogenesis and cancer biology. Although protein-coding gene signatures and single protein pathway(More)
Many current therapies for metastatic castration-resistant prostate cancer (mCRPC) are aimed at AR signaling; however, resistance to these therapies is inevitable. To personalize CRPC therapy in an individual with clinical progression despite maximal AR signaling blockade, it is important to characterize the status of AR activity within their cancer.(More)
The mTOR (mammalian target of rapamycin) inhibitor, everolimus, affects tumor growth by targeting cellular metabolic proliferation pathways and delays renal cell carcinoma (RCC) progression. Preclinical evidence suggests that baseline elevated tumor glucose metabolism as quantified by FDG-PET ([(18)F] fluorodeoxy-glucose positron emission tomography) may(More)
The CDKN2 (MISI) gene is located at 9p21; its product, p 16. inhibits the cyclin D/CDK4 complex that phosphorylates pRb, thus negatively regulating cell cycle progression IM. CDKN2 mutations are more common in cultured human uroepithelial cells (HUC) than in uncultured bladder cancers. We examined the status of CDKN2/pl6 in early and late passage (P)(More)
Bone metastases of 16 prostate cancer patients were scanned twice 1 week apart by dynamic contrast enhanced (DCE)-MRI at 2-s resolution using a two-dimensional gradient-echo pulse sequence. With a multiple reference tissue method (MRTM), the local tissue arterial input function (AIF) was estimated using the contrast agent enhancement data from tumor(More)