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Characterization of the Inflammatory Microenvironment and Identification of Potential Therapeutic Targets in Wilms Tumors

Translational oncology, 2014-08, Vol.7 (4), p.484-492

2014

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Generation of a Wt1 conditional deletion, nuclear red fluorescent protein reporter allele in the mouse

Differentiation (London), 2024-07, Vol.138, p.100791, Article 100791

2024

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Identification of germline DICER1 mutations and loss of heterozygosity in familial Wilms tumor using whole genome sequencing

Journal of medical genetics, 2015-11, Vol.53 (6), p.385-388

2015

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Abstract 5047: Impact of kidney progenitor cell differentiation status in Wilms tumorigenesis

Cancer research (Chicago, Ill.), 2013-04, Vol.73 (8_Supplement), p.5047-5047

2013

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Nephron Progenitor But Not Stromal Progenitor Cells Give Rise to Wilms Tumors in Mouse Models with β-Catenin Activation or Wt1 Ablation and Igf2 Upregulation1

Neoplasia (New York, N.Y.), 2016-02, Vol.18 (2), p.71-81

2016

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Nephron Progenitor But Not Stromal Progenitor Cells Give Rise to Wilms Tumors in Mouse Models with [beta]-Catenin Activation or Wt1 Ablation and Igf2 Upregulation

Neoplasia (New York, N.Y.), 2016-02, Vol.18 (2), p.71-81

2016

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Knock-in of the Wt1 R394W mutation causes MDS and cooperates with Flt3/ITD to drive aggressive myeloid neoplasms in mice

Oncotarget, 2018-10, Vol.9 (82), p.35313-35326

2018

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Genetic changes associated with relapse in favorable histology Wilms tumor: A Children’s Oncology Group AREN03B2 study

Cell reports. Medicine, 2022-06, Vol.3 (6), p.100644, Article 100644

2022

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A Wilms Tumor 1 (WT1) Mutation Causes Myelodysplastic Syndrome in a Knock-in Mouse Model, and a Mixed Myelodysplastic/Myeloproliferative Neoplam in Double Knock-in Mice with WT1 and FLT3/ITD Mutations

Blood, 2015-12, Vol.126 (23), p.312-312

2015

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Reprogramming of Sertoli cells to fetal-like Leydig cells byWt1ablation

Proceedings of the National Academy of Sciences - PNAS, 2015-03, Vol.112 (13), p.4003-4008

2015

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Abstract 5353: Comprehensive Ggnomic analysis of diffuse hyperplastic perilobar nephroblastomatosis (DHPLN)

Cancer research (Chicago, Ill.), 2011-04, Vol.71 (8_Supplement), p.5353-5353

2011

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Clinical outcome and biological predictors of relapse following nephrectomy only for very low risk Wilms tumor (VLR WT): A report from Children’s Oncology Group AREN0532

Journal of clinical oncology, 2015-05, Vol.33 (15_suppl), p.10023-10023

2015

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Abstract LB-180: The genetic landscape of Wilms tumor

Cancer research (Chicago, Ill.), 2016-07, Vol.76 (14_Supplement), p.LB-180-LB-180

2016

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Reply to B. Royer-Pokora et al

Journal of clinical oncology, 2011-06, Vol.29 (16), p.e487-e488

2011

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Abstract 1439: Loss of expression of SWI/SNF subunits in high risk Wilms tumor is accompanied by global gene expression changes

Cancer research (Chicago, Ill.), 2012-04, Vol.72 (8_Supplement), p.1439-1439

2012

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Monitoring Therapy with MEK Inhibitor U0126 in a Novel Wilms Tumor Model in Wt1 Knockout Igf2 Transgenic Mice Using super(18)F-FDG PET with Dual-Contrast Enhanced CT and MRI: Early Metabolic Response Without Inhibition of Tumor Growth

Molecular imaging and biology, 2013-04, Vol.15 (2), p.175-185

2013

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Monitoring Therapy with MEK Inhibitor U0126 in a Novel Wilms Tumor Model in Wt1 Knockout Igf2 Transgenic Mice Using ^sup 18^F-FDG PET with Dual-Contrast Enhanced CT and MRI: Early Metabolic Response Without Inhibition of Tumor Growth

Molecular imaging and biology, 2013-04, Vol.15 (2), p.175

2013

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Clinically Relevant Subsets Identified by Gene Expression Patterns Support a Revised Ontogenic Model of Wilms Tumor: A Children's Oncology Group Study12

Neoplasia (New York, N.Y.), 2012-08, Vol.14 (8), p.742-756

2012

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Characterization of the Inflammatory Microenvironment and Identification of Potential Therapeutic Targets in Wilms Tumors12

Translational oncology, 2014-06, Vol.7 (4), p.484-492

2014

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Wt1 negatively regulates Î²-catenin signaling during testis development

Development (Cambridge), 2008-05, Vol.135 (10), p.1875

2008

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Genotype/phenotype correlations in Wilms' tumor

Medical and pediatric oncology, 1996-11, Vol.27 (5), p.408-414

Huff, Vicki

1996

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UNIVERSAL NEPHROBLASTOMATOSIS WITH BILATERAL HYPERPLASTIC NEPHROMEGALY IN SIBLINGS

Pediatric and developmental pathology, 2006, Vol.preprint (2008), p.1

2006

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Genome-wide loss of heterozygosity analysis ofWT1-wild-type andWT1-mutant Wilms tumors

Genes chromosomes & cancer, 2005, Vol.43 (2), p.172-180

2005

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Characterization of the Inflammatory Microenvironment and Identification of Potential Therapeutic Targets in Wilms Tumors

Generation of a Wt1 conditional deletion, nuclear red fluorescent protein reporter allele in the mouse

Identification of germline DICER1 mutations and loss of heterozygosity in familial Wilms tumor using whole genome sequencing

Abstract 5047: Impact of kidney progenitor cell differentiation status in Wilms tumorigenesis

Nephron Progenitor But Not Stromal Progenitor Cells Give Rise to Wilms Tumors in Mouse Models with β-Catenin Activation or Wt1 Ablation and Igf2 Upregulation1

Nephron Progenitor But Not Stromal Progenitor Cells Give Rise to Wilms Tumors in Mouse Models with [beta]-Catenin Activation or Wt1 Ablation and Igf2 Upregulation

Knock-in of the Wt1 R394W mutation causes MDS and cooperates with Flt3/ITD to drive aggressive myeloid neoplasms in mice

Genetic changes associated with relapse in favorable histology Wilms tumor: A Children’s Oncology Group AREN03B2 study

A Wilms Tumor 1 (WT1) Mutation Causes Myelodysplastic Syndrome in a Knock-in Mouse Model, and a Mixed Myelodysplastic/Myeloproliferative Neoplam in Double Knock-in Mice with WT1 and FLT3/ITD Mutations

Reprogramming of Sertoli cells to fetal-like Leydig cells byWt1ablation

Abstract 5353: Comprehensive Ggnomic analysis of diffuse hyperplastic perilobar nephroblastomatosis (DHPLN)

Clinical outcome and biological predictors of relapse following nephrectomy only for very low risk Wilms tumor (VLR WT): A report from Children’s Oncology Group AREN0532

Abstract LB-180: The genetic landscape of Wilms tumor

Reply to B. Royer-Pokora et al

Abstract 1439: Loss of expression of SWI/SNF subunits in high risk Wilms tumor is accompanied by global gene expression changes

Recurrent DGCR8, DROSHA, and SIX Homeodomain Mutations in Favorable Histology Wilms Tumors

The Wilms Tumor Gene, Wt1, Is Critical for Mouse Spermatogenesis via Regulation of Sertoli Cell Polarity and Is Associated with Non-Obstructive Azoospermia in Humans: e1003645

Monitoring Therapy with MEK Inhibitor U0126 in a Novel Wilms Tumor Model in Wt1 Knockout Igf2 Transgenic Mice Using super(18)F-FDG PET with Dual-Contrast Enhanced CT and MRI: Early Metabolic Response Without Inhibition of Tumor Growth

Monitoring Therapy with MEK Inhibitor U0126 in a Novel Wilms Tumor Model in Wt1 Knockout Igf2 Transgenic Mice Using ^sup 18^F-FDG PET with Dual-Contrast Enhanced CT and MRI: Early Metabolic Response Without Inhibition of Tumor Growth

Clinically Relevant Subsets Identified by Gene Expression Patterns Support a Revised Ontogenic Model of Wilms Tumor: A Children's Oncology Group Study12

Characterization of the Inflammatory Microenvironment and Identification of Potential Therapeutic Targets in Wilms Tumors12

Wt1 negatively regulates Î²-catenin signaling during testis development

Genotype/phenotype correlations in Wilms' tumor

UNIVERSAL NEPHROBLASTOMATOSIS WITH BILATERAL HYPERPLASTIC NEPHROMEGALY IN SIBLINGS

Genome-wide loss of heterozygosity analysis ofWT1-wild-type andWT1-mutant Wilms tumors

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