Renin-induced hypertension in Wilms tumor patients

2007 ◽  
Vol 48 (5) ◽  
pp. 500-503 ◽  
Author(s):  
M.H. Maas ◽  
K. Cransberg ◽  
M. van Grotel ◽  
R. Pieters ◽  
M.M. van den Heuvel-Eibrink
2018 ◽  
Vol 66 (1) ◽  
pp. e27430 ◽  
Author(s):  
Douglas S. M. Iaboni ◽  
Yueh-Yun Chi ◽  
Yeonil Kim ◽  
Jeffrey S. Dome ◽  
Conrad V. Fernandez

1995 ◽  
Vol 24 (5) ◽  
pp. 305-309 ◽  
Author(s):  
Jane M. Olson ◽  
Anne Hamilton ◽  
Norman E. Breslow

2014 ◽  
Vol 111 ◽  
pp. S107
Author(s):  
M. Ramos Albiac ◽  
D. Mosquera ◽  
M. Hermida-López ◽  
J. Giralt

2014 ◽  
Vol 433 ◽  
pp. 235-241 ◽  
Author(s):  
Elke Hammer ◽  
Florian D. Ernst ◽  
Andrea Thiele ◽  
Narasimha Kumar Karanam ◽  
Christina Kujath ◽  
...  

2021 ◽  
Author(s):  
Verena Waehle ◽  
Rosemarie Ungricht ◽  
Philipp S. Hoppe ◽  
Joerg Betschinger

SUMMARYThe loss or failure of cell differentiation is a hallmark of cancer, yet whether perturbation of differentiation is causal or consequential to malignant transformation is largely unclear. Wilms tumor is the most widespread kidney cancer in children. Here, we establish a model for Wilms tumorigenesis in human kidney organoids. We show that loss of the tumor suppressor WT1 during organoid formation induces overgrowth of kidney progenitor cells at the expense of differentiating tubules. Functional and gene expression analyses demonstrate that absence of WT1 halts progenitor cell progression at a pre-epithelialized cell state and recapitulates the transcriptional changes detected in a subgroup of Wilms tumor patients with ectopic myogenesis. By “transplanting” WT1 mutant cells into wild-type kidney organoids, we find that their propagation requires an untransformed microenvironment. Genetic engineering of cancer lesions in human organoids therefore permits phenotypic modeling of tumor initiation and progression, and complements the current toolbox of pre-clinical Wilms tumor models.


Author(s):  
Shotaro Matsudera ◽  
Yoshihito Kano ◽  
Yasuko Aoyagi ◽  
Kohki Tohyama ◽  
Kei Ogino ◽  
...  

Background: Comprehensive genomic profiling (CGP) was widely adopted in Japan after its coverage by national healthcare insurance began in June 2019. We investigated the clinical utility of CGP in pediatric and adolescent young adults (AYA) solid tumor patients. Procedure: Between November 2017 and December 2019, 13 patients who progressed with or who were likely to progress with standard therapies were recruited to the PROFILE-F study to undergo CGP using either FoundationOne® CDx or FoundationOne® Heme. Results: The median age was 28 years old. Tumor types were as follows: neuroblastoma (n=1), Wilms’ tumor (n=1), rhabdomyosarcoma (n=2), Ewing sarcoma (n=1), gastric cancer (n=1), rectal cancer (n=1), osteosarcoma (n=1), neuroendocrine tumor (n=2), salivary gland carcinoma (n=1), tracheal adenoid cystic carcinoma (n=1), and thymic cancer (n=1). In 92% of cases, at least one genomic alteration was identified, including CDKN2A (four cases), TP53 (three cases), and MYC (two cases). Actionable aberrations were found in 10 cases (77%), and a clinical trial candidate was found in seven cases (54%). However, no patients were able to receive biomarker-matched therapy according to their genomic alterations. Conclusions: Further efforts to increase basket trials and collection of clinical genomic data to predict response are necessary to advance precision cancer medicine in pediatric and AYA populations.


1997 ◽  
Vol 19 (4) ◽  
pp. 397
Author(s):  
M. R. del Olmo ◽  
M. Alvarez de Món ◽  
B. Lopez-Ibor ◽  
M. J. Cilleruelo ◽  
I. Sánchez ◽  
...  

1995 ◽  
Vol 13 (7) ◽  
pp. 1546-1556 ◽  
Author(s):  
K Sorensen ◽  
G Levitt ◽  
D Sebag-Montefiore ◽  
C Bull ◽  
I Sullivan

PURPOSE To study late cardiac function in a single diagnostic group (children with Wilms' tumor) with good long-term survival; to compare patients treated with anthracyclines (doxorubicin) with patients treated without anthracyclines and with a normal child/adolescent group; and to examine the risk factors involved in late cardiac dysfunction. PATIENTS AND METHODS Echocardiographic studies were performed on 97 Wilms' tumor patients treated with anthracyclines (mean cumulative dose, 303 mg/m2) with a mean follow-up time of 7.1 years, on 39 Wilms' tumor patients treated without anthracyclines with a mean follow-up time of 8.9 years, and on 50 normal subjects. Left ventricular (LV) dimensions, end systolic wall stress (a measure of afterload), and load-dependent and -independent measures of contractility were compared between groups. Potential risk factors, including age at diagnosis, follow-up duration, sex, pubertal status, cardiac irradiation, dose-intensity, and cumulative dose of anthracyclines, were studied by multivariate analysis. RESULTS Twenty-five percent of the anthracycline-treated group showed cardiac abnormalities. All but one of these patients had increased LV afterload. Risk factors for increased afterload were anthracycline cumulative dose (P < .05) and anthracycline dose-intensity (P < .02). Wilms' tumor patients treated without anthracyclines had thickened LV walls compared with normal subjects (P < .05). CONCLUSION Total dose and dose-intensity of anthracycline were risk factors for increased LV afterload in long-term Wilms' tumor survivors treated on standard protocols. The increase in afterload accounted for reduced LV shortening, whereas contractility was rarely abnormal. The new finding that Wilms' tumor survivors who do not receive anthracyclines have mild LV hypertrophy may provide some protection against anthracycline-induced cardiotoxic effects.


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