Identical Genetic Changes in Different Histologic Components of Wilms' Tumors

Zhuang, Zhengping; Merino, María J.; Vortmeyer, Alexander O.; Bryant, Bonita R.; Lash, Alexander E.; Wang, Chaoyu; Deavers, Michael T.; Shelton, Wilfred F.; Kapur, Sudesh; Chandra, Roma

doi:10.1093/jnci/89.15.1148

Cited by 28 publications

(25 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Such progenitor cells in glioblastoma multiforme may also give rise to the development of glomeruloid microvascular proliferations, which constantly express SMA [11,24]. Sarcomatous components carry the same genetic alterations as epithelial tumor cells [12,28,29]. This observation pro- vides an additional evidence for this hypothesis (Fig.…”

Section: Discussionmentioning

confidence: 77%

Analysis of the TP53 gene in laser-microdissected glioblastoma vasculature

et al. 2003

View full text Add to dashboard Cite

Malignant transformation of human gliomas is accompanied by extensive proliferation of stromal blood vessels. Recent data suggest mesenchymal transdifferentiation of neoplastic cells in various human cancers, including colon and breast cancer as well as gliosarcoma. In this study, we have analyzed proliferating stromal blood vessels in glioblastoma multiforme for the presence of mutations in the tumor suppressor gene TP53. Using tissue arrays derived from glioblastoma specimens, cases with significant immunohistochemical p53 accumulation were selected for molecular genetic detection of TP53 mutations in exons 5 to 8. None of the tumors included in this series displayed properties of gliosarcoma. Proliferating glomeruloid stromal vessels were isolated by laser microdissection from paraffin sections. In six cases, single-strand conformation polymorphism analysis for mutations of the TP53 gene in stromal blood vessels compared with adjacent tumor cells and subsequent DNA sequencing of the resulting DNA fragments were carried out. Glioblastoma cells of these cases exhibited TP53 mutations in exons 5, 7 and 8. None of these tumors showed TP53 mutations in microdissected samples from glomeruloid vessels. The absence of TP53 mutations in vascular stromal components of glioblastoma multiforme supports the hypothesis that microvascular proliferations originate from the tumor stroma and are not derived from transdifferentiated glioblastoma cells.

show abstract

Section: Discussionmentioning

confidence: 77%

Analysis of the TP53 gene in laser-microdissected glioblastoma vasculature

et al. 2003

View full text Add to dashboard Cite

show abstract

“…[19][20][21] In the tumour that we studied, such epithelial-to-mesenchymal transition (EMT) was present in LOH-bearing, presumably tumour-derived cells, and it is possible that it occurred in vivo, since it was evident from the first passage. It is of course impossible to prove that EMT indeed occurred in vivo.…”

Section: Discussionmentioning

confidence: 99%

A pleiomorphic GH pituitary adenoma from a Carney complex patient displays universal allelic loss at the protein kinase A regulatory subunit 1A (PRKARIA) locus

Bossis

2004

Journal of Medical Genetics

View full text Add to dashboard Cite

“…Here again, while a broad pan-mesodermal multi-potentiality remained, the mesenchyme loses its nephron epithelial potential. Culture with TGFβ2 results in the formation of a blastemal and chondrogenic phenotypes, as is frequently observed in Wilms’ tumors [57], suggesting a misdirection of differentiation or loss of specification. As nephrospheres can be derived from Sall1- or Osr1-positive populations that will include CM, the loss of renal potential by these cultures may simply indicate that the CM component itself is selectively lost, leaving only the stromal progenitor population.…”

Section: Introductionmentioning

confidence: 96%

Defining and redefining the nephron progenitor population

et al. 2011

View full text Add to dashboard Cite

It has long been appreciated that the mammalian kidney arises via reciprocal interactions between an epithelial ureteric epithelium and the surrounding metanephric mesenchyme. More recently, lineage tracing has confirmed that the portion of the metanephric mesenchyme closest to the advancing ureteric tips, the cap mesenchyme, represents the progenitor population for the nephron epithelia. This Six2+Cited1+ population undergoes self-renewal throughout nephrogenesis while retaining the potential to epithelialize. In contrast, the Foxd1+ portion of the metanephric mesenchyme shows no epithelial potential, developing instead into the interstitial, perivascular, and possibly endothelial elements of the kidney. The cap mesenchyme rests within a nephrogenic niche, surrounded by the stroma and the ureteric tip. While the role of Wnt signaling in nephron induction is known, there remains a lack of clarity over the intrinsic and extrinsic regulation of cap mesenchyme specification, self-renewal, and nephron potential. It is also not known what regulates cessation of nephrogenesis, but there is no nephron generation in response to injury during the postnatal period. In this review, we will examine what is and is not known about this nephron progenitor population and discuss how an increased understanding of the regulation of this population may better explain the observed variation in final nephron number and potentially facilitate the reinitiation or prolongation of nephron formation.

show abstract

Identical Genetic Changes in Different Histologic Components of Wilms' Tumors

Cited by 28 publications

References 18 publications

Analysis of the TP53 gene in laser-microdissected glioblastoma vasculature

Analysis of the TP53 gene in laser-microdissected glioblastoma vasculature

A pleiomorphic GH pituitary adenoma from a Carney complex patient displays universal allelic loss at the protein kinase A regulatory subunit 1A (PRKARIA) locus

Defining and redefining the nephron progenitor population

Contact Info

Product

Resources

About