Evaluation of ENU-Induced Gliomas in Rats: Nomenclature, Immunochemistry, and Malignancy

Zook, Bernard C.; Simmens, Samuel J.; Jones, Robert

doi:10.1177/019262330002800124

Cited by 45 publications

(51 citation statements)

References 29 publications

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“…H&E. X200. plastic oligodendroglia (102). Takahashi (88) Figure 11), but, unlike in rats, pineal tumors have been mentioned but not described in mice (25,91 (Figure 12).…”

Section: Features Demonstrated By Special Methodsmentioning

confidence: 99%

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Morphologic Characterization of Spontaneous Nervous System Tumors in Mice and Rats

et al. 2000

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“…H&E. X200. plastic oligodendroglia (102). Takahashi (88) Figure 11), but, unlike in rats, pineal tumors have been mentioned but not described in mice (25,91 (Figure 12).…”

Section: Features Demonstrated By Special Methodsmentioning

confidence: 99%

“…Certain tumorlike lesions, such as lipomas (lipomatous hamartoma) and epidermoid cysts, appear to be more frequent in mice than in rats (3,48 (14,102).…”

Section: Comments On the Reports Dealing With Spontaneous Primary Rodmentioning

confidence: 99%

Morphologic Characterization of Spontaneous Nervous System Tumors in Mice and Rats

et al. 2000

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“…16 The ENU-induced rat gliomas from the study by Wang et al 1 showed cytological features similar to low-grade or anaplastic oligodendrogliomas, but lacked diffuse brain invasion. 1 Taken together, the histopathology of these model tumors is consistent with the nondiffuse gliomas, such as pilocytic astrocytomas, gangliogliomas, or pleomorphic xanthoastrocytoma, and their lack of invasion further supports the use of this model for studying these entities.…”

Section: Role Of Braf In Tumorigenesismentioning

confidence: 97%

BRAF Mutations Open Doors for N-Ethyl-N-Nitrosourea–Induced Gliomagenesis

McNeill

Irvin

Miller

2016

The American Journal of Pathology

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In this issue of the American Journal of Pathology, Wang et al 1 identified recurrent Braf mutations in N-ethyl-Nnitrosourea (ENU)einduced rat gliomas by DNA sequencing. Their results provide a platform for preclinical development of novel targeted therapies for BRAF-mutant gliomas. Precision oncology promises to revolutionize cancer therapy by stratifying tumors on the basis of their molecular characteristics and using rationally designed treatments in molecularly defined patient populations. 2 Although the field of oncology is transitioning into the precision medicine era, conventional diagnostics, based on tissue type, tumor pathology, and patient demographics, remain essential to quality care. One natural pathological division for gliomas, the most common primary brain tumors in humans, is based on their invasion, with nondiffuse gliomas forming well-circumscribed tumors and diffuse gliomas invading the normal brain. 3 Within these two broad diagnostic categories, gliomas are further subdivided on the basis of patient demographics into pediatric and adult diseases and further into specific diagnostic entities based on their histological appearance.

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“…This results in the eventual development of neural tumors in virtually all offspring after a latency of greater than 4 months. Tumors are of variable types including mixed oligoastrocytomas, oligodendrogliomas, astrocytomas, and neurinomas [Zook et al, 2000]. Initiation occurs rapidly since ENU is cleared within minutes [Swann and Magee, 1971;Mü ller and Rajewsky, 1983] and transformation of brain cells isolated from exposed rats in the neonatal period has been reported [Laerum and Rajewsky, 1975;Roscoe and Claisse, 1978].…”

Section: Evaluating the Relationship Of Neural Stem Cells And Glioma mentioning

confidence: 99%

“…While the ENU model continues to be utilized by investigators [Blass-Kampmann et al, 1998;Adey et al, 2000;Zook et al, 2000;Kish et al, 2001], it is mostly to study the events that occur at initiation (i.e., genetic mutations) or progression (after large tumors are apparent). Little work is currently ongoing that examines the latency period, however, and to date, there are no data that suggests that a promotion stage, similar to that observed in epithelial cancers, occurs in the development of glioma [Koestner, 1990].…”

Section: Applying Concepts From Neural Stem Cellmentioning

confidence: 99%

Neural stem cells and neuro‐oncology: Quo vadis?

Recht

Jang

Savarese

et al. 2002

J of Cellular Biochemistry

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Conventionally, gliomas are assumed to arise via transformation of an intraparenchymal glial cell that forms a mass that then expands centrifugally, eventually invading surrounding tissues. We propose an alternative model in which gliomas arise via initiation and promotion of cells within the brain's subependymal layer or subventricular zone, the source of a recently characterized pool of neural cells with the properties of self-renewal and multipotentiality (i.e., stem cells) that persists into adulthood. In this model, the particular histological subtype of glioma would represent the effects of temporal and spatial environmental influences rather than the particular cell of origin and the disease's centrifugal point would be the subependymal layer. The implications of such a model are discussed.

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Evaluation of ENU-Induced Gliomas in Rats: Nomenclature, Immunochemistry, and Malignancy

Cited by 45 publications

References 29 publications

Morphologic Characterization of Spontaneous Nervous System Tumors in Mice and Rats

Morphologic Characterization of Spontaneous Nervous System Tumors in Mice and Rats

BRAF Mutations Open Doors for N-Ethyl-N-Nitrosourea–Induced Gliomagenesis

Neural stem cells and neuro‐oncology: Quo vadis?

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