Combined activation of Ras and Akt in neural progenitors induces glioblastoma formation in mice

By Eric C. Holland, J. Celestino, Chengkai Dai, L. Schaefer, R. Sawaya, G. Fuller. Nature Genetics, 2000

950 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/c080e53873b0c3210e387add1159f015535011e0

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Citations in the corpus

PI3K/Akt: getting it right matters (2008, background): “…neural progenitor cells have observed increased tumor formation, but only when Akt1-transgenic animals were crossed with animals carrying activated alleles of v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (Kras) or mutated middle T oncoprotein (Holland et al., 2000; Hutchinson et al., 2001).”
Human cortical glial tumors contain neural stem‐like cells expressing astroglial and neuronal markers in vitro (2002, background): “…progenitor cells in the developing CNS (Lendahl et al., 1990), with tumors experimentally induced by PDGF-B viral gene transfer (Uhrbum et al., 1998), and with reactive astrocytes (Lin et al., 1995), argues that nestin-positive cells may be somehow involved in gliomagenesis (Holland et al., 2000).”
Malignant astrocytic glioma: genetics, biology, and paths to treatment. (2007, background): “…develop gliomas with many of the features of the human disease (Table 2; Weissenberger et al. 1997; Uhrbom et al. 1998; Kamijo et al. 1999; Holland et al. 2000; Reilly et al. 2000; Dai et al. 2001; Ding et al. 2001, 2003; Rich et al. 2001; Sonoda et al. 2001; Bachoo et al. 2002; Uhrbom et…”
Cells of origin in cancer (2011, methodology): “The models have predominantly included conditionally targeted mice, the RCAS–TVA system — in which gene transfer is mediated by an oncogene-carrying RCAS retrovirus to somatic cells in TVA transgenic mic”
Brain tumour stem cells (2006, background): “Similarly, a series of classic studies proposed that deletion of tumour suppressors and/or activation of oncogenes, such as Ras and Akt, in undifferentiated nestin-expressing cells results in a higher frequency of tumour formation than such alterations in GFAP-expressing astrocyte”
Malignant glioma: genetics and biology of a grave matter. (2001, result): “Similar results were obtained when Ras and activated Akt were targeted to nestin-positive rather than GFAP-positive cells (Holland et al. 2000).”
Isolation of cancer stem cells from adult glioblastoma multiforme (2004, methodology): “The application of principles used for studying the NSCs to tumor biology indicates a link between normal neurogenesis and brain tumorigenesis (Holland et al., 1998; 2000; Holland, 2001; Kabos et al., 2002; Ehtesham et al., 2004).”
Activation of the PI3K/Akt pathway and chemotherapeutic resistance. (2002, background): “First, studies in transgenic mice that overexpress constitutively active Akt in a tissue-specific manner show that Akt, in concert with other genetic alterations, contributes to tumor formation in tissues such as skin, breast, lymph node, ovary, and brain (Ackler et al., 2002; Holland et al., 2000; ”
The phosphatidylinositol 3-Kinase–AKT pathway in human cancer (2002, background): “Direct evidence for this hypothesis comes from a study in which retroviral transfer of activated alleles of both Ras and Akt into glial progenitor cells in the mouse brain produced glioblastomas, whereas transfer of either gene alone did no”
The biology of cancer stem cells. (2007, background): “The hypothesis that an early neural stem or progenitor cell gives rise to tumors is also supported by the observation that glial tumor development arises from a nestin-positive progenitor population rather than from differentiated astrocytes (Holland et al. 2000).”