Activation of a novel human transforming gene, ret, by DNA rearrangement

Takahashi, Masahide; Ritz, Jérôme; Cooper, Geoffrey M.

doi:10.1016/0092-8674(85)90115-1

Cited by 719 publications

(406 citation statements)

References 33 publications

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“…The functional receptor for Gdnf is the Ret tyrosine kinase (REarranged during Transfection) originally discovered by Takahashi and colleagues who showed a novel gene rearrangement and oncogenic activation in a transfection assay of NIH 3T3 fibroblasts with lymphoma DNA (Takahashi et al, 1985). Using serum-free short-term cultures of SSCs and a spermatogonial stem cell line (Hofmann et al, 2005a), our group recently elucidated some of the pathways induced by Gdnf in these cells.…”

Section: Src Signaling Pathwaymentioning

confidence: 99%

Gdnf signaling pathways within the mammalian spermatogonial stem cell niche

Hofmann

2008

Molecular and Cellular Endocrinology

203

178

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SummaryMammalian spermatogenesis is a complex process in which male germ-line stem cells develop to ultimately form spermatozoa. Spermatogonial stem cells, or SSCs, are found in the basal compartment of the seminiferous epithelium. They self-renew to maintain the pool of stem cells throughout life, or they differentiate to generate a large number of germ cells. A balance between SSC self-renewal and differentiation in the adult testis is therefore essential to maintain normal spermatogenesis and fertility. Maintenance and self-renewal are tightly regulated by extrinsic signals from the surrounding microenvironment, called the spermatogonial stem cell niche. By physically supporting the SSCs and providing them with growth factors, the Sertoli cell is the main component of the niche. In addition, adhesion molecules that connect the SSCs to the basement membrane and cellular components of the interstitium between the seminiferous tubules are important regulators of the niche function. This review mainly focuses on glial cell line-derived neurotrophic factor (Gdnf), which is produced by Sertoli cells to maintain SSCs self-renewal, and the downstream signaling pathways induced by this crucial growth factor. Interactions between Gdnf and other signaling pathways that maintain self-renewal, as well as the role of novel SSC-and Sertoli cell-specific transcription factors, are also discussed.

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Section: Src Signaling Pathwaymentioning

confidence: 99%

Gdnf signaling pathways within the mammalian spermatogonial stem cell niche

Hofmann

2008

Molecular and Cellular Endocrinology

203

178

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“…c-ret, ®rst isolated as an oncogene using the NIH3T3 cell transformation assay, encodes a member of the RTK superfamily (Takahashi et al, 1985). To date, closely related homologues of c-ret have been cloned from three vertebrate species, namely human, mouse and chicken (Takahashi et al, 1988;Iwamoto et al, 1993;Pachnis et al, 1993;Robertson and Mason, 1995;Schuchardt et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

The zebrafish homologue of the ret receptor and its pattern of expression during embryogenesis

et al. 1997

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The c-ret proto-oncogene, a member of the receptor tyrosine kinase gene superfamily, plays a critical role in the development of the excretory system and the enteric and autonomic nervous systems of mammalian embryos. To study the potential function of the c-ret locus in lower vertebrates, we have isolated its zebra®sh homologue, ret1 and established its expression pattern during embryogenesis. Ret1 mRNA ®rst appears during early somitogenesis in the presumptive brain, spinal cord and excretory system. Within the CNS, expression of ret1 is detected in primary motor and sensory (Rohon ± Beard) neurons. Ret1 transcripts are also expressed in subsets of neural crest cells and cranial ganglia as well as in the enteric nervous system. In the excretory system, expression is detected in the developing nephric duct and the pronephros. Our ®ndings reveal a remarkable similarity in the expression pattern of c-ret between higher and lower vertebrates, suggesting that the function of this locus has been conserved throughout vertebrate evolution. Furthermore, the conservation of ret1 expression in cell types which remain una ected by the mammalian c-ret mutations, such as motor and sensory neurons, suggests a function of this receptor in these cell lineages.

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“…The RET proto-oncogene located on chromosome 10q11.2 encodes a protein structurally related to transmembrane receptors with an intracellular tyrosine kinase domain (Takahashi et al, 1985;Takahashi and Cooper, 1987). The ligands for RET have been recently identified as neurotrophic factors of the glial-cell-line derived neurotrophic factor (GDNF) family, including GDNF, neurturin, artemin, and perseptin (reviewed in Airaksinen et al, 1999;Baloh et al, 2000).…”

mentioning

confidence: 99%

Association of RET codon 691 polymorphism in radiation-induced human thyroid tumours with C-cell hyperplasia in peritumoural tissue

et al. 2002

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The RET proto-oncogene encodes a protein structurally related to transmembrane receptors with an intracellular tyrosine kinase domain. In human thyroid gland, the RET proto-oncogene is normally expressed in parafollicular C-cells. Thyroid C-cell hyperplasia is associated with inherited medullary thyroid carcinomas and is considered as a pre-neoplastic stage of C-cells disease. It has also been observed in thyroid tissues adjacent to follicular and papillary carcinomas. In order to study the relationship between a misfunctioning of the RET proto-oncogene and the presence of C-cell hyperplasia, we compared a series of thyroid glands presenting sporadic or radiation-associated tumours, as well as samples of unrelated normal thyroid tissues, for alteration in exons 10 and 11 of the gene and for the presence or absence of C-cell hyperplasia. Here we report a significantly higher frequency of C-cell hyperplasia present in peritumoural thyroid tissues of radiation-induced epithelial thyroid tumours, than in peritumoural of sporadic thyroid tumours or in control normal thyroid tissues (P=0.001). A G691S RET polymorphism was present with a higher frequency in radiation-induced epithelial thyroid tumours (55%) than in sporadic tumours (20%) and in control normal thyroid tissues (15%). Interestingly, this polymorphism was associated in the majority (88%) of radiation-induced tumours with a C-cell hyperplasia in the peritumoural tissues. Several explanations for this association are discussed.

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Activation of a novel human transforming gene, ret, by DNA rearrangement

Cited by 719 publications

References 33 publications

Gdnf signaling pathways within the mammalian spermatogonial stem cell niche

Gdnf signaling pathways within the mammalian spermatogonial stem cell niche

The zebrafish homologue of the ret receptor and its pattern of expression during embryogenesis

Association of RET codon 691 polymorphism in radiation-induced human thyroid tumours with C-cell hyperplasia in peritumoural tissue

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