Proto Oncogene

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Ximing J Yang - One of the best experts on this subject based on the ideXlab platform.

Isabella Ceccherini - One of the best experts on this subject based on the ideXlab platform.

  • cDNA sequence and genomic structure of the rat RET Proto-Oncogene.
    Dna Sequence, 2009
    Co-Authors: Ivana Matera, Manuel De Miguel-rodríguez, José M. Fernández-santos, Giuseppe Santamaria, Aldamaria Puliti, Hugo Galera-davidson, Giovanni Romeo, Roberto Ravazzolo, Isabella Ceccherini
    Abstract:

    The RET Proto-Oncogene, a member of the Receptor Tyrosine Kinase family, plays a crucial role during the development of the excretory system and the enteric nervous system, as demonstrated by in vivo animal studies and by its involvement in the pathogenesis of several human neurocristopathies like Hirschsprung disease and Multiple Endocrine Neoplasia type 2. Using a multistep RT-PCR approach we have isolated and sequenced the cDNA of the whole rat RET Proto-Oncogene, reporting the deduced amino acid sequence in comparison with the human and mouse counterparts. Moreover, two different isoforms (RET9 and RET51) have been confirmed in the rat, while a third RET isoform demonstrated in human (RET43) has not resulted to be conserved in this species. Finally, we have determined the genomic structure of the rat RET Proto-Oncogene comparing the exon-intron boundaries and intron sizes with the known structure of the human homologous gene. Our findings will facilitate the molecular study of appropriate rat models o...

  • cDNA sequence and genomic structure of the rat RET Proto-Oncogene.
    Dna Sequence, 2009
    Co-Authors: Ivana Matera, Manuel De Miguel-rodríguez, José M. Fernández-santos, Giuseppe Santamaria, Aldamaria Puliti, Hugo Galera-davidson, Giovanni Romeo, Roberto Ravazzolo, Isabella Ceccherini
    Abstract:

    The RET Proto-Oncogene, a member of the Receptor Tyrosine Kinase family, plays a crucial role during the development of the excretory system and the enteric nervous system, as demonstrated by in vivo animal studies and by its involvement in the pathogenesis of several human neurocristopathies like Hirschsprung disease and Multiple Endocrine Neoplasia type 2. Using a multistep RT-PCR approach we have isolated and sequenced the cDNA of the whole rat RET Proto-Oncogene, reporting the deduced amino acid sequence in comparison with the human and mouse counterparts. Moreover, two different isoforms (RET9 and RET51) have been confirmed in the rat, while a third RET isoform demonstrated in human (RET43) has not resulted to be conserved in this species. Finally, we have determined the genomic structure of the rat RET Proto-Oncogene comparing the exon-intron boundaries and intron sizes with the known structure of the human homologous gene. Our findings will facilitate the molecular study of appropriate rat models of RET related human diseases.

  • Somatic in frame deletions not involving juxtamembranous cysteine residues strongly activate the RET Proto-Oncogene.
    Oncogene, 1997
    Co-Authors: Isabella Ceccherini, Ivana Matera, Giuseppe Santamaria, Maria Gullo, Italia Bongarzone, Cristina Romei, Piera Mondellini, Furio Pacini, Barbara Pasini, Lucio Scopsi
    Abstract:

    Somatic in frame deletions not involving juxtamembranous cysteine residues strongly activate the RET Proto-Oncogene

  • GERM LINE MUTATIONS OF THE RET Proto-Oncogene IN JAPANESE PATIENTS WITH MULTIPLE ENDOCRINE NEOPLASIA TYPE 2A AND TYPE 2B
    Japanese Journal of Cancer Research, 1994
    Co-Authors: Shoichi Maruyama, Toshihide Iwashita, Hiroomi Funahashi, Mutsushi Matsuyama, Tsuneo Imai, Isabella Ceccherini, Seiichi Matsuo, Giovanni Romeo, Masahide Takahashi
    Abstract:

    : We investigated mutations of the ret Proto-Oncogene in Japanese patients with multiple endocrine neoplasia (MEN) type 2A and type 2B. DNAs from pheochromocytomas and/or medullary thyroid carcinomas (MTCs) of five MEN 2A and three MEN 2B patients were amplified by a polymerase chain reaction (PCR) and analyzed. Tumors of four MEN 2A patients had missense mutations in Cys 634 in the extracellular domain of the ret Proto-Oncogene. The same mutations were detected in normal tissues of the patients, indicating that the mutations had arisen in the germ line. Using a reverse transcriptase(RT)-PCR, both normal and mutant transcripts of the ret Proto-Oncogene were detected in a tumor of one patient with MEN 2A mutation. In addition, three MEN 2B patients examined had the same point mutation (ATG-->ACG) at codon 918 in the tyrosine kinase domain of the ret Proto-Oncogene. Since all mutations identified in this study generated new restriction enzyme sites or eliminated a restriction site, the mutant alleles of affected family members could be readily detected without sequencing.

Masahide Takahashi - One of the best experts on this subject based on the ideXlab platform.

  • Ret: Proto-Oncogene activated by recombination (vertebrates)
    The Protein Kinase FactsBook, 1995
    Co-Authors: Masahide Takahashi
    Abstract:

    The RET Proto-Oncogene encodes a transmembrane PTK and is activated to an Oncogene by recombination with other cellular sequences. Rearrangement of the RET gene was found in 11%–33% of thyroid papillary carcinomas from European and American patients, while the frequency of rearrangement was low (

  • A single missense mutation in codon 918 of the RET Proto-Oncogene in sporadic medullary thyroid carcinomas.
    Endocrine Journal, 1995
    Co-Authors: Shigeto Maeda, Hiroyuki Namba, Ken Tanigawa, Shiroh Noguchi, Noboru Takamura, Takashi Kanematsu, Shigenobu Nagataki, Masahide Takahashi, Shunichi Yamashita
    Abstract:

    The RET Proto-Oncogene is expressed in human medullary thyroid carcinoma and pheochromocytoma.Recently germline mutations of the RET Proto-Oncogene were reported in four syndromes (MEN 2A, MEN 2B, familial medullary thyroid carcinoma and Hirschprung's disease) and somatic mutation was also found in sporadic medullary thyroid carcinoma. To determine the incidence of RET mutations in medullary thyroid carcinoma in Japan, we investigated 14 medullary thyroid carcinomas (comprising 1 case of MEN 2A, 1 case of MEN 2B, 2 cases of familial medullary thyroid carcinoma and 10 cases of sporadic). Tumors from all cases were screened by PCR-SSCP on exons 10 and 11. DNA sequencing on these exons was performed for the hereditary medullary thyroid carcinoma cases. The PCR products of exon 16 from tumor DNA were analyzed by means of Fok1 restriction enzyme digestion analysis and mutations confirmed by DNA sequencing. We found no structural abnormalities in either exon 10 or exon 11 in any of the cases examined, but in four of 10 sporadic cases we detected a common point mutation at codon 918 (ATG to ACG) in exon 16, where methionine was replaced with threonine. Our results support the theory that a point mutation of exon 16 of the RET Proto-Oncogene may be related to the Oncogenesis of sporadic medullary thyroid carcinomas. However, further studies on the entire RET Proto-Oncogene are needed to clarify the relationship between its expression and thyroid tumorigenesis.

  • GERM LINE MUTATIONS OF THE RET Proto-Oncogene IN JAPANESE PATIENTS WITH MULTIPLE ENDOCRINE NEOPLASIA TYPE 2A AND TYPE 2B
    Japanese Journal of Cancer Research, 1994
    Co-Authors: Shoichi Maruyama, Toshihide Iwashita, Hiroomi Funahashi, Mutsushi Matsuyama, Tsuneo Imai, Isabella Ceccherini, Seiichi Matsuo, Giovanni Romeo, Masahide Takahashi
    Abstract:

    : We investigated mutations of the ret Proto-Oncogene in Japanese patients with multiple endocrine neoplasia (MEN) type 2A and type 2B. DNAs from pheochromocytomas and/or medullary thyroid carcinomas (MTCs) of five MEN 2A and three MEN 2B patients were amplified by a polymerase chain reaction (PCR) and analyzed. Tumors of four MEN 2A patients had missense mutations in Cys 634 in the extracellular domain of the ret Proto-Oncogene. The same mutations were detected in normal tissues of the patients, indicating that the mutations had arisen in the germ line. Using a reverse transcriptase(RT)-PCR, both normal and mutant transcripts of the ret Proto-Oncogene were detected in a tumor of one patient with MEN 2A mutation. In addition, three MEN 2B patients examined had the same point mutation (ATG-->ACG) at codon 918 in the tyrosine kinase domain of the ret Proto-Oncogene. Since all mutations identified in this study generated new restriction enzyme sites or eliminated a restriction site, the mutant alleles of affected family members could be readily detected without sequencing.

  • Identification of the ret Proto-Oncogene products in neuroblastoma and leukemia cells.
    Oncogene, 1991
    Co-Authors: Masahide Takahashi, Buma Y, Masahiko Taniguchi
    Abstract:

    : Monoclonal and/or polyclonal antibodies were generated against the products synthesized from two portions of the ret Proto-Oncogene (c-ret) cDNA expressed in Escherichia coli. These antibodies were reactive in immunoblotting with 150 kd and 170 kd proteins in cell lysates from three human neuroblastoma cell lines expressing the ret Proto-Oncogene. When the neuroblastoma cells were treated with tunicamycin, a protein with an apparent molecular weight of 120 kd, which is consistent with that of the c-ret protein predicted from the cDNA sequence, appeared on immunoblots. These results indicated that the 150 kd and 170 kd proteins in neuroblastoma cells are produced from a single polypeptide of 120 kd by posttranslational glycosylation. Furthermore, the antibodies detected a unique 190 kd protein as well as 150 kd protein in a cell lysate from THP-1 human monocytic leukemia cell line, suggesting that glycosylated forms of the c-ret protein are different between neuroblastoma and leukemia cells.

Rossella Elisei - One of the best experts on this subject based on the ideXlab platform.

  • a comprehensive overview of the role of the ret Proto Oncogene in thyroid carcinoma
    Nature Reviews Endocrinology, 2016
    Co-Authors: Cristina Romei, Raffaele Ciampi, Rossella Elisei
    Abstract:

    The rearranged during transfection (RET) Proto-Oncogene was identified in 1985 and, very soon thereafter, a rearrangement named RET/PTC was discovered in papillary thyroid carcinoma (PTC). After this discovery, other RET rearrangements were found in PTCs, particularly in those induced by radiation. For many years, it was thought that these genetic alterations only occurred in PTC, but, in the past couple of years, some RET/PTC rearrangements have been found in other human tumours. 5 years after the discovery of RET/PTC rearrangements in PTC, activating point mutations in the RET Proto-Oncogene were discovered in both hereditary and sporadic forms of medullary thyroid carcinoma (MTC). In contrast to the alterations found in PTC, the activation of RET in MTC is mainly due to activating point mutations. Interestingly, in the past year, RET rearrangements that were different to those described in PTC were observed in sporadic MTC. The identification of RET mutations is relevant to the early diagnosis of hereditary MTC and the prognosis of sporadic MTC. The diagnostic and prognostic role of the RET/PTC rearrangements in PTC is less relevant but still important in patient management, particularly for deciding if a targeted therapy should be initiated. In this Review, we discuss the pathogenic, diagnostic and prognostic roles of the RET Proto-Oncogene in both PTC and MTC.

  • A comprehensive overview of the role of the RET Proto-Oncogene in thyroid carcinoma
    Nature Reviews Endocrinology, 2016
    Co-Authors: Cristina Romei, Raffaele Ciampi, Rossella Elisei
    Abstract:

    Since mutations in theRET Proto-Oncogene were discovered in thyroid carcinoma 20 years ago, research has focused on determining the prevalence of these alterations, their role in disease development and potential clinical applications. In this Review, the authors discuss these findings with respect to the pathogenic, diagnostic and prognostic roles of RETin patients with papillary thyroid carcinoma and medullary thyroid carcinoma. The rearranged during transfection (RET) Proto-Oncogene was identified in 1985 and, very soon thereafter, a rearrangement named RET/PTC was discovered in papillary thyroid carcinoma (PTC). After this discovery, other RET rearrangements were found in PTCs, particularly in those induced by radiation. For many years, it was thought that these genetic alterations only occurred in PTC, but, in the past couple of years, some RET/PTC rearrangements have been found in other human tumours. 5 years after the discovery of RET/PTC rearrangements in PTC, activating point mutations in the RET Proto-Oncogene were discovered in both hereditary and sporadic forms of medullary thyroid carcinoma (MTC). In contrast to the alterations found in PTC, the activation of RET in MTC is mainly due to activating point mutations. Interestingly, in the past year, RET rearrangements that were different to those described in PTC were observed in sporadic MTC. The identification of RET mutations is relevant to the early diagnosis of hereditary MTC and the prognosis of sporadic MTC. The diagnostic and prognostic role of the RET/PTC rearrangements in PTC is less relevant but still important in patient management, particularly for deciding if a targeted therapy should be initiated. In this Review, we discuss the pathogenic, diagnostic and prognostic roles of the RET Proto-Oncogene in both PTC and MTC.

Duy T Nguyen - One of the best experts on this subject based on the ideXlab platform.

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