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Draft:Masahide Takahashi

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  • Comment: The education section is still entirely unsourced. Greenman (talk) 08:35, 2 November 2023 (UTC)
  • Comment: Large sections are unsourced for a WP:BLP. Bullet points are not ideal. Prose style is ideal standard per WP:MOS. Often the bullet is removed as not compliant. Article is unlinked. scope_creepTalk 21:10, 18 July 2023 (UTC)
  • Comment: There is a good chance that the subject is notable per WP:NPROF, but in its current state, the draft doesn't seem to cite sources that are independent of the subject. The Biography section is a bulleted list and doesn't cite any sources, which I'd argue is not compliant with Wikipedia's WP:BLP policy. Also note that the lead section is not very well written; see WP:LEAD for help. Best regards, --Johannes (Talk) (Contribs) (Articles) 20:42, 22 March 2023 (UTC)
Masahide Takahashi
Born (1954-11-18) November 18, 1954 (age 69)
Alma materNagoya University
Scientific career
FieldsPathology

Biography

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Masahide Takahashi is Professor Emeritus of Nagoya University, and Director and Designated Professor of International Center for Cell and Gene Therapy, Fujita Health University in Japan. His pioneering work is the discovery of the RET proto-oncogene encoding a receptor tyrosine kinase [1][2]Alterations of the RET proto-oncogene are responsible for various human cancers and developmental disorders, including thyroid cancer, non-small-cell lung cancer, multiple endocrine neoplasia type 2 (hereditary cancer syndrome), and Hirschsprung’s disease (developmental disorder of the enteric nervous system) [3] [4] [5] [6]

Education

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Masahide Takahashi was born in Japan, in 1954 and graduated from Nagoya University School of Medicine in 1979. He majored in Pathology at Nagoya University Graduate School of Medicine and received his PhD degree in 1983. [7]. [8].

Carrier and research

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Takahashi studied as a research fellow at Dana-Farber Cancer Institute and Harvard Medical School in Boston between 1983 and 1985. After returning to Japan, he worked as a researcher at Aichi Cancer Center Research Institute in Nagoya between 1985 and1990, and moved to Nagoya University as an Assistant Professor. He became Professor of Pathology at Nagoya University in 1996. He was appointed as Dean of Nagoya University School of Medicine between 2012 and 2017, and Trustee and Vice President of Nagoya University between 2017 and 2020. He became Director and Professor of the International Center for Cell and Gene Therapy at Fujita Health University in 2020 [9]. His research group has elucidated the molecular mechanisms of disease development caused by alteration of the RET proto-oncogene. In collaboration with Dr Arnon Rosenthal’s group, they found that glial cell line-derived neurotrophic factor (DNF) is a ligand for RET receptor [10] [11] [12]. The group has studied physiological roles of GDNF/RET signaling in the development of the enteric nervous system and kidney as well as spermatogenesis [13] [14] . In the process of the study of GDNF/RET signaling, Takahashi discovered a new actin-binding protein, named Girdin, which plays pivotal roles in cell motility including cancer cell invasion and metastasis, and neuronal migration [15] [16]

Awards and honors

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  • 1990: Young Investigator Award of the Japanese Cancer Association
  • 1993: Academic Research Award of the Japanese Society of Pathology
  • 2001: The Japan Pathology Award.
  • 2006: Yomiuri-Tokai Medical Award (the Yomiuri Shinbun Co.)
  • 2010: The Chunichi Cultural Award (the Chunichi Shinbun Co.)
  • 2019: Medical Award of The Japan Medical Association
  • 2020: Princess Takamatsu Cancer Research Fund Prize

[17]

  • 2020: Medal with Purple Ribbon from the Government of Japan

[18]

Footnote

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  1. ^ Takahashi M, Ritz J, Cooper GM. Activation of a novel human transforming gene, ret, by DNA rearrangement. Cell. 1985;42:581-588. DOI: 10.1016/0092-8674(85)90115-1
  2. ^ Takahashi M, Buma Y, Iwamoto T, Inaguma Y, Ikeda H, Hiai H. Cloning and expression of the ret proto-oncogene encoding a tyrosine kinase with two potential transmembrane domains. Oncogene. 1988;3:571-578.
  3. ^ Takahashi M. RET receptor signaling: Function in development, metabolic disease, and cancer. Proceedings of the Japan Academy Series B. 2022;98:112-125. DOI: 10.2183/pjab.98.008
  4. ^ Takahashi M. The GDNF/RET signaling pathway and human diseases. Cytokine and Growth Factor Reviews. 2001;12;361-373. DOI: 10.1016/s1359-6101(01)00012-0
  5. ^ Arighi E, Borrello MG, Sariola H. RET tyrosine kinase signaling in development and cancer. Cytokine and Growth Factor Reviews. 2005;16:441-467. DOI: 10.1016/j.cytogfr.2005.05.010
  6. ^ Ibáñez CF. Structure and physiology of the RET receptor tyrosine kinase. Cold Spring Harb Perspect Biol. 2013 5(2):a009134. doi: 10.1101/cshperspect.a009134. PMID: 23378586
  7. ^ "Masahide Takahashi - My portal - researchmap".
  8. ^ "ORCID".
  9. ^ "Masahide Takahashi - My portal - researchmap".
  10. ^ Treanor JJ, Goodman L, de Sauvage F, et al. Characterization of a multicomponent receptor for GDNF. Nature. 1996;382:80-83. DOI: 10.1038/382080a0
  11. ^ Klein RD, Sherman D, Ho WH, et al. A GPI-linked protein that interacts with Ret to form a candidate neurturin receptor. Nature. 1997;387:717-721. DOI: 10.1038/42722
  12. ^ Kawai K, Takahashi, M. Intracellular RET signaling pathways activated by GDNF. Cell and Tissue Research. 2020;382:113-123. DOI: 10.1007/s00441-020-03262-1
  13. ^ Jijiwa M, Fukuda T, Kawai K, et al. A targeting mutation of tyrosine 1062 in Ret causes a marked decrease of enteric neurons and renal hypoplasia. Molecular and Cellular Biology. 2004;24:8026-8036. DOI: 10.1128/MCB.24.18.8026-8036.2004
  14. ^ Jijiwa M, Kawai K, Fukihara J, et al. GDNF-mediated signaling via RET tyrosine 1062 is essential for maintenance of spermatogonial stem cells. Genes to Cells. 2008;13:365-374. DOI: 10.1111/j.1365-2443.2008.01171.x
  15. ^ Enomoto A, Murakami H, Asai N, et al. Akt/PKB regulates actin organization and cell motility via Girdin/APE. Dev Cell. 2005;9:389-402. doi: 10.1016/j.devcel.2005.08.001.
  16. ^ Enomoto A, Asai N, Namba T, et al. Roles of disrupted-in-schizophrenia 1-interacting protein girdin in postnatal development of the dentate gyrus.Neuron. 2009;63:774-87. doi: 10.1016/j.neuron.2009.08.015.
  17. ^ "Princess Takamatsu Cancer Research Fundprincess Takamatsu Cancer Research Fundprincess Takamatsu Cancer Research Fund".
  18. ^ "Nagoya University Awards".


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