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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
MasahideTakahashi
Born (1954-11-18) November 18, 1954 (age 70)
Alma materNagoya University
Scientific career
FieldsPathology

Biography

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Masahide Takahashi is a Japanese pathologist and oncologist. He is a Professor Emeritus of Nagoya University, and Designated Professor of International Center for Cell and Gene Therapy, Fujita Health University in Japan.

[1] [2] [3] His pioneering work is the discovery of the RET proto-oncogene that plays a crucial role in cancer and development. [3] [4] [5]

Education

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Takahashi was born in Japan in 1954. He acquired his degree in M.D. from Nagoya University School of Medicine in 1979, followed by Ph.D. from the same university in 1983. [1] [2] [3]

Carrier and research

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After completing his Ph.D., Takahashi took a position at Dana-Farber Cancer Institute and Harvard Medical School in Boston. He served at the institute as a Research Fellow for two years and half (1983 and 1985), where he discovered the RET oncogene. [4] [5] He became a 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. [1] [2] [3] Takahashi’s research group has studied physiological and pathological roles of the RET protooncogene in cancer and development [5] [6] . 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). His group elucidated the molecular mechanisms of the disease development caused by RET alterations [5] [6] In 1996 and 1997, Takahashi in collaboration with Arnon Rosenthal’s group. (Genentech Inc, USA) discovered that the RET ligand is an equal to neurotrophic factors, glial cell line-derived neurotrophic factor (GDNF) and neurturin [7] [8] . Takahashi extensively studied physiological roles of GDNF/RET signaling in the development of the enteric nervous system and kidney as well as spermatogenesis [9] .
Following the functional analysis of the RET protooncogene, the alliance then worked upon molecular mechanism of cell motility, through which discovered a new actin-binding protein called Girdin which turned out to have a crucial role in motility of cancer cells and neuronal cells that are responsible for cancer invasion and metastasis, and neurogenesis. [10] [11]

Awards and honors

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He received The Japan Pathology Award from the Japanese Society of Pathology in 2001. [3] In 2019, Medical Award of The Japan Medical Association was given to Takahashi. [3] In 2020, he was awarded Princess Takamatsu Cancer Research Fund Prize, [12] and Medal of Honour (Medal with Purple Ribbon) from the Japanese Geovernment [13] for his seminal work on the RET proto-oncogene.


Footnote

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  1. ^ a b c Masahide Takahashi: researchmap https://researchmap.jp/masa1118?lang=en
  2. ^ a b c Masahide Takahashi: ORCID https://orcid.org/0000-0002-2803-2683
  3. ^ a b c d e f RET gene :”the” thyroid oncogene, The story of the RET oncogene from discovery to inhibitor development. The Thyroidologist, issue 5, summer 2024https://www.eurothyroid.com/public/thyroidologist.html
  4. ^ a b 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
  5. ^ a b c d 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
  6. ^ a b 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
  7. ^ 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
  8. ^ 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
  9. ^ 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
  10. ^ 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.
  11. ^ 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;63:774-787. doi: 10.1016/j.neuron.2009.08.015.
  12. ^ Princess Takamatsu Cancer Research Fund http://www.ptcrf.or.jp/english/index.html#prize
  13. ^ Recipients of the 2020 Autumn Conferment of Japanese Orders and Medals of Honor Announced https://en.nagoya-u.ac.jp/awards/recipients_of_the_2020_autumn_conferment_of_japanese_orders_and_medals_of_honor_announced.html


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