• Refine Query
  • Source
  • Publication year
  • to
  • Language
  • 3
  • Tagged with
  • 3
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

MCL1 inhibition is effective against a subset of small-cell lung cancer with high MCL1 and low BCL-XL expression / MCL1阻害はMCL1高発現/BCL-XL低発現の小細胞肺癌に有効である

Yasuda, Yuto 27 July 2020 (has links)
京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第22688号 / 医博第4632号 / 新制||医||1045(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 武藤 学, 教授 小川 誠司, 教授 溝脇 尚志 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM
2

Resistance to HSP90 inhibition involving loss of MCL1 addiction

Busacca, S., Law, E.W.P., Powley, I.R., Proia, D.A., Sequeira, M., Le Quesne, J., Klabatsa, A., Edwards, J.M., Matchett, K.B., Luo, J.L., Pringle, J.H., El-Tanani, Mohamed, MacFarlane, M., Fennell, D.A. 22 June 2015 (has links)
Yes / Inhibition of the chaperone heat-shock protein 90 (HSP90) induces apoptosis, and it is a promising anti-cancer strategy. The mechanisms underpinning apoptosis activation following HSP90 inhibition and how they are modified during acquired drug resistance are unknown. We show for the first time that, to induce apoptosis, HSP90 inhibition requires the cooperation of multi BH3-only proteins (BID, BIK, PUMA) and the reciprocal suppression of the pro-survival BCL-2 family member MCL1, which occurs via inhibition of STAT5A. A subset of tumour cell lines exhibit dependence on MCL1 expression for survival and this dependence is also associated with tumour response to HSP90 inhibition. In the acquired resistance setting, MCL1 suppression in response to HSP90 inhibitors is maintained; however, a switch in MCL1 dependence occurs. This can be exploited by the BH3 peptidomimetic ABT737, through non-BCL-2-dependent synthetic lethality.
3

Combinatorial Activation of STAT3 by EGF and Thrombin in Endothelial Cells

Waitkus, Matthew S. 10 March 2014 (has links)
No description available.

Page generated in 0.0243 seconds