Urban Lendahl

Urban Lendahl

Professor
E-postadress: urban.lendahl@ki.se
Besöksadress: Solnavägen 9, 17165 Stockholm
Postadress: C5 Cell- och molekylärbiologi, C5 CMB Lendahl, 171 77 Stockholm
Del av:

Om mig

  • Professor i genetik.

Forskningsbeskrivning

  • Notch-signalering, cancerbiologi, vaskulärbiologi, utvecklingsbiologi

Artiklar

Alla övriga publikationer

Forskningsbidrag

  • Consequences of misregulated Notch signaling in breast cancer
    Swedish Cancer Society
    1 January 2015
    Breast cancer, with 7,000 new patients annually, despite improved treatment, continues to pose a major medical problem, and there are many aspects of breast cancer that we do not yet understand. In recent years, it has become increasingly apparent that an important signaling mechanism called Notch signaling is often misregulated in breast cancer. This is evident, among other things, through a connection between high Notch signaling and poor prognosis for the patient. Notch signaling is important for most of the body's organs and tissues that develop normally, but when it is mutated or expressed at too high a level, this can lead to cancer. Increased Notch signaling is linked to breast cancer, and we want to understand the role this plays in several important stages of the tumor process. In this application, we want to find out how Notch in animal models can initiate breast cancer, and what other genes are involved in this. We also want to understand how Notch affects the interaction between tumor and surrounding stroma tissue. Finally, we also want to learn more about how Notch signaling interacts with other important signaling pathways in the tumor cells, inter alia with the mechanism that handles situations with low oxygen pressure in the tissue, which often occurs in tumors. The overall and long-term aim of the project is to be able to contribute to developing new and improved therapies for breast cancer. It is becoming increasingly clear that misregulated Notch signaling contributes to breast cancer, and we focus our research on understanding how this error regulation leads both to tumor emergence and how the tumor interacts with and benefits from surrounding tissue. We also hope to contribute to the development of principles for new combination treatments where at the same time you counter Notch signaling and other signal mechanisms to obtain a better and more specific treatment for breast cancer.
  • Consequences of misregulated Notch signaling in breast cancer
    Swedish Cancer Society
    1 January 2014
    Breast cancer, with 7,000 new patients annually, despite improved treatment, continues to pose a major medical problem, and there are many aspects of breast cancer that we do not yet understand. In recent years, it has become increasingly apparent that an important signaling mechanism called Notch signaling is often misregulated in breast cancer. This is evident, among other things, through a connection between high Notch signaling and poor prognosis for the patient. Notch signaling is important for most of the body's organs and tissues that develop normally, but when it is mutated or expressed at too high a level, this can lead to cancer. Increased Notch signaling is linked to breast cancer, and we want to understand the role this plays in several important stages of the tumor process. In this application, we want to find out how Notch in animal models can initiate breast cancer, and what other genes are involved in this. We also want to understand how Notch affects the interaction between tumor and surrounding stroma tissue. Finally, we also want to learn more about how Notch signaling interacts with other important signaling pathways in the tumor cells, inter alia with the mechanism that handles situations with low oxygen pressure in the tissue, which often occurs in tumors. The overall and long-term aim of the project is to be able to contribute to developing new and improved therapies for breast cancer. It is becoming increasingly clear that misregulated Notch signaling contributes to breast cancer, and we focus our research on understanding how this error regulation leads both to tumor emergence and how the tumor interacts with and benefits from surrounding tissue. We also hope to contribute to the development of principles for new combination treatments where at the same time you counter Notch signaling and other signal mechanisms to obtain a better and more specific treatment for breast cancer.
  • Swedish Research Council
    1 January 2014 - 31 December 2018
  • Swedish Research Council
    1 January 2014 - 31 December 2018
  • Knut and Alice Wallenberg Foundation
    1 January 2013 - 1 January 2016
  • Swedish Research Council
    1 January 2013 - 31 December 2015
  • Swedish Research Council
    1 January 2011 - 31 December 2013
  • Swedish Research Council
    1 July 2009 - 30 June 2014

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