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2012.02.27 20:16

March KSEA-SD bioseminar

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KSEA-SD bioseminar (9th of March, Friday)

Dear all Korean bioscientists in San Diego,
Please mark your calendar down for the KSEA-SD bioseminar.
When: 11:50AM - 1PM, March 9th (Friday)
Where: TSRI CB107
Speaker: Jung-whan Kim, D.V.M., PhD. Randall S. Johnson's lab at UCSD
Title: Stromal Fibroblast HIF-1 Signaling in Mammary Tumorigenesis
As always, we will be serving lunch and refreshments and in addition we will continue the raffle drawing for a gift card out of the people on the sign-up sheet.
KSEA-SD seminar series are kindly supported by KSEA-SD chapter, Imgenex, and BMS Korea.  
The following is the link for BMS-Korea :
If you need more information, please visit website and contact to 오수림 부사장님 at BMS-Korea ( 
Here is the IMGENEX March's promotion info, and the following is the link: 
If you have further question, please contact to Dr. Hyun Ku Lee at Imgenex :
On behalf of all members, I'd like to thank all our supporters.
Best regards,
Hong Sook Kim

Stromal Fibroblast HIF-1 Signaling in Mammary


Solid tumors consist of malignant cells and
associated stromal cells including fibroblasts, endothelial cells, inflammatory


cells and adipocytes. Tumor-associated stromal alterations are integral components of the tumor microenvironment that contribute to tumor growth and progression. Stromal fibroblastic cells are prominent cell populations of the tumor microenvironment and have been implicated in the development of various cancers including breast cancer. Tumor fibrosis and chaotic vascularization contribute to the low oxygen tension, or hypoxia, frequently found in advanced tumors. Although functional roles of hypoxic responses in malignant cells have been intensively investigated in a number of pre-clinical and experimental studies, how tumor-associated fibroblast hypoxic signaling contributes to the process of tumorigenesis is poorly understood.

   Using a fibroblast-specific promoter-Cre (Fsp1-cre), key aspects of the genetic network regulating hypoxic response were removed from tumor stromal fibroblasts, including the VHL, HIF-1α and VEGF-A genes. It was found that loss of HIF-1α and its target gene VEGF-A altered tumor progression in a mammary cancer model, accelerating tumor growth while normalizing tumor vasculature and reducing myeloid cell infiltration. This was correlated with improved blood perfusion and tumor oxygenation in the mutant tumors, and indicates that fibroblast HIF-1 response is a critical component of tumor vascularization.

   These findings identify HIF-1/VEGF-mediated hypoxic signaling in stromal fibroblasts as a crucial mediator of tumor progression. Aberrant tumor vascularization reduces perfusion and oxygenation of tumors, which in turn inhibits chemo- and radiation therapy. Ablation of Hif-1α or Vegf in stromal fibroblasts induces vascular normalization and increase tumor oxygenation, which indicate that these cells and this pathway could be important target for combination treatment to improved therapeutic efficacy.

   Future research plan to be presented seeks to (i) evaluate fibroblast hypoxic signaling as a potentially important adjunct to chemo- and radiation therapeutic regimens for breast and other types of cancer; (ii) to characterize the impact of targeting tumor-associated fibroblasts on tumorigenesis and treatment response; (iii) to investigate mechanisms of adipocyte-mediated pro-tumorigenic action and the link between obesity and cancer risk and progression.


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