Person:
Huang, Yu-Hwa

Profile Picture

Email Address

AA Acceptance Date

Birth Date

Research Projects

Organizational Units

Job Title

Last Name

Huang

First Name

Yu-Hwa

Name

Huang, Yu-Hwa
Author's Publications: search.filters.isAuthorOfPublication.22b3a71d-8b10-43d3-98ce-33f2f662485c

Search Results

Now showing 1 - 2 of 2
  • Thumbnail Image
    Publication
    CEACAM1 as a multi-purpose target for cancer immunotherapy
    (Taylor & Francis, 2017) Dankner, Matthew; Gray-Owen, Scott D.; Huang, Yu-Hwa; Blumberg, Richard; Beauchemin, Nicole
    ABSTRACT CEACAM1 is an extensively studied cell surface molecule with established functions in multiple cancer types, as well as in various compartments of the immune system. Due to its multi-faceted role as a recently appreciated immune checkpoint inhibitor and tumor marker, CEACAM1 is an attractive target for cancer immunotherapy. Herein, we highlight CEACAM1's function in various immune compartments and cancer types, including in the context of metastatic disease. This review outlines CEACAM1's role as a therapeutic target for cancer treatment in light of these properties.
  • Thumbnail Image
    Publication
    CEACAM1 dampens antitumor immunity by down-regulating NKG2D ligand expression on tumor cells
    (The Rockefeller University Press, 2011) Chen, Zhangguo; Chen, Lanfen; Olszak, Torsten; Zeissig, Sebastian; Kuo, Timothy T.; Mandelboim, Ofer; Beauchemin, Nicole; Lanier, Lewis L.; Baker, Kristi; Huang, Yu-Hwa; Blumberg, Richard
    Although carcinoembryonic antigen (CEA)–related cell adhesion molecule 1 (CEACAM1) has been viewed as a tumor suppressor, increasing clinical evidence shows that high levels of CEACAM1 expression on tumors correlates with poor prognosis and high risk of metastasis. Here, we examined the consequences of CEACAM1 expression on tumor cells. We show that tumor cell–associated CEACAM1 causes intracellular retention of various NKG2D ligands in mouse and human tumor cells. CEACAM1-silenced tumor cells expressed more cell surface NKG2D ligands and exhibited greater sensitivity to natural killer cell–mediated cytolysis in vitro and rejection in vivo. Our studies reveal a novel mechanism through which CEACAM1-bearing tumor cells may escape immune-surveillance.