Our Science

Chih-Chi Andrew Hu, Ph.D.

Chih-Chi Andrew Hu, Ph.D.

  • Associate Professor, Translational Tumor Immunology Program
  • 215-495-6976, office
Summary

The research interests of the Hu lab include the analysis of the mechanisms of B cell development and B cell cancer formation. We investigate endoplasmic reticulum-associated stress signaling molecules, which play important roles in the quality control of secretory and integral membrane proteins. We are especially interested in knowing how B cell cancers employ these signaling molecules to work in favor of their survival, spreading and chemoresistance in response to therapies. These signaling molecules may also play a role in tumor development in other organs, and are being evaluated in melanoma and other tumor types. We take biochemical, cell biological, and immunological approaches to study these questions in mouse tumor models and human cancer cells.

Selected Publications

1. Zhao C, Brown RSH, Tang CHA, Hu CCA, and Schlieker C. Site-specific proteolysis mobilizes Torsin A from the membrane of the endoplasmic reticulum in response to ER stress and B cell stimulation. J. Biol. Chem. 2016 Apr. 29; 291(18): 9469-9481.

2. Tang CHA, Zundell JA, Ranatunga S, Lin C, Nefedova Y, Del Valle JR, and Hu CCA. Agonist-mediated activation of STING induces apoptosis in malignant B cells. Cancer Res. 2016 Apr. 15; 76(8): 2137-2152.

3. Tang CHA, Ranatunga S, Kriss CL, Cubitt CL, Tao J, Pinilla-Ibarz JA, Del Valle JR, and Hu CCA. Inhibition of ER stress-associated IRE-1/XBP-1 pathway reduces leukemic cell survival. J. Clin. Invest. 2014 Jun. 2; 124(6): 2585-2598.

4. Ranatunga S, Tang CHA, Kang CW, Kriss CL, Kloppenburg BJ, Hu CCA, and Del Valle JR. Synthesis of novel tricyclic chromenone-based inhibitors of IRE-1 RNase activity. J. Med. Chem. 2014 May 22; 57(10): 4289-4301.

5. Kriss CL, Pinilla-Ibarz JA, Mailloux AW, Powers JJ, Tang CHA, Kang CW, Zanesi N, Epling-Burnette PK, Sotomayor EM, Croce CM, Del Valle JR, and Hu CCA. Overexpression of TCL1 activates the endoplasmic reticulum stress response: a novel mechanism of leukemic progression in mice. Blood. 2012 Aug. 2; 120(5): 1027-1038.