Tina Chang Albershardt

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Normalization to a reference gene is the method of choice for quantitative PCR analysis. The stability of reference genes is critical for accurate gene expression analysis, as significant variations in reference gene expression can alter experimental results and conclusions. In this study, we evaluated the expression stability of five commonly used(More)
Our previous studies found that B16-F10 melanoma growth in the rear footpad of immunocompetent mice induces marked B cell accumulation within tumor-draining popliteal lymph nodes (TDLN). This B cell accumulation drives TDLN remodeling that precedes and promotes metastasis, indicating a tumor-promoting role for TDLN B cells. Here we show that phenotypic(More)
We have engineered an integration-deficient lentiviral vector, LV305, to deliver the tumor antigen NY-ESO-1 to human dendritic cells in vivo through pseudotyping with a modified Sindbis virus envelop protein. Mice immunized once with LV305 developed strong, dose-dependent, multifunctional, and cytotoxic NY-ESO-1-specific cluster of differentiation 8 (CD8) T(More)
4005. P299<lb>Phosphopeptides as novel tumor antigens in colorectal cancer<lb>Sarah A Penny, Jennifer G Abelin, Abu Z Saeed, Stacy A Malaker,<lb>Paisley T Myers, Jeffrey Shabanowitz, Stephen T Ward, Donald F<lb>Hunt, Mark Cobbold<lb>University of Birmingham, Birmingham, England, UK; University of<lb>Virginia, Charlottesville, VA, USA; Stanford University,(More)
Tumor-draining lymph nodes (TDLNs) often enlarge in human cancer patients and in murine tumor models, due to lymphocyte accumulation and lymphatic sinus growth. B lymphocytes within TDLNs can drive lymph node hypertrophy in response to tumor growth, however little is known about the mechanisms directing the preferential accumulation of B lymphocytes(More)
Methods B16F10-OVA melanoma bearing C57BL/6 mice were immunized with the lentiviral vector DCVex on 10 days after tumor challenge to induce OVA specific effector and memory CD8 T cells. Mice were then treated 12 days later intratumorally with the TLR4 agonist GLAAS (glucopyranosyl adjuvant system), which induces the T cell homing chemokines CXCL9 and(More)
The clinical efficacy of tumor-specific effector T cells can be limited by their proper trafficking to the site of the tumor and the immunosuppressed local environment. Strategies to improve homing of effector cells to tumors and to enhance activity of these effector cells could further unlock the potential of active cancer immunotherapy. G100 is the(More)
The dysregulation of immune checkpoints by tumors is an important mechanism of immune resistance, as administration of checkpoint inhibitors has resulted in impressive clinical responses in patients with late stage cancers. However, a subset of patients exhibits insufficient or no clinical response presumably due to the absence of tumor-specific cytotoxic T(More)
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