S. K. Dissanayake

发表

Resistance to Metastatic Disease in STAT6-Deficient Mice Requires Hemopoietic and Nonhemopoietic Cells and Is IFN-γ Dependent1

J. Berzofsky, S. Ostrand-Rosenberg, M. Terabe, 2002, The Journal of Immunology.

Activation of Tumor-specific CD4+ T Lymphocytes by Major Histocompatibility Complex Class II Tumor Cell Vaccines

Peter W. Chen, B. Ksander, S. Ostrand-Rosenberg, 2004, Cancer Research.

The Wnt5A/Protein Kinase C Pathway Mediates Motility in Melanoma Cells via the Inhibition of Metastasis Suppressors and Initiation of an Epithelial to Mesenchymal Transition*

M. Bittner, J. Trent, R. Moon, 2007, Journal of Biological Chemistry.

Wnt5A regulates expression of tumor-associated antigens in melanoma via changes in signal transducers and activators of transcription 3 phosphorylation.

Stephen M Hewitt, Kyle J Hewitt, V. Sondak, 2008, Cancer research.

The Orphan Tyrosine Kinase Receptor, ROR2, Mediates Wnt5A Signaling in Metastatic Melanoma

Arnell Carter, A. Weeraratna, D. Taub, 2009, Oncogene.

Tumor cells transduced with the MHC class II Transactivator and CD80 activate tumor-specific CD4+ T cells whether or not they are silenced for invariant chain.

B. Ksander, K. Knutson, M. Disis, 2006, Cancer research.

Claudin-1 overexpression in melanoma is regulated by PKC and contributes to melanoma cell motility

P. Meltzer, A. Weeraratna, D. Taub, 2006, Oncogene.

Presentation of Endogenously Synthesized MHC Class II-Restricted Epitopes by MHC Class II Cancer Vaccines Is Independent of Transporter Associated with Ag Processing and the Proteasome1

S. Ostrand-Rosenberg, S. K. Dissanayake, Natalia Tuera, 2005, The Journal of Immunology.

Antagonists of tumor-specific immunity: tumor-induced immune suppression and host genes that co-opt the anti-tumor immune response.

P. Sinha, S. Ostrand-Rosenberg, S. K. Dissanayake, 2004, Breast disease.

Detecting PKC phosphorylation as part of the Wnt/calcium pathway in cutaneous melanoma.

A. Weeraratna, S. K. Dissanayake, 2008, Methods in molecular biology.