W S Dalton

Overexpression of a dominant-negative signal transducer and activator of transcription 3 variant in tumor cells leads to production of soluble factors that induce apoptosis and cell cycle arrest.

R. Jove, G. Niu, W. Dalton, 2001, Cancer research.

The tumor microenvironment as a determinant of cancer cell survival: a possible mechanism for de novo drug resistance

W. Dalton, K. Shain, T. Landowski, 2000, Current opinion in oncology.

STAT proteins as novel targets for cancer therapy. Signal transducer an activator of transcription.

R. Jove, W. Dalton, W S Dalton, 1999, Current opinion in oncology.

Breast cancer resistance protein is localized at the plasma membrane in mitoxantrone- and topotecan-resistant cell lines.

J. Schellens, W. Dalton, J. Allen, 2000, Cancer research.

Expression of cytokeratin confers multiple drug resistance.

W. Dalton, A. Cress, J. Anderson, 1994, Proceedings of the National Academy of Sciences of the United States of America.

The clinical relevance of multidrug resistance.

W. Dalton, R. Dorr, W S Dalton, 1990, Cancer investigation.

Synergistic inhibition by verapamil and quinine of P-glycoprotein-mediated multidrug resistance in a human myeloma cell line model.

W. Dalton, M. Lehnert, D. Roe, 1991, Blood.

Dysregulation of CD95/CD95 ligand-apoptotic pathway in CD3(+) large granular lymphocyte leukemia.

J. H. Liu, Jin Hong Liu, W. Dalton, 1998, Blood.

Atypical multidrug resistance: breast cancer resistance protein messenger RNA expression in mitoxantrone-selected cell lines.

M Dietel, M. Dietel, W. Dalton, 1999, Journal of the National Cancer Institute.