This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Turturro, F. Articles by Link, C. J. Search for Related Content PubMed PubMed Citation Articles by Turturro, F. Articles by Link, C. J., Jr.

In Vitro Adenoviral Vector p53-mediated Transduction and Killing Correlates with Expression of Coxsackie-Adenovirus Receptor and ß₅ Integrin in SUDHL-1 Cells Derived from Anaplastic Large-Cell Lymphoma¹

Human Gene Therapy Research Institute [F. T., P. S., J. L.], John Stoddard Cancer Center, Iowa Methodist Medical Center, and VA Central Iowa Health Care System, Des Moines, IA [F. T.]

Adenoviral vector-mediated p53 expression induced apoptosis is a well established gene therapy approach that has been evaluated extensively in epithelial tumors but only recently in lymphoid malignancies mainly due to the known resistance of the lymphoid lineage to adenovirus infection. Recently, it was shown that this resistance is not absolute and that cell lines derived from anaplastic large cell lymphoma (ALCL) and some other lymphoid malignancies are efficiently transduced by adenoviral vectors. Normal circulating T lymphocytes do not express coxsackie-adenovirus receptor (CAR) and ß integrins and are relatively resistant to infection by adenovirus. These molecules serve as receptors for adenovirus entry into the cells. ALCL-derived SUDHL-1 cells were evaluated for transduction efficiency and expression of p53 after infection with an adenoviral vector containing wild-type p53 (AdWTp53). Cells derived from ALCL and circulating mononucleated cells (MNCs) were also evaluated for expression of CAR and ß integrins. AdWTp53-mediated expression of p53 resulted in p21/WAF1 induction, G₁ arrest, and apoptosis in SUDHL-1 cells. The expression of CAR and ß₅ integrin was high in SUDHL-1 cells and comparable to levels observed with epithelial tumor cells, but it was absent in MNCs. The susceptibility to adenoviral vector transduction of the tumor-derived cells implies an important biological difference between them and circulating MNCs, possibly underlying the malignant transformation that ALCL cells undergo. Further studies will be required to evaluate this initial observation in more cell lines and tissue derived from ALCL.

This article has been cited by other articles:

				H. Tanaka, T. Shirakawa, Z. Zhang, K. Hamada, A. Gotoh, and K.-i. Nibu A Replication-Selective Adenoviral Vector for Head and Neck Cancers Arch Otolaryngol Head Neck Surg, July 1, 2005; 131(7): 630 - 634. [Abstract] [Full Text] [PDF]

				R. Borenstein, O. Singer, A. Moseri, and N. Frenkel Use of Amplicon-6 Vectors Derived from Human Herpesvirus 6 for Efficient Expression of Membrane-Associated and -Secreted Proteins in T Cells J. Virol., May 1, 2004; 78(9): 4730 - 4743. [Abstract] [Full Text] [PDF]

				C. J. Cohen, Z. Q. Xiang, G.-P. Gao, H. C. J. Ertl, J. M. Wilson, and J. M. Bergelson Chimpanzee adenovirus CV-68 adapted as a gene delivery vector interacts with the coxsackievirus and adenovirus receptor J. Gen. Virol., January 1, 2002; 83(1): 151 - 155. [Abstract] [Full Text] [PDF]

				F. Turturro, M. D. Arnold, A. Y. Frist, and K. Pulford Model of Inhibition of the NPM-ALK Kinase Activity by Herbimycin A Clin. Cancer Res., January 1, 2002; 8(1): 240 - 245. [Abstract] [Full Text] [PDF]

				P. K. Tan, A.-I. Michou, J. M. Bergelson, and M. Cotten Defining CAR as a cellular receptor for the avian adenovirus CELO using a genetic analysis of the two viral fibre proteins J. Gen. Virol., June 1, 2001; 82(6): 1465 - 1472. [Abstract] [Full Text]