The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.
Complete responses of relapsed lymphoma following genetic modification of tumor-antigen presenting cells and T-lymphocyte transfer
Open accessAbstract
Epstein-Barr virus (EBV)–associated tumors developing in immunocompetent individuals present a challenge to immunotherapy, since they lack expression of immunodominant viral antigens. However, the tumors consistently express viral proteins including LMP2, which are immunologically “weak” but may nonetheless be targets for immune T cells. We previously showed that a majority of cytotoxic T lymphocytes (CTLs) reactivated using EBV-transformed B-lymphoblastoid cells lines (LCLs) contained minor populations of LMP2-specific T cells and homed to tumor sites. However, they did not produce remissions in patients with bulky disease. We have now used gene transfer into antigen-presenting cells (APCs) to augment the expression and immunogenicity of LMP2. These modified APCs increased the frequency of LMP2-specific CTLs by up to 100-fold compared with unmodified LCL-APCs. The LMP2-specific population expanded and persisted in vivo without adverse effects. Nine of 10 patients treated in remission of high-risk disease remain in remission, and 5 of 6 patients with active relapsed disease had a tumor response, which was complete in 4 and sustained for more than 9 months. It is therefore possible to generate immune responses to weak tumor antigens by ex vivo genetic modification of APCs and the CTLs so produced can have substantial antitumor activity. This study is registered at http://www.cancer.gov/clinicaltrials (protocol IDs: BCM-H-9936, NCT00062868, NCT00070226).
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Cites
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Cited by
Savoldo, B., Ramos, C. A., Liu, E., Mims, M. P., Keating, M. J., Carrum, G., Kamble, R. T., Bollard, C. M., Gee, A. P., Mei, Z., et al. (2011) · Journal of Clinical Investigation · doi:10.1172/jci46110 · Cited by 1,023
Self-citationER Stress Sensor XBP1 Controls Anti-tumor Immunity by Disrupting Dendritic Cell Homeostasis
Cubillos-Ruiz, J. R., Silberman, P. C., Rutkowski, M. R., Chopra, S., Perales-Puchalt, A., Song, M., Zhang, S., Bettigole, S. E., Gupta, D., Holcomb, K., et al. (2015) · Cell · doi:10.1016/j.cell.2015.05.025 · Cited by 933
Paths to stemness: building the ultimate antitumour T cell
Gattinoni, L., Klebanoff, C. A., & Restifo, N. P. (2012) · Nature Reviews Cancer · doi:10.1038/nrc3322 · Cited by 599
Di Stasi, A., De Angelis, B., Rooney, C. M., Zhang, L., Mahendravada, A., Foster, A. E., Heslop, H. E., Brenner, M. K., Dotti, G., & Savoldo, B. (2009) · Blood · doi:10.1182/blood-2009-03-209650 · Cited by 533
Self-citationBollard, C. M., Gottschalk, S., Torrano, V., Diouf, O., Ku, S., Hazrat, Y., Carrum, G., Ramos, C., Fayad, L., Shpall, E. J., et al. (2014) · Journal of Clinical Oncology · doi:10.1200/jco.2013.51.5304 · Cited by 503
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Metadata
- Authors
- Bollard, C. M., Gottschalk, S., Leen, A. M., Weiss, H., Straathof, K. C., Carrum, G., Khalil, M., Wu, M.-F., Huls, M. H., Chang, C.-C., Gresik, M. V., Gee, A. P., Brenner, M. K., Rooney, C. M., & Heslop, H. E.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2007-10-15
- Volume
- 110
- Issue
- 8
- Pages
- 2838-2845
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W1975615991
- Cited by
- 278
- References
- 33
- FWCI
- 9.43
- Type
- journal article
- Language
- en
- Open access
- green
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- Bollard, C. M., Gottschalk, S., Leen, A. M., Weiss, H., Straathof, K. C., Carrum, G., Khalil, M., Wu, M.-F., Huls, M. H., Chang, C.-C., Gresik, M. V., Gee, A. P., Brenner, M. K., Rooney, C. M., & Heslop, H. E. (2007). Complete responses of relapsed lymphoma following genetic modification of tumor-antigen presenting cells and T-lymphocyte transfer. Blood. https://doi.org/10.1182/blood-2007-05-091280
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
