The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Inhibition of interleukin-8 reduces tumorigenesis of human non-small cell lung cancer in SCID mice.
Open accessAbstract
The salient feature of solid tumor growth is the strict dependence on local angiogenesis. We have previously demonstrated that IL-8 is an angiogenic factor present in freshly isolated specimens of human non-small cell lung cancer (NSCLC). Using a model of human NSCLC tumorigenesis in SCID mice, we now report that IL-8 acts as a promoter of human NSCLC tumor growth through its angiogenic properties. Passive immunization with neutralizing antibodies to IL-8 resulted in more than 40% reduction in tumor size and was associated with a decline in tumor-associated vascular density and angiogenic activity. IL-8 did not act as an autocrine growth factor for NSCLC proliferation. The reduction in primary tumor size in response to neutralizing antibodies to IL-8 was also accompanied by a trend toward a decrease in spontaneous metastasis to the lung. These data support the notion that IL-8 plays a significant role in mediating angiogenic activity during tumorigenesis of human NSCLC, thereby offering a potential target for immunotherapy against solid tumors.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Kim, K. J., Li, B., Winer, J., Armanini, M., Gillett, N., Phillips, H. S., & Ferrara, N. (1993) · Nature · doi:10.1038/362841a0 · Cited by 3,605
Interleukin-8 as a macrophage-derived mediator of angiogenesis
Koch, A. E., Polverini, P. J., Kunkel, S. L., Harlow, L. A., DiPietro, L. A., Elner, V. M., Elner, S. G., & Strieter, R. M. (1992) · Science · doi:10.1126/science.1281554 · Cited by 2,135
Self-citationInduction of angiogenesis during the transition from hyperplasia to neoplasia
Folkman, J., Watson, K., Ingber, D., & Hanahan, D. (1989) · Nature · doi:10.1038/339058a0 · Cited by 1,879
The Functional Role of the ELR Motif in CXC Chemokine-mediated Angiogenesis
Strieter, R. M., Polverini, P. J., Kunkel, S. L., Arenberg, D. A., Burdick, M. D., Kasper, J., Dzuiba, J., Van Damme, J., Walz, A., Marriott, D., et al. (1995) · Journal of Biological Chemistry · doi:10.1074/jbc.270.45.27348 · Cited by 1,222
Self-citationWalz, A., Burgener, R., Car, B., Baggiolini, M., Kunkel, S. L., & Strieter, R. M. (1991) · The Journal of experimental medicine · doi:10.1084/jem.174.6.1355 · Cited by 353
Self-citation
Cited by
Gerard, C., & Rollins, B. J. (2001) · Nature Immunology · doi:10.1038/84209 · Cited by 1,357
Phenotype and Genotype of Pancreatic Cancer Cell Lines
Deer, E. L., González-Hernández, J., Coursen, J. D., Shea, J. E., Ngatia, J., Scaife, C. L., Firpo, M. A., & Mulvihill, S. J. (2010) · Pancreas · doi:10.1097/mpa.0b013e3181c15963 · Cited by 936
Chemokines and Their Receptors in the Central Nervous System
Bajetto, A., Bonavia, R., Barbero, S., Florio, T., & Schettini, G. (2001) · Frontiers in Neuroendocrinology · doi:10.1006/frne.2001.0214 · Cited by 416
Arenberg, D. A., Keane, M. P., DiGiovine, B., Kunkel, S. L., Morris, S. B., Xue, Y. Y., Burdick, M. D., Glass, M. C., Iannettoni, M. D., & Strieter, R. M. (1998) · Journal of Clinical Investigation · doi:10.1172/jci3145 · Cited by 259
Self-citationNeutrophils: important contributors to tumor progression and metastasis
Swierczak, A., Mouchemore, K. A., Hamilton, J. A., & Anderson, R. L. (2015) · Cancer and Metastasis Reviews · doi:10.1007/s10555-015-9594-9 · Cited by 220
Metadata
- Authors
- Arenberg, D. A., Kunkel, S. L., Polverini, P. J., Glass, M., Burdick, M. D., & Strieter, R. M.
- Venue
- Journal of Clinical Investigation
- Published
- 1996-06-15
- Volume
- 97
- Issue
- 12
- Pages
- 2792-2802
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2056088187
- Cited by
- 403
- References
- 5
- FWCI
- 6.80
- Type
- journal article
- Language
- en
- Open access
- bronze
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Inhibition of interleukin-8 reduces tumorigenesis of human non-small cell lung cancer in SCID mice. https://app.cochat.ai/papers/10.1172/jci118734
- The paper
- Arenberg, D. A., Kunkel, S. L., Polverini, P. J., Glass, M., Burdick, M. D., & Strieter, R. M. (1996). Inhibition of interleukin-8 reduces tumorigenesis of human non-small cell lung cancer in SCID mice. Journal of Clinical Investigation. https://doi.org/10.1172/jci118734
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
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.
