The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
FcRγ Activation Regulates Inflammation-Associated Squamous Carcinogenesis
Open accessAbstract
SUMMARY Chronically activated leukocytes recruited to premalignant tissues functionally contribute to cancer development; however, mechanisms underlying pro- versus anti-tumor programming of neoplastic tissues by immune cells remain obscure. Using the K14-HPV16 mouse model of squamous carcinogenesis, we report that B cells and humoral immunity foster cancer development by activating Fcγ receptors (FcγRs) on resident and recruited myeloid cells. Stromal accumulation of autoantibodies in premalignant skin, through their interaction with activating FcγRs, regulate recruitment, composition, and bioeffector functions of leukocytes in neoplastic tissue, which in turn promote neoplastic progression and subsequent carcinoma development. These findings support a model in which B cells, humoral immunity, and activating FcγRs are required for establishing chronic inflammatory programs that promote de novo carcinogenesis.
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
Mantovani, A., Allavena, P., Sica, A., & Balkwill, F. (2008) · Nature · doi:10.1038/nature07205 · Cited by 11,399
Fcγ receptors as regulators of immune responses
Nimmerjahn, F., & Ravetch, J. V. (2008) · Nature Reviews Immunology · doi:10.1038/nri2206 · Cited by 2,947
MMP-9 Supplied by Bone Marrow–Derived Cells Contributes to Skin Carcinogenesis
Coussens, L. M., Tinkle, C. L., Hanahan, D., & Werb, Z. (2000) · Cell · doi:10.1016/s0092-8674(00)00139-2 · Cited by 1,306
Self-citationInflammatory mast cells up-regulate angiogenesis during squamous epithelial carcinogenesis
Coussens, L. M., Raymond, W. W., Bergers, G., Laig-Webster, M., Behrendtsen, O., Werb, Z., Caughey, G. H., & Hanahan, D. (1999) · Genes & Development · doi:10.1101/gad.13.11.1382 · Cited by 946 · cited 7×
“FcγRIII+ mast cells regulate tissue remodeling, angiogenesis, and keratinocyte hyperproliferation in HPV16 mice (Coussens et al., 1999; Coussens et al., 2000), thus we evaluated whether FcRγ-dependent activation of mast cells was in part necessary for neoplastic progression.”
InfluentialSelf-citation“Re-educating” tumor-associated macrophages by targeting NF-κB
Hagemann, T., Lawrence, T., McNeish, I., Charles, K. A., Kulbe, H., Thompson, R. G., Robinson, S. C., & Balkwill, F. R. (2008) · The Journal of Experimental Medicine · doi:10.1084/jem.20080108 · Cited by 792
Cited by
Immunity, Inflammation, and Cancer
Grivennikov, S. I., Greten, F. R., & Karin, M. (2010) · Cell · doi:10.1016/j.cell.2010.01.025 · Cited by 10,755
Macrophage plasticity and polarization: in vivo veritas
Sica, A., & Mantovani, A. (2012) · Journal of Clinical Investigation · doi:10.1172/jci59643 · Cited by 6,335
Protective and pathogenic functions of macrophage subsets
Murray, P. J., & Wynn, T. A. (2011) · Nature Reviews Immunology · doi:10.1038/nri3073 · Cited by 5,269
The immune contexture in human tumours: impact on clinical outcome
Fridman, W. H., Pagès, F., Sautès-Fridman, C., & Galon, J. (2012) · Nature reviews. Cancer · doi:10.1038/nrc3245 · Cited by 4,981
Alternative activation of macrophages: mechanism and functions
Gordon, S., & Martinez, F. O. (2010) · Immunity · doi:10.1016/j.immuni.2010.05.007 · Cited by 4,197
Metadata
- Authors
- Andreu, P., Johansson, M., Affara, N. I., Pucci, F., Tan, T., Junankar, S., Korets, L., Lam, J., Tawfik, D., DeNardo, D. G., Naldini, L., de Visser, K. E., De Palma, M., & Coussens, L. M.
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2010-02
- Volume
- 17
- Issue
- 2
- Pages
- 121-134
- ISSN
- 1535-6108 (ISSN-L)
- OpenAlex
- W2130085747
- Cited by
- 590
- References
- 5
- FWCI
- 20.49
- 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: FcRγ Activation Regulates Inflammation-Associated Squamous Carcinogenesis. https://app.cochat.ai/papers/10.1016/j.ccr.2009.12.019
- The paper
- Andreu, P., Johansson, M., Affara, N. I., Pucci, F., Tan, T., Junankar, S., Korets, L., Lam, J., Tawfik, D., DeNardo, D. G., Naldini, L., de Visser, K. E., De Palma, M., & Coussens, L. M. (2010). FcRγ Activation Regulates Inflammation-Associated Squamous Carcinogenesis. Cancer Cell. https://doi.org/10.1016/j.ccr.2009.12.019
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.