The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
STAT3 SIGNALING: Anticancer Strategies and Challenges
Open accessAbstract
Multiple lines of evidence place STAT3 at a central node in the development, progression, and maintenance of many human tumors, and STAT3 has been validated as an anti-cancer target in several contexts. STAT3 modulates the transcription of a variety of genes involved in the regulation of critical functions, including cell differentiation, proliferation, apoptosis, angiogenesis, metastasis, and immune responses. For many cancers, elevated levels of activated STAT3 have been associated with a poor prognosis. We review approaches that have been pursued to target STAT3, and we highlight some of the promises and challenges associated with developing an anticancer drug that might therapeutically inhibit the STAT3 signaling pathway.
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
Principles of interleukin (IL)-6-type cytokine signalling and its regulation
HEINRICH, P. C., BEHRMANN, I., HAAN, S., HERMANNS, H. M., MÜLLER-NEWEN, G., & SCHAPER, F. (2003) · Biochemical Journal · doi:10.1042/bj20030407 · Cited by 3,272 · cited 11×
“STAT3 is structurally typical of the STAT family: an N-terminal coiled-coiled domain involved in protein–protein interactions; a DNA binding domain; a Src homology-2 (SH-2) domain; and a C-terminal transactivation domain (5, 22).”
BackgroundInfluentialInterleukin-6-type cytokine signalling through the gp130/Jak/STAT pathway
HEINRICH, P. C., BEHRMANN, I., MÜLLER-NEWEN, G., SCHAPER, F., & GRAEVE, L. (1998) · Biochemical Journal · doi:10.1042/bj3340297 · Cited by 2,130
Inhibitors of Cytokine Signal Transduction
Wormald, S., & Hilton, D. J. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.r300030200 · Cited by 440
STAT3 nuclear import is independent of tyrosine phosphorylation and mediated by importin-α3
Liu, L., McBride, K. M., & Reich, N. C. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0501643102 · Cited by 348
Nucleocytoplasmic shuttling of persistently activated STAT3
Herrmann, A., Vogt, M., Mönnigmann, M., Clahsen, T., Sommer, U., Haan, S., Poli, V., Heinrich, P. C., & Müller-Newen, G. (2007) · Journal of Cell Science · doi:10.1242/jcs.03482 · Cited by 94
Cited by
The Role of Resveratrol in Cancer Therapy
Ko, J.-H., Sethi, G., Um, J.-Y., Shanmugam, M. K., Arfuso, F., Kumar, A. P., Bishayee, A., & Ahn, K. S. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18122589 · Cited by 800
STAT3 regulates arginase-I in myeloid-derived suppressor cells from cancer patients
Vasquez-Dunddel, D., Pan, F., Zeng, Q., Gorbounov, M., Albesiano, E., Fu, J., Blosser, R. L., Tam, A. J., Bruno, T., Zhang, H., et al. (2013) · Journal of Clinical Investigation · doi:10.1172/jci60083 · Cited by 507
Crescenzo, R., Abate, F., Lasorsa, E., Tabbo’, F., Gaudiano, M., Chiesa, N., Di Giacomo, F., Spaccarotella, E., Barbarossa, L., Ercole, E., et al. (2015) · Cancer Cell · doi:10.1016/j.ccell.2015.03.006 · Cited by 443
The role of JAK-STAT signaling within the CNS
Nicolas, C. S., Amici, M., Bortolotto, Z. A., Doherty, A., Csaba, Z., Fafouri, A., Dournaud, P., Gressens, P., Collingridge, G. L., & Peineau, S. (2013) · JAK-STAT · doi:10.4161/jkst.22925 · Cited by 351
Cancer Immunotherapy by Targeting IDO1/TDO and Their Downstream Effectors
Platten, M., von Knebel Doeberitz, N., Oezen, I., Wick, W., & Ochs, K. (2015) · Frontiers in Immunology · doi:10.3389/fimmu.2014.00673 · Cited by 340
Metadata
- Authors
- Johnston, P. A., & Grandis, J. R.
- Venue
- Molecular Interventions
- Publisher
- CLOCKSS Archive
- Published
- 2011-02-01
- Volume
- 11
- Issue
- 1
- Pages
- 18-26
- ISSN
- 1534-0384 (ISSN-L)
- OpenAlex
- W1991013609
- Cited by
- 406
- References
- 5
- FWCI
- 11.17
- Type
- journal article
- Language
- en
- Open access
- green
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: STAT3 SIGNALING: Anticancer Strategies and Challenges. https://app.cochat.ai/papers/10.1124/mi.11.1.4
- The paper
- Johnston, P. A., & Grandis, J. R. (2011). STAT3 SIGNALING: Anticancer Strategies and Challenges. Molecular Interventions. https://doi.org/10.1124/mi.11.1.4
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.
