ArticleCancer immunology, immunotherapy : CII2007
In situ expression of IFN-gamma-inducible T cell alpha chemoattractant in breast cancer mounts an enhanced specific anti-tumor immunity which leads to tumor regression.
Article in Cancer immunology, immunotherapy : CII, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- C-X-C ligand 10 and C-X-C receptor 3 status can predict tamoxifen treatment response in breast cancer patients.Breast cancer research and treatment · 2014Trial
- The trifunctional antibody catumaxomab amplifies and shapes tumor-specific immunity when applied to gastric cancer patients in the adjuvant setting.Human vaccines & immunotherapeutics · 2013Trial
- Immunomodulatory potential of natural products from herbal medicines as immune checkpoints inhibitors: Helping to fight against cancer via multiple targets.Medicinal research reviews · 2022Review
- CXCL11 Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2021Review
- The paramount role of cytokines and chemokines in papillary thyroid cancer: a review and experimental results.Immunologic research · 2018Review
- Identification of a gene expression signature associated with the metastasis suppressor function of NME1: prognostic value in human melanoma.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Delivery of interleukin-15 to B16 melanoma by electroporation leads to tumor regression and long-term survival.Technology in cancer research & treatment · 2014Article
- CXCR3 deficiency enhances tumor progression by promoting macrophage M2 polarization in a murine breast cancer model.Immunology · 2014Article
- Chemokine receptor trio: CXCR3, CXCR4 and CXCR7 crosstalk via CXCL11 and CXCL12.Cytokine & growth factor reviews · 2013Review
- Modulation of CXCR3 ligand secretion by prostaglandin E2 and cyclooxygenase inhibitors in human breast cancer.Breast cancer research : BCR · 2012Article
- CXCR7/CXCR4 heterodimer constitutively recruits beta-arrestin to enhance cell migration.The Journal of biological chemistry · 2011Article
- Chemokine receptor CXCR3 promotes growth of glioma.Carcinogenesis · 2011Article
- Integrating individual functional moieties of CXCL10 and CXCL11 into a novel chimeric chemokine leads to synergistic antitumor effects: a strategy for chemokine-based multi-target-directed cancer therapy.Cancer immunology, immunotherapy : CII · 2010Article
- Decreased expression of miR-125b and miR-100 in oral cancer cells contributes to malignancy.Genes, chromosomes & cancer · 2009Article
- The Role of CXCL11 and its Receptors in Cancer: Prospective but Challenging Clinical Targets.Cancer control : journal of the Moffitt Cancer CenterReview
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased evidence indicates that chemokines are involved in tumor growth. ITAC, a key member of chemokines, possesses the ability to recruit T cells and enhance immune responses. Therefore, ITAC might contribute to antitumor immunity. In this study, we evaluated the relationship between the expression of ITAC and human breast cancer advancement. We further investigated whether forced expression of ITAC in tumor sites could mediate enhanced antitumor immunity in a murine breast cancer model. Results showed that ITAC expression level was down-regulated in 31 breast cancer specimens compared to normal mammary tissues, and associated negatively with the stages of breast cancer. Contrarily, forced expression of ITAC in murine 4T1 tumor cells resulted in tumor regression after initial growth upon injection into naïve Balb/c mice. More lymphocytes were recruited to the site of tumor inoculated by 4T1-ITAC and more than 80% of these T cells expressed the ITAC receptor, CXCR3. ITAC-recruited TILs exhibited 4T1-specific proliferation and cytotoxicity, and an increased IFN-gamma but decreased IL-4 production. Importantly, forced expression of ITAC in 4T1 tumor nodules inhibited tumor growth. These findings demonstrated that the decreased expression of ITAC is associated with the advancement of breast cancer in patients. Forced expression of ITAC in tumor site not only induces increased T cell-recruitment and elicits a specific antitumor immunity, but also mediates regression of established 4T1 tumors, indicating the potential application of ITAC-expressing tumor cells in cancer immunotherapy and vaccine designing.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.