Chang, S., Parker, S. L., Pham, T., Buzdar, A. U. & Hursting, S. D. Inflammatory breast carcinoma incidence and survival: the Surveillance, Epidemiology, and End Results Program of the National Cancer Institute, 1975–1992. Cancer 82, 2366–2372 (1998).
Hance, K. W., Anderson, W. F., Devesa, S. S., Young, H. A. & Levine, P. H. Trends in inflammatory breast carcinoma incidence and survival: the Surveillance, Epidemiology, and End Results Program at the National Cancer Institute. J. Natl Cancer Inst. 97, 966–975 (2005).
Schlichting, J. A., Soliman, A. S., Schairer, C., Schottenfeld, D. & Merajver, S. D. Inflammatory and non-inflammatory breast cancer survival by socioeconomic position in the Surveillance, Epidemiology, and End Results database, 1990–2008. Breast Cancer Res. Treat. 134, 1257–1268 (2012).
Fouad, T. M. et al. Inflammatory breast cancer: a proposed conceptual shift in the UICC-AJCC TNM staging system. Lancet Oncol. 18, e228–e232 (2017).
Anderson, W. F., Schairer, C., Chen, B. E., Hance, K. W. & Levine, P. H. Epidemiology of inflammatory breast cancer (IBC). Breast Dis. 22, 9–23 (2005).
Boussen, H. et al. Inflammatory breast cancer in Tunisia: epidemiological and clinical trends. Cancer 116, 2730–2735 (2010).
Bonnier, P. et al. Inflammatory carcinomas of the breast: a clinical, pathological, or a clinical and pathological definition? Int. J. Cancer 62, 382–385 (1995).
Manfrin, E. et al. Comparison between invasive breast cancer with extensive peritumoral vascular invasion and inflammatory breast carcinoma: a clinicopathologic study of 161 cases. Am. J. Pathol. 142, 299–306 (2014).
Charpin, C. et al. Inflammatory breast carcinoma: an immunohistochemical study using monoclonal anti-pHER-2/neu, pS2, cathepsin, ER and PR. Anticancer Res. 12, 591–597 (1992).
Lehman, H. L. et al. Modeling and characterization of inflammatory breast cancer emboli grown in vitro. Int. J. Cancer 132, 2283–2294 (2013).
Xiao, Y. et al. The lymphovascular embolus of inflammatory breast cancer exhibits a Notch 3 addiction. Oncogene 30, 287–300 (2011).
Ye, Y. et al. Early to intermediate steps of tumor embolic formation involve specific proteolytic processing of E-cadherin regulated by Rab7. Mol. Cancer Res. 10, 713–726 (2012).
Charafe-Jauffret, E. et al. Aldehyde dehydrogenase 1-positive cancer stem cells mediate metastasis and poor clinical outcome in inflammatory breast cancer. Clin. Cancer Res. 16, 45–55 (2010). This study reports the expression of stem cell markers in IBC and their association with clinical outcome.
Li, J. et al. Triple-negative subtype predicts poor overall survival and high locoregional relapse in inflammatory breast cancer. Oncologist 16, 1675–1683 (2011).
Masuda, H. et al. Long-term treatment efficacy in primary inflammatory breast cancer by hormonal receptor- and HER2-defined subtypes. Ann. Oncol. 25, 384–391 (2014). This is the largest data set to show that the unique aggressive nature of IBC influences overall survival regardless of molecular subtype.
Kertmen, N. et al. Molecular subtypes in patients with inflammatory breast cancer; a single center experience. J. BUON 20, 35–39 (2015).
Parton, M. et al. High incidence of HER-2 positivity in inflammatory breast cancer. Breast 13, 97–103 (2004).
Van der Auwera, I. et al. Integrated miRNA and mRNA expression profiling of the inflammatory breast cancer subtype. Br. J. Cancer 103, 532–541 (2010).
Lehman, H. L. et al. Regulation of inflammatory breast cancer cell invasion through Akt1/PKBalpha phosphorylation of RhoC GTPase. Mol. Cancer Res. 10, 1306–1318 (2012).
Masuda, H. et al. Comparison of molecular subtype distribution in triple-negative inflammatory and non-inflammatory breast cancers. Breast Cancer Res. 15, R112 (2013).
Dawood, S. et al. International expert panel on inflammatory breast cancer: consensus statement for standardized diagnosis and treatment. Ann. Oncol. 22, 515–523 (2011).
Rosso, K. J. et al. Improved locoregional control in a contemporary cohort of nonmetastatic inflammatory breast cancer patients undergoing surgery. Ann. Surg. Oncol. 24, 2981–2988 (2017).
Ross, J. S. et al. Comprehensive genomic profiling of inflammatory breast cancer cases reveals a high frequency of clinically relevant genomic alterations. Breast Cancer Res. Treat. 154, 152–162 (2015).
Morrow, R. J., Etemadi, N., Yeo, B. & Ernst, M. Challenging a misnomer? The role of inflammatory pathways in inflammatory breast cancer. Mediators Inflamm. 2017, 4754827 (2017).
Arora, J. et al. Inflammatory breast cancer tumor emboli express high levels of anti-apoptotic proteins: use of a quantitative high content and high-throughput 3D IBC spheroid assay to identify targeting strategies. Oncotarget 8, 25848–25863 (2017).
S. M., R. et al. Immune and molecular determinants of response to neoadjuvant chemotherapy in inflammatory breast cancer. J. Clin. Oncol. 35, 11501 (2017).
Iwamoto, T. et al. Different gene expressions are associated with the different molecular subtypes of inflammatory breast cancer. Breast Cancer Res. Treat. 125, 785–795 (2011).
Van Laere, S. et al. Distinct molecular phenotype of inflammatory breast cancer compared to non-inflammatory breast cancer using Affymetrix-based genome-wide gene-expression analysis. Br. J. Cancer 97, 1165–1174 (2007).
Van Laere, S. J. et al. Uncovering the molecular secrets of inflammatory breast cancer biology: an integrated analysis of three distinct Affymetrix gene expression datasets. Clin. Cancer Res. 19, 4685–4696 (2013). This study performs a comprehensive, systems biological analysis of IBC consortium genomic data in an attempt to uncover the genomic secrets of IBC.
Woodward, W. A. et al. Genomic and expression analysis of microdissected inflammatory breast cancer. Breast Cancer Res. Treat. 138, 761–772 (2013). This paper describes the microdissection of IBC in an attempt to eliminate the stromal effect on the genomics of IBC.
Bertucci, F. et al. Gene expression profiles of inflammatory breast cancer: correlation with response to neoadjuvant chemotherapy and metastasis-free survival. Ann. Oncol. 25, 358–365 (2014). This study reports a comprehensive analysis of IBC consortium genomic data, evaluating the difference in response to chemotherapy — a new approach to unravel the distinct genomics of IBC.
Lehmann, B. D. et al. Identification of human triple-negative breast cancer subtypes and preclinical models for selection of targeted therapies. J. Clin. Invest. 121, 2750–2767 (2011).
Manai, M. et al. MARCKS protein overexpression in inflammatory breast cancer. Oncotarget 8, 6246–6257 (2017).
Boersma, B. J. et al. A stromal gene signature associated with inflammatory breast cancer. Int. J. Cancer 122, 1324–1332 (2008).
Matsuda, N. et al. Identification of frequent somatic mutations in inflammatory breast cancer. Breast Cancer Res. Treat. 163, 263–272 (2017).
Debeb, B. G. et al. EZH2 expression correlates with locoregional recurrence after radiation in inflammatory breast cancer. J. Exp. Clin. Cancer Res. 33, 58 (2014).
Putcha, P. et al. HDAC6 activity is a non-oncogene addiction hub for inflammatory breast cancers. Breast Cancer Res. 17, 149 (2015).
Lee, J. et al. A class I histone deacetylase inhibitor, entinostat, enhances lapatinib efficacy in HER2-overexpressing breast cancer cells through FOXO3-mediated Bim1 expression. Breast Cancer Res. Treat. 146, 259–272 (2014).
Lim, B. et al. Open-label phase 1b study of entinostat, and lapatinib alone, and in combination with trastuzumab in patients with HER2+ metastatic breast cancer after progression on trastuzumab [abstract]. J. Clin. Oncol. 34 (Suppl.), 609 (2016).
Debeb, B. G. et al. Histone deacetylase inhibitor-induced cancer stem cells exhibit high pentose phosphate pathway metabolism. Oncotarget 7, 28329–28339 (2016).
Maltseva, D. V. et al. miRNome of inflammatory breast cancer. BMC Res. 7, 871 (2014).
Huo, L. et al. MicroRNA expression profiling identifies decreased expression of miR-205 in inflammatory breast cancer. Mod. Path. 29, 330–346 (2016).
Anfossi, S. et al. High serum miR-19a levels are associated with inflammatory breast cancer and are predictive of favorable clinical outcome in patients with metastatic HER2+ inflammatory breast cancer. PLoS ONE 9, e83113 (2014).
Mesci, A. et al. Targeting of CCBE1 by miR-330-3p in human breast cancer promotes metastasis. Br. J. Cancer 116, 1350–1357 (2017).
Rokavec, M., Li, H., Jiang, L. & Hermeking, H. The p53/miR-34 axis in development and disease. J. Mol. Cell. Biol. 6, 214–230 (2014).
Lerebours, F. et al. miRNA expression profiling of inflammatory breast cancer identifies a 5-miRNA signature predictive of breast tumor aggressiveness. Int. J. Cancer 133, 1614–1623 (2013).
Debeb, B. G. et al. miR-141-mediated regulation of brain metastasis from breast cancer. J. Natl. Cancer Inst. 108, djw026 (2016). This study shows that a specific miRNA mediates one of the most aggressive metastatic patterns in IBC.
Van Laere, S., Limame, R., Van Marck, E. A., Vermeulen, P. B. & Dirix, L. Y. Is there a role for mammary stem cells in inflammatory breast carcinoma?: a review of evidence from cell line, animal model, and human tissue sample experiments. Cancer 116, 2794–2805 (2010).
Gong, Y. et al. Aldehyde dehydrogenase 1 expression in inflammatory breast cancer as measured by immunohistochemical staining. Clin. Breast Cancer 14, e81–88 (2014).
Rosenthal, D. T. et al. RhoC impacts the metastatic potential and abundance of breast cancer stem cells. PLoS ONE 7, e40979 (2012).
van Golen, K. L. et al. Mitogen activated protein kinase pathway is involved in RhoC GTPase induced motility, invasion and angiogenesis in inflammatory breast cancer. Clin. Exp. Metastasis 19, 301–311 (2002).
Wynn, M. L. et al. RhoC GTPase is a potent regulator of glutamine metabolism and N-acetylaspartate production in inflammatory breast cancer cells. J. Biol Chem. 291, 13715–13729 (2016).
van Golen, K. L., Wu, Z. F., Qiao, X. T., Bao, L. W. & Merajver, S. D. RhoC GTPase, a novel transforming oncogene for human mammary epithelial cells that partially recapitulates the inflammatory breast cancer phenotype. Cancer Res. 60, 5832–5838 (2000).
Arias-Pulido, H. et al. SRC-1 expression is a prognostic factor of breast cancer-specific and disease-free survival in inflammatory breast cancer [abstract]. Cancer Res. 71 (Suppl.), P4-01-19 (2011).
Herold, C. I. et al. Phase II trial of dasatinib in patients with metastatic breast cancer using real-time pharmacodynamic tissue biomarkers of Src inhibition to escalate dosing. Clin. Cancer Res. 17, 6061–6070 (2011).
Wolfe, A. R. et al. High-density and very-low-density lipoprotein have opposing roles in regulating tumor-initiating cells and sensitivity to radiation in inflammatory breast cancer. Int. J. Radiat. Oncol. Biol. Phys. 91, 1072–1080 (2015).
Lacerda, L. et al. Simvastatin radiosensitizes differentiated and stem-like breast cancer cell lines and is associated with improved local control in inflammatory breast cancer patients treated with postmastectomy radiation. Stem Cells Transl Med. 3, 849–856 (2014).
Denoyelle, C. et al. Cerivastatin, an inhibitor of HMG-CoA reductase, inhibits the signaling pathways involved in the invasiveness and metastatic properties of highly invasive breast cancer cell lines: an in vitro study. Carcinogenesis 22, 1139–1148 (2001).
Park, Y. H., Jung, H. H., Ahn, J. S. & Im, Y. H. Statin induces inhibition of triple negative breast cancer (TNBC) cells via PI3K pathway. Biochem. Biophys. Res. Commun. 439, 275–279 (2013).
Wang, J. & Kitajima, I. Pitavastatin inactivates NF-kappaB and decreases IL-6 production through Rho kinase pathway in MCF-7 cells. Oncol. Rep. 17, 1149–1154 (2007).
Klawitter, J., Shokati, T., Moll, V., Christians, U. & Klawitter, J. Effects of lovastatin on breast cancer cells: a proteo-metabonomic study. Breast Cancer Res. 12, R16 (2010).
Ghosh-Choudhury, N., Mandal, C. C., Ghosh-Choudhury, N. & Ghosh Choudhury, G. Simvastatin induces derepression of PTEN expression via NFkappaB to inhibit breast cancer cell growth. Cell. Signal. 22, 749–758 (2010).
Gopalan, A., Yu, W., Sanders, B. G. & Kline, K. Simvastatin inhibition of mevalonate pathway induces apoptosis in human breast cancer cells via activation of JNK/CHOP/DR5 signaling pathway. Cancer Lett. 329, 9–16 (2013).
Campbell, M. J. et al. Breast cancer growth prevention by statins. Cancer Res. 66, 8707–8714 (2006).
Wolfe, A. R. et al. Mesenchymal stem cells and macrophages interact through IL-6 to promote inflammatory breast cancer in pre-clinical models. Oncotarget 7, 82482–82492 (2016).
Lacerda, L. et al. Mesenchymal stem cells mediate the clinical phenotype of inflammatory breast cancer in a preclinical model. Breast Cancer Res. 17, 42 (2015).
Wolfe, A. R. et al. Simvastatin prevents triple-negative breast cancer metastasis in pre-clinical models through regulation of FOXO3a. Breast Cancer Res. Treat. 154, 495–508 (2015).
Nelson, E. R. et al. 27-Hydroxycholesterol links hypercholesterolemia and breast cancer pathophysiology. Science 342, 1094–1098 (2013).
Van den Eynden, G. G. et al. Overexpression of caveolin-1 and -2 in cell lines and in human samples of inflammatory breast cancer. Breast Cancer Res. Treat. 95, 219–228 (2006).
Joglekar, M., Elbazanti, W. O., Weitzman, M. D., Lehman, H. L. & van Golen, K. L. Caveolin-1 mediates inflammatory breast cancer cell invasion via the Akt1 pathway and RhoC GTPase. J. Cell. Biochem. 116, 923–933 (2015).
Wang, X. et al. TIG1 promotes the development and progression of inflammatory breast cancer through activation of Axl kinase. Cancer Res. 73, 6516–6525 (2013).
Van der Auwera, I. et al. Increased angiogenesis and lymphangiogenesis in inflammatory versus noninflammatory breast cancer by real-time reverse transcriptase-PCR gene expression quantification. Clin. Cancer Res. 10, 7965–7971 (2004).
Van der Auwera, I. et al. Tumor lymphangiogenesis in inflammatory breast carcinoma: a histomorphometric study. Clin. Cancer Res. 11, 7637–7642 (2005).
Wedam, S. B. et al. Antiangiogenic and antitumor effects of bevacizumab in patients with inflammatory and locally advanced breast cancer. J. Clin. Oncol. 24, 769–777 (2006).
Bertucci, F. et al. Bevacizumab plus neoadjuvant chemotherapy in patients with HER2-negative inflammatory breast cancer (BEVERLY-1): a multicentre, single-arm, phase 2 study. Lancet Oncol. 17, 600–611 (2016).
Pierga, J. Y. et al. Neoadjuvant bevacizumab, trastuzumab, and chemotherapy for primary inflammatory HER2-positive breast cancer (BEVERLY-2): an open-label, single-arm phase 2 study. Lancet Oncol. 13, 375–384 (2012).
Levine, P. H. et al. Evaluation of lymphangiogenic factors, vascular endothelial growth factor D and E-cadherin in distinguishing inflammatory from locally advanced breast cancer. Clin. Breast Cancer 12, 232–239 (2012).
Raposo, T. P., Pires, I., Prada, J., Queiroga, F. L. & Argyle, D. J. Exploring new biomarkers in the tumour microenvironment of canine inflammatory mammary tumours. Vet. Comp. Oncol. 15, 655–666 (2016).
Oladapo, H. O. et al. Pharmacological targeting of GLI1 inhibits proliferation, tumor emboli formation and in vivo tumor growth of inflammatory breast cancer cells. Cancer Lett. 411, 136–149 (2017).
Kenny, P. A. et al. The morphologies of breast cancer cell lines in three-dimensional assays correlate with their profiles of gene expression. Mol. Oncol. 1, 84–96 (2007).
Cabioglu, N. et al. Expression of growth factor and chemokine receptors: new insights in the biology of inflammatory breast cancer. Ann. Oncol. 18, 1021–1029 (2007).
Zhang, D. et al. Epidermal growth factor receptor tyrosine kinase inhibitor reverses mesenchymal to epithelial phenotype and inhibits metastasis in inflammatory breast cancer. Clin. Cancer Res. 15, 6639–6664 (2009). This manuscript reports that EGFR signalling is active in IBC and is the basis of an ongoing randomized phase II study evaluating panitumumab.
Sauer, S. J. et al. Bisphenol A activates EGFR and ERK promoting proliferation, tumor spheroid formation and resistance to EGFR pathway inhibition in estrogen receptor-negative inflammatory breast cancer cells. Carcinogenesis 38, 252–260 (2017).
Silvera, D. & Schneider, R. J. Inflammatory breast cancer cells are constitutively adapted to hypoxia. Cell Cycle 8, 3091–3096 (2009).
Vermeulen, P. B., Van Laere, S. J. & Dirix, L. Y. Inflammatory breast carcinoma as a model of accelerated self-metastatic expansion by intravascular growth. Br. J. Cancer 101, 1028–1029 (2009).
Jolly, M. K. et al. Inflammatory breast cancer: a model for investigating cluster-based dissemination. npj Breast Cancer 3, 21 (2017).
Topalian, S. L., Weiner, G. J. & Pardoll, D. M. Cancer immunotherapy comes of age. J. Clin. Oncol. 29, 4828–4836 (2011).
Cimino-Mathews, A. et al. PD-L1 (B7-H1) expression and the immune tumor microenvironment in primary and metastatic breast carcinomas. Hum. Pathol. 47, 52–63 (2016).
Hamm, C. A. et al. Genomic and immunological tumor profiling identifies targetable pathways and extensive CD8+ /PDL1+ immune infiltration in inflammatory breast cancer tumors. Mol. Cancer Ther. 15, 1746–1756 (2016).
Jhaveri, K. et al. Hyperactivated mTOR and JAK2/STAT3 pathways: molecular drivers and potential therapeutic targets of inflammatory and invasive ductal breast cancers after neoadjuvant chemotherapy. Clin. Breast Cancer 16, 113–122.e1 (2016).
Su, S. et al. A positive feedback loop between mesenchymal-like cancer cells and macrophages is essential to breast cancer metastasis. Cancer Cell 25, 605–620 (2014).
Bochet, L. et al. Adipocyte-derived fibroblasts promote tumor progression and contribute to the desmoplastic reaction in breast cancer. Cancer Res. 73, 5657–5668 (2013).
Oleinika, K., Nibbs, R. J., Graham, G. J. & Fraser, A. R. Suppression, subversion and escape: the role of regulatory T cells in cancer progression. Clin. Exp. Immun. 171, 36–45 (2013).
Schmidt, T., Ben-Batalla, I., Schultze, A. & Loges, S. Macrophage-tumor crosstalk: role of TAMR tyrosine kinase receptors and of their ligands. Cell. Mol. Life Sci. 69, 1391–1414 (2012).
Quail, D. F. & Joyce, J. A. Microenvironmental regulation of tumor progression and metastasis. Nat. Med. 19, 1423–1437 (2013).
Sica, A. Macrophages give Gas(6) to cancer. Blood 115, 2122–2123 (2010).
Mego, M. et al. Circulating tumor cells (CTCs) are associated with abnormalities in peripheral blood dendritic cells in patients with inflammatory breast cancer. Oncotarget 8, 35656–35658 (2016).
Bertucci, F. et al. PDL1 expression in inflammatory breast cancer is frequent and predicts for the pathological response to chemotherapy. Oncotarget 6, 13506–13519 (2015). This study is the first analysis of residual IBC after neoadjuvant chemotherapy and searches for relevant biomarkers, including those related to the microenvironment.
Datta, J. et al. Anti-HER2 CD4(+) T-helper type 1 response is a novel immune correlate to pathologic response following neoadjuvant therapy in HER2-positive breast cancer. Breast Cancer Res. 17, 71 (2015).
Cohen, N. et al. Fibroblasts drive an immunosuppressive and growth-promoting microenvironment in breast cancer via secretion of Chitinase 3-like 1. Oncogene 36, 4457–4468 (2017).
Baroni, S. et al. Exosome-mediated delivery of miR-9 induces cancer-associated fibroblast-like properties in human breast fibroblasts. Cell Death Dis. 7, e2312 (2016).
Zhang, Z. et al. Loss of exosomal miR-320a from cancer-associated fibroblasts contributes to HCC proliferation and metastasis. Cancer Lett. 397, 33–42 (2017).
Colpaert, C. G. et al. Inflammatory breast cancer shows angiogenesis with high endothelial proliferation rate and strong E-cadherin expression. Br. J. Cancer 88, 718–725 (2003).
Goswami, S. & Sharma-Walia, N. Osteoprotegerin secreted by inflammatory and invasive breast cancer cells induces aneuploidy, cell proliferation and angiogenesis. BMC Cancer 15, 935 (2015).
Aaronson, D. S. & Horvath, C. M. A road map for those who don’t know JAK-STAT. Science 296, 1653–1655 (2002).
Ogony, J., Choi, H. J., Lui, A., Cristofanilli, M. & Lewis-Wambi, J. Interferon-induced transmembrane protein 1 (IFITM1) overexpression enhances the aggressive phenotype of SUM149 inflammatory breast cancer cells in a signal transducer and activator of transcription 2 (STAT2)-dependent manner. Breast Cancer Res. 18, 25 (2016).
US National Library of Medicine. ClinicalTrials.gov https://www.clinicaltrials.gov/ct2/show/NCT02041429 (2017).
Bieche, I. et al. Molecular profiling of inflammatory breast cancer: identification of a poor-prognosis gene expression signature. Clin. Cancer Res. 10, 6789–6795 (2004).
Marotta, L. L. et al. The JAK2/STAT3 signaling pathway is required for growth of CD44( + )CD24(-) stem cell-like breast cancer cells in human tumors. J. Clin. Invest. 121, 2723–2735 (2011). This manuscript reports a connection between stem cell markers and hyperactivated JAK–STAT signalling, which could lead to translational drug development. Currently, a clinical trial is ongoing to study the clinical efficacy of a JAK inhibitor on the basis of this study.
Kim, H. S. et al. COX2 overexpression is a prognostic marker for Stage III breast cancer. Breast Cancer Res. Treat. 132, 51–59 (2012).
Ristimaki, A. et al. Prognostic significance of elevated cyclooxygenase-2 expression in breast cancer. Cancer Res. 62, 632–635 (2002).
Wang, X. et al. EGFR signaling promotes inflammation and cancer stem-like activity in inflammatory breast cancer. Oncotarget 8, 67904–67917 (2017).
Zelenay, S. et al. Cyclooxygenase-dependent tumor growth through evasion of immunity. Cell 162, 1257–1270 (2015).
Subbaramaiah, K. et al. Increased levels of COX-2 and prostaglandin E2 contribute to elevated aromatase expression in inflamed breast tissue of obese women. Cancer Discov. 2, 356–365 (2012).
Lee, J., Banu, S. K., Burghardt, R. C., Starzinski-Powitz, A. & Arosh, J. A. Selective inhibition of prostaglandin E2 receptors EP2 and EP4 inhibits adhesion of human endometriotic epithelial and stromal cells through suppression of integrin-mediated mechanisms. Biol. Reprod. 88, 77 (2013).
Robertson, F. M. et al. Differential regulation of the aggressive phenotype of inflammatory breast cancer cells by prostanoid receptors EP3 and EP4. Cancer 116, 2806–2814 (2010).
Zheng, Z. et al. Correlation between epidermal growth factor receptor and tumor stem cell markers CD44/CD24 and their relationship with prognosis in breast invasive ductal carcinoma. Med. Oncol. 32, 275 (2015).
Mu, Z. et al. AZD8931, an equipotent, reversible inhibitor of signaling by epidermal growth factor receptor (EGFR), HER2, and HER3: preclinical activity in HER2 non-amplified inflammatory breast cancer models. J. Exp. Clin. Cancer Res. 33, 47 (2014).
Matsuda, N. et al. Phase II study of panitumumab, nab-paclitaxel, and carboplatin followed by FEC neoadjuvant chemotherapy for patients with primary HER-2 negative inflammatory breast cancer [abstract]. J. Clin. Oncol. 33 (Suppl.), 1087 (2015).
Joglekar-Javadekar, M. et al. Characterization and targeting of platelet-derived growth factor receptor alpha (PDGFRA) in inflammatory breast cancer (IBC). Neoplasia 19, 564–573 (2017).
Dong, J. et al. VEGF-null cells require PDGFR alpha signaling-mediated stromal fibroblast recruitment for tumorigenesis. J. EMBO 23, 2800–2810 (2004).
Jechlinger, M. et al. Autocrine PDGFR signaling promotes mammary cancer metastasis. J. Clin. Invest. 116, 1561–1570 (2006).
Seymour, L. & Bezwoda, W. R. Positive immunostaining for platelet derived growth factor (PDGF) is an adverse prognostic factor in patients with advanced breast cancer. Breast Cancer Res. Treat. 32, 229–233 (1994).
Carvalho, I., Milanezi, F., Martins, A., Reis, R. M. & Schmitt, F. Overexpression of platelet-derived growth factor receptor alpha in breast cancer is associated with tumour progression. Breast Cancer Res. 7, R788–795 (2005).
Drygin, D. et al. Protein kinase CK2 modulates IL-6 expression in inflammatory breast cancer. Biochem. Biophys. Res. Commun. 415, 163–167 (2011).
Wang, W. et al. Effector T cells abrogate stroma-mediated chemoresistance in ovarian cancer. Cell 165, 1092–1105 (2016).
Mahooti, S. et al. Breast carcinomatous tumoral emboli can result from encircling lymphovasculogenesis rather than lymphovascular invasion. Oncotarget 1, 131–147 (2010).
Babaei, Z. et al. Relationship of obesity with serum concentrations of leptin, CRP and IL-6 in breast cancer survivors. J. Egypt. Natl Canc. Inst. 27, 223–229 (2015).
Markkula, A., Simonsson, M., Ingvar, C., Rose, C. & Jernstrom, H. IL6 genotype, tumour ER-status, and treatment predicted disease-free survival in a prospective breast cancer cohort. BMC Cancer 14, 759 (2014).
Ammanamanchi, S., Kim, S. J., Sun, L. Z. & Brattain, M. G. Induction of transforming growth factor-beta receptor type II expression in estrogen receptor-positive breast cancer cells through SP1 activation by 5-aza-2′-deoxycytidine. J. Biol. Chem. 273, 16527–16534 (1998).
Ellis, D. L. & Teitelbaum, S. L. Inflammatory carcinoma of the breast. A pathologic definition. Cancer 33, 1045–1047 (1974).
Ohshiro, K., Schwartz, A. M., Levine, P. H. & Kumar, R. Alternate estrogen receptors promote invasion of inflammatory breast cancer cells via non-genomic signaling. PLoS ONE 7, e30725 (2012).
Anderson, W. F., Chu, K. C. & Chang, S. Inflammatory breast carcinoma and noninflammatory locally advanced breast carcinoma: distinct clinicopathologic entities? J. Clin. Oncol. 21, 2254–2259 (2003).
Fernandez, S. V. et al. Inflammatory breast cancer (IBC): clues for targeted therapies. Breast Cancer Res. Treat. 140, 23–33 (2013).
Wang, L., Zuo, X., Xie, K. & Wei, D. The role of CD44 and cancer stem cells. Methods Mol. Biol. 1692, 31–42 (2018).
Fei, M. et al. TNF-alpha from inflammatory dendritic cells (DCs) regulates lung IL-17A/IL-5 levels and neutrophilia versus eosinophilia during persistent fungal infection. Proc. Natl Acad. Sci. USA 108, 5360–5365 (2011).
Hilkens, C. M., Kalinski, P., de Boer, M. & Kapsenberg, M. L. Human dendritic cells require exogenous interleukin-12-inducing factors to direct the development of naive T-helper cells toward the Th1 phenotype. Blood 90, 1920–1926 (1997).
Hallahan, D. E., Spriggs, D. R., Beckett, M. A., Kufe, D. W. & Weichselbaum, R. R. Increased tumor necrosis factor alpha mRNA after cellular exposure to ionizing radiation. Proc. Natl Acad. Sci. USA 86, 10104–10107 (1989).
Curran, E. et al. STING pathway activation stimulates potent immunity against acute myeloid leukemia. Cell Rep. 15, 2357–2366 (2016).
Alpaugh, M. L., Tomlinson, J. S., Shao, Z. M. & Barsky, S. H. A novel human xenograft model of inflammatory breast cancer. Cancer Res. 59, 5079–5084 (1999).
Kurebayashi, J. et al. Isolation and characterization of a new human breast cancer cell line, KPL-4, expressing the Erb B family receptors and interleukin-6. Br. J. Cancer 79, 707–717 (1999).
Hall, C. S. et al. Novel inflammatory breast cancer cell line, MDA-IBC-1 expresses and secretes WISP3, a putative tumor suppressor in inflammatory breast cancer [abstract]. Cancer Res. 69 (Suppl.), 1051 (2009).
Klopp, A. H. et al. Mesenchymal stem cells promote mammosphere formation and decrease E-cadherin in normal and malignant breast cells. PLoS ONE 5, e12180 (2010).
Nokes, B. T. et al. In vitro assessment of the inflammatory breast cancer cell line SUM 149: discovery of 2 single nucleotide polymorphisms in the RNase L gene. J. Cancer 4, 104–116 (2013).
Holliday, D. L. & Speirs, V. Choosing the right cell line for breast cancer research. Breast Cancer Res. 13, 215 (2011).
Shirakawa, K. et al. Inflammatory breast cancer: vasculogenic mimicry and its hemodynamics of an inflammatory breast cancer xenograft model. Breast Cancer Res. 5, 136–139 (2003).