Molecular Profiling of Inflammatory Breast Cancer

Bièche, Ivan; Lerebours, Florence; Tozlu, Sengül; Espié, Marc; Marty, M.; Lidereau, Rosette

doi:10.1158/1078-0432.ccr-04-0306

Cited by 214 publications

(172 citation statements)

References 28 publications

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“…We found 181 genes which were 2-fold differentially changed. In other studies, IGFBP7 was screened in the microarray (25,26), which may be related with tumor metastasis. By identification and quantification of membrane proteins, network 2 (grouped by IPa) shows 12-related genes involved in the endocrine system, disorders, metabolic disease cell-to-cell signaling and interaction.…”

Section: Discussionmentioning

confidence: 99%

IGFBP7 functions as a potential lymphangiogenesis inducer in non-small cell lung carcinoma

et al. 2015

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Abstract. Lymphangiogenesis is not only involved in the processes of embryonic development, tissue repair and chronic inflammation, but also in tumor lymphatic metastasis. Metastatic tumor cells spreading through lymphatic vessels occur in non-small cell lung carcinoma (NSCLC), with regional lymph node metastasis often being the most important prognostic factor for carcinoma patients. Recent research has identified a range of lymphangiogenic growth factors that could conceivably play a great role in promoting tumor lymphangiogenesis and lymphatic metastasis. The most extensively accepted signaling pathways promoting lymphangiogenesis in tumors include the secreted lymphangiogenic proteins: vascular endothelial growth factor-C (VEGF-C) and VEGF-D, and their cognate receptor on lymphatic endothelium VEGF receptor-3 (VEGFR-3). Targeting VEGF pathway strategy sometimes failed to decrease tumor metastasis in vivo experiments and clinical trials. It is unclear whether the tumor cells induced the lymphangiogenesis process, while VEGF pathway could not completely illustrate the mechanism of tumor cell lymphatic metastasis. To explore the novel tumor lymphangiogenesis targets, we screened 181 candidate genes between high lymphatic vascular density (LVD) and low LVD in lung adenocarcinomas using Human Genome U133 Plus 2.0 Microarray. Insulin-like growth factor binding protein 7 (IGFBP7) was proven to be associated with metastatic clinicopathological features and high LVD. Furthermore, by assessing the capability of lymphatic endothelial cell forming lymphatic vessel-like structures in vitro, it appears to enhance lymphangiogenesis.

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Section: Discussionmentioning

confidence: 99%

IGFBP7 functions as a potential lymphangiogenesis inducer in non-small cell lung carcinoma

et al. 2015

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“…25 Tumor-derived CCL5 is detected in many clinical specimens of breast and cervical cancers; greater plasma levels in patients with progressive and more advanced disease than those in remission, [26][27][28] and it constitutes a prominent part of a poor prognosis signature of inflammatory BC. 29,30 An analysis of large core needle biopsies of 113 invasive breast carcinomas revealed that the concentration of CCL5 was significantly higher in the groups of patients with axillary lymph node metastasis than those without. 31 Most BC-derived cell lines spontaneously produce large amounts of CCL5, and the incidence of CCL5 expression detected in tissue sections of breast carcinomas is considerably higher than in normal duct epithelial cells or in those of benign breast lumps.…”

Section: Ccl5 and Human Breast Cancer (Bc)mentioning

confidence: 99%

CCL5 as a potential immunotherapeutic target in triple-negative breast cancer

Zhang

Kim

et al. 2013

Cell Mol Immunol

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Breast cancer (BC) is a leading cause of mortality among women in the world. To date, a number of molecules have been established as disease status indicators and therapeutic targets. The best known among them are estrogen receptor-a (ER-a), progesterone receptor (PR) and HER-2/neu. About 15%-20% BC patients do not respond effectively to therapies targeting these classes of tumor-promoting factors. Thus, additional targets are strongly and urgently sought after in therapy for human BCs negative for ER, PR and HER-2, the so-called triple-negative BC (TNBC). Recent clinical work has revealed that CC chemokine ligand 5 (CCL5) is strongly associated with the progression of BC, particularly TNBC. How CCL5 contributes to the development of TNBC is not well understood. Experimental animal studies have begun to address the mechanistic issue. In this article, we will review the clinical and laboratory work in this area that has led to our own hypothesis that targeting CCL5 in TNBCs will have favorable therapeutic outcomes with minimal adverse impact on the general physiology.

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“…In terms of breast cancer, a number of studies have suggested that RANTES is associated with breast malignancy. In patients with breast cancer, advanced disease, early relapse, and poor prognosis are significantly correlated with elevated RANTES expression levels in biopsy specimens and serum (26)(27)(28). Therefore, the precise role of RANTES signaling in breast cancer should be clarified.…”

Section: Introductionmentioning

confidence: 99%

STAT3-RANTES Autocrine Signaling Is Essential for Tamoxifen Resistance in Human Breast Cancer Cells

Lee

et al. 2013

Molecular Cancer Research

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The acquisition of tamoxifen resistance is a major therapeutic problem in breast cancer. We developed a tamoxifen-resistant MCF-7 (TRM-7) cell line to elucidate the molecular mechanisms and factors associated with acquisition of such resistance. We showed that phosphorylation of STAT3 at tyrosine 705 (Y705) and RANTES expression are increased in response to tamoxifen in human breast cancer cells. On the basis of these results, we hypothesize that upregulated STAT3 phosphorylation and RANTES may be correlated with the development of drug resistance. Here, we showed that STAT3 and RANTES contribute to the maintenance of drug resistance. STAT3 phosphorylation is constitutively retained via a RANTES autocrine loop, which in turn upregulates antiapoptotic signals in TRM-7 cells. STAT3-RANTES autocrine signaling affected expression of anti-apoptotic BCL-2 family genes and prevented TRM-7 cells from undergoing programmed cell death by inhibiting PARP and caspase-9 cleavage. Subsequently, blockade of STAT3 and RANTES in TRM-7 cells resulted in reduction of antiapoptotic signals, which was rescued by exogenous RANTES treatment; drug resistance was also restored. Taken together, our results suggested that STAT3-RANTES autocrine signaling is essential for maintenance of drug resistance and inhibition of programmed cell death. These mechanisms of STAT3-RANTES autocrine signaling suggest a novel strategy for management of patients with tamoxifen-resistant tumors. Mol Cancer Res; 11(1); 31-42. Ó2012 AACR. IntroductionBreast cancer is the second most common cancer worldwide after lung cancer, the fifth most common cause of cancer death, and the leading cause of cancer death in women. The global burden of breast cancer exceeds that of all other cancers, and its incidence is increasing (1). In women younger than 50 years with breast cancer, chemotherapy increases the 15-year survival rate by 10%,

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Molecular Profiling of Inflammatory Breast Cancer

Cited by 214 publications

References 28 publications

IGFBP7 functions as a potential lymphangiogenesis inducer in non-small cell lung carcinoma

IGFBP7 functions as a potential lymphangiogenesis inducer in non-small cell lung carcinoma

CCL5 as a potential immunotherapeutic target in triple-negative breast cancer

STAT3-RANTES Autocrine Signaling Is Essential for Tamoxifen Resistance in Human Breast Cancer Cells

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