Inflammatory breast cancer (IBC): clues for targeted therapies

Inflammatory breast cancer (IBC) is the most aggressive type of advanced breast cancer characterized by rapid proliferation, early metastatic development and poor prognosis. Since there are few preclinical models of IBC, there is a general lack of understanding of the complexity of the disease. Rece...

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Vydané v:	Breast cancer research and treatment Ročník 140; číslo 1; s. 23 - 33
Hlavní autori:	Fernandez, Sandra V., Robertson, Fredika M., Pei, Jianming, Aburto-Chumpitaz, Lucy, Mu, Zhaomei, Chu, Khoi, Alpaugh, R. K., Huang, Yong, Cao, Yu, Ye, Zaiming, Cai, Kathy Q., Boley, Kimberly M., Klein-Szanto, Andres J., Devarajan, Karthik, Addya, Sankar, Cristofanilli, Massimo
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	Boston Springer US 01.07.2013 Springer Springer Nature B.V
Predmet:	Adenosine Triphosphatases - genetics Analysis Anaplastic Lymphoma Kinase Animals ATPases Associated with Diverse Cellular Activities Biological and medical sciences Brain Neoplasms - pathology Brain Neoplasms - secondary Breast cancer Cadherins - metabolism Cancer research Cancer therapies CD4 Antigens - genetics Cell adhesion & migration Cell Line, Tumor Chromosomes, Human, Pair 8 DNA-Binding Proteins - genetics Epithelial-Mesenchymal Transition Female Focal Adhesion Kinase 1 - metabolism Focal Adhesion Kinase 2 - metabolism Gene Expression Regulation, Neoplastic Genes, myc Gynecology. Andrology. Obstetrics Humans Inflammatory Breast Neoplasms - genetics Inflammatory Breast Neoplasms - metabolism Inflammatory Breast Neoplasms - pathology Loss of Heterozygosity Lung Neoplasms - secondary Mammary gland diseases Medical sciences Medicine Medicine & Public Health Metastasis Mice Mice, SCID Molecular Targeted Therapy Multiple tumors. Solid tumors. Tumors in childhood (general aspects) Neoplasms, Experimental - genetics Neoplasms, Experimental - pathology Oncology Preclinical Study Prognosis Receptor Protein-Tyrosine Kinases - genetics Receptor, Notch3 Receptors, Notch - genetics Tumors Xenograft Model Antitumor Assays ALK NOTCH3 MYC FAK1/PTK2 CD44 ATAD2 Transmembrane protein Breast disease Targeted therapy Notch3 gene Cell adhesion molecule Breast cancer Inflammation Malignant tumor Mammary gland diseases Treatment C-Onc gene myc Gene Anaplastic lymphoma kinase Protooncogene Cancer
ISSN:	0167-6806, 1573-7217, 1573-7217
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Popis
Shrnutí:	Inflammatory breast cancer (IBC) is the most aggressive type of advanced breast cancer characterized by rapid proliferation, early metastatic development and poor prognosis. Since there are few preclinical models of IBC, there is a general lack of understanding of the complexity of the disease. Recently, we have developed a new model of IBC derived from the pleural effusion of a woman with metastatic secondary IBC. FC-IBC02 cells are triple negative and form clusters (mammospheres) in suspension that are strongly positive for E-cadherin, β-catenin and TSPAN24, all adhesion molecules that play an important role in cell migration and invasion. FC-IBC02 cells expressed stem cell markers and some, but not all of the characteristics of cells undergoing epithelial mesenchymal transition (EMT). Breast tumor FC-IBC02 xenografts developed quickly in SCID mice with the presence of tumor emboli and the development of lymph node and lung metastases. Remarkably, FC-IBC02 cells were able to produce brain metastasis in mice on intracardiac or intraperitoneal injections. Genomic studies of FC-IBC02 and other IBC cell lines showed that IBC cells had important amplification of 8q24 where MYC, ATAD2 and the focal adhesion kinase FAK1 are located. MYC and ATAD2 showed between 2.5 and 7 copies in IBC cells. FAK1, which plays important roles in anoikis resistance and tumor metastasis, showed 6–4 copies in IBC cells. Also, CD44 was amplified in triple-negative IBC cells (10–3 copies). Additionally, FC-IBC02 showed amplification of ALK and NOTCH3. These results indicate that MYC, ATAD2, CD44, NOTCH3, ALK and/or FAK1 may be used as potential targeted therapies against IBC.
Bibliografia:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23
ISSN:	0167-6806 1573-7217 1573-7217
DOI:	10.1007/s10549-013-2600-4