Serial analysis of gene expression of lobular carcinoma in situ identifies down regulation of claudin 4 and overexpression of matrix metalloproteinase 9

Cao, Dengfeng; Polyák, Kornélia; Halushka, Marc K.; Nassar, Hind; Kouprina, Nina; Iacobuzio‐Donahue, Christine A.; Wu, Xinyan; Sukumar, Saraswati; Hicks, Jessica L.; Marzo, Angelo De; Argani, Pedram

doi:10.1186/bcr2189

Cited by 28 publications

(25 citation statements)

References 40 publications

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“…Most importantly these studies, as well as that by Morandi and co-workers (116), demonstrated the common loss of 16q in ALH and LCIS with ILC, supporting an evolutionary link among the three types of lesions. Gene-expression profiling of classic ILC and LCIS reveals a gene-expression signature that overlaps significantly with that observed in low grade IDCs (117). Thus, this gene-expression data, in conjunction with the CGH data, support a common evolutionary –16q, low-grade gene-expression pathway (Figure 6) that encompasses ( a ) ILC and its precursor lesions (ALH and LCIS), and ( b ) low-grade IDC and its precursor lesions (FEA, ADH and low-grade DCIS).…”

Section: Gene-expression Analysis Of Invasive Ductal Carcinomamentioning

confidence: 80%

Preinvasive Breast Cancer

Sgroi

2010

Annu. Rev. Pathol. Mech. Dis.

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Preinvasive breast cancer accounts for approximately one-third of all newly diagnosed breast cancer cases in the United States and constitutes a spectrum of neoplastic lesions with varying degrees of differentiation and clinical behavior. High-throughput genetic, epigenetic, and gene-expression analyses have enhanced our understanding of the relationship of these early neoplastic lesions to normal breast tissue, and they strongly suggest that preinvasive breast cancer develops and evolves along two distinct molecular genetic and biological pathways that correlate with tumor grade. Although unique epigenetic and gene-expression changes are not observed in the tumor epithelial compartment during the transition from preinvasive to invasive disease, distinct molecular alterations are observed in the tumor-stromal and myoepithelial cells. This suggests that the stromal and myoepithelial microenvironment of preinvasive breast cancer actively participates in the transition from preinvasive to invasive disease. An improved understanding of the transition from preinvasive to invasive breast cancer will pave the way for novel preventative and therapeutic strategies.

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Section: Gene-expression Analysis Of Invasive Ductal Carcinomamentioning

confidence: 80%

Preinvasive Breast Cancer

Sgroi

2010

Annu. Rev. Pathol. Mech. Dis.

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“…Thus, the BRC aggressive phenotype also coincides with the cell capacity to crosstalk with other lineages. Macrophages have already been described as potent protease producers [57] and MMP9 has been found overexpressed in breast cancer [58, 59] and greatly expressed by M2 macrophages [60]. MMP1 has also been proposed as a marker of progression into BRC [61].…”

Section: Discussionmentioning

confidence: 99%

MMP1, MMP9, and COX2 Expressions in Promonocytes Are Induced by Breast Cancer Cells and Correlate with Collagen Degradation, Transformation-Like Morphological Changes in MCF-10A Acini, and Tumor Aggressiveness

Chimal-Ramírez

Espinoza-Sánchez

Utrera-Barillas

et al. 2013

BioMed Research International

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Tumor-associated immune cells often lack immune effector activities, and instead they present protumoral functions. To understand how tumors promote this immunological switch, invasive and noninvasive breast cancer cell (BRC) lines were cocultured with a promonocytic cell line in a Matrigel-based 3D system. We hypothesized that if communication exists between tumor and immune cells, coculturing would result in augmented expression of genes associated with tumor malignancy. Upregulation of proteases MMP1 and MMP9 and inflammatory COX2 genes was found likely in response to soluble factors. Interestingly, changes were more apparent in promonocytes and correlated with the aggressiveness of the BRC line. Increased gene expression was confirmed by collagen degradation assays and immunocytochemistry of prostaglandin 2, a product of COX2 activity. Untransformed MCF-10A cells were then used as a sensor of soluble factors with transformation-like capabilities, finding that acini formed in the presence of supernatants of the highly aggressive BRC/promonocyte cocultures often exhibited total loss of the normal architecture. These data support that tumor cells can modify immune cell gene expression and tumor aggressiveness may importantly reside in this capacity. Modeling interactions in the tumor stroma will allow the identification of genes useful as cancer prognostic markers and therapy targets.

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“…36 However, complete genomic DNA gains at the probes spanning HGF were only observed in three cases ( Figure 1). On the other hand, DNA losses tended to be small focal changes and recurrently mapped to 7p22, 7p12.3, and 7q11.23 in which three earlier reported candidate tumor suppressor genes, that is MAD1L1 (7p22.3), 37 TNS3 (7p12.3), 38 and CLDN4 (7q11.23), 39 were located. …”

Section: Genomic Profiling Of Chromosome 7 By Ultrahigh-resolution Acghmentioning

confidence: 93%

Prognostic implication of MET overexpression in myxofibrosarcomas: an integrative array comparative genomic hybridization, real-time quantitative PCR, immunoblotting, and immunohistochemical analysis

Lee

Fang

et al. 2010

Modern Pathology

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It remains obscure in myxofibrosarcoma about the basis of tumorigenesis, progression, and metastasis. Chromosome 7 gains are common in some sarcomas, including myxofibrosarcoma, whereas the specific oncogenes are yet to be characterized. We performed an integrative study of MET gene at 7q31.2 to elucidate its implication in myxofibrosarcoma. Focused on candidate oncogenes on chromosome 7, 385K array comparative genomic hybridization was used to profile DNA copy number alterations of 12 samples. MET transcript was successfully quantified by real-time RT-PCR for 16 laser-microdissected tumors and two myxofibrosarcoma cell lines (NMFH-1, OH931). MET immunoexpression was assessable in 86 primary localized tumors with followup. To analyze endogenous MET expression and activation, NMFH-1 and OH931 cells, both with wild-type MET gene, were subjected to Western blotting and hepatocyte growth factor-treated NMFH-1 cells were evaluated for the kinetics of MET tyrosine phosphorylation. Non-random large-scale gains on 7q were detected in five cases, delineating three recurrent amplicons, 7q21.11-7q21.3, 7q22.1-22.3, and 7q31.1-7q32.3, in which the locus of MET displayed increased copy number, among others. MET mRNA was upregulated in OH931, NMFH-1, and nine tumors (56%), whereas neither gene dosage nor mRNA expression of MET was associated with clinicopathological factors. In contrast, MET protein overexpression, present in 67% of cases, was highly related to deep location (P ¼ 0.004), higher grades (P ¼ 0.001), and more advanced stages (Po0.001). Importantly, MET overexpression independently portended inferior metastasis-free survival (P ¼ 0.004) and overall survival (P ¼ 0.0221). Expressing activating phospho-MET at Tyr 1234 /Tyr 1235 , OH931 cells had more abundant total MET than NMFH-1 cells, whereas the latter became promptly phosphorylated on stimulation of

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Serial analysis of gene expression of lobular carcinoma in situ identifies down regulation of claudin 4 and overexpression of matrix metalloproteinase 9

Cited by 28 publications

References 40 publications

Preinvasive Breast Cancer

Preinvasive Breast Cancer

MMP1, MMP9, and COX2 Expressions in Promonocytes Are Induced by Breast Cancer Cells and Correlate with Collagen Degradation, Transformation-Like Morphological Changes in MCF-10A Acini, and Tumor Aggressiveness

Prognostic implication of MET overexpression in myxofibrosarcomas: an integrative array comparative genomic hybridization, real-time quantitative PCR, immunoblotting, and immunohistochemical analysis

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