Ontology highlight
ABSTRACT:
PROVIDER: PRJNA988050 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR25036201.fastq.gz | Fastqsanger.gz | |||
| SRR25036201_1.fastq.gz | Fastqsanger.gz | |||
| SRR25036201_2.fastq.gz | Fastqsanger.gz | |||
| SRR25036202.fastq.gz | Fastqsanger.gz |
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Project description:Invasive lobular carcinoma (ILC) of the breast accounts for 5-15% of breast cancers and is characterized by loss of E-cadherin and believed to arise via a linear histological progression. Genomic studies have identified a clonal relationship between ILC and concurrent lobular carcinoma in situ (LCIS) lesions, suggesting that LCIS may be a precursor lesion. It has been shown that an LCIS diagnosis confers a 15-20% risk of progression to ILC, over a lifetime. Currently no molecular test or markers can identify LCIS lesions likely to progress to ILC. Since microRNA (miRNA) expression changes have been detected in a number of other cancer types, we explored whether their dysregulation might be detected during progression from LCIS to ILC. Using the Illumina miRNA profiling platform, designed for simultaneous analysis of 470 mature miRNAs, we analyzed the profiles of archived normal breast epithelium, LCIS lesions found alone, LCIS lesions concurrent with ILC, and the concurrent ILCs, as a model of linear histological progression toward ILC. We identified two sets of differentially expressed miRNAs, the first set highly expressed in normal epithelium, including hsa-miR-224, -139, -10b, -450, 140 and -365 and the second set upregulated during lobular neoplasia, including hsa-miR-375, -203, -425-5p, -183, -565 and -182. Using quantitative RT-PCR, we validated a trend of increased expression for hsa-mir-375, hsa-mir-182, and hsa-mir-183 correlating with ILC progression. As we detected increased expression of hsa-miR-375 in LCIS lesions synchronous with ILC, we sought to determine whether hsa-mir-375 might induce phenotypes reminiscent of lobular neoplasia by expressing it in the MCF10A 3D culture model of mammary acinar morphogenesis. Increased expression of hsa-miR-375 resulted in loss of cellular organization and acquisition of a hyperplastic phenotype. These data suggest that dysregulated miRNA expression contributes to lobular neoplastic progression. 6 specimens were analyzed in duplicate. One frozen normal lobular epithelium and the matched FFPE (1 month old) normal lobular epithelium. One lobular carcinoma in situ (LCIS) found alone, one LCIS synchronous with an invasive lobular carcinoma (ILC), the synchronous ILC (from a different archived block), and one ILC found alone without presence of any other breast cancer.
2011-04-11 | E-GEOD-28514 | biostudies-arrayexpress
Project description:The identification of genomic alterations occurring in neoplastic lesions provides insight into both lesion occurrence and disease progression. In this study we used microarray comparative genomic hybridization (CGH) to investigate genetic changes in atypical lobular hyperplasia (ALH) and lobular carcinoma in situ (LCIS), as the presence of these lobular neoplastic lesions is an indicator of risk in the development of invasive breast cancer. DNA was extracted from microdissected archival breast tissue containing ALH or LCIS, lacking adjacent invasive carcinoma, and subjected to whole-genome tiling path microarray-CGH using the submegabase resolution tiling set (SMRTr)-array platform. Twelve ALH and 13 LCIS lesions were examined. Copy number alterations were identified using statistical criteria and validated with Real-Time PCR and fluorescence in situ hybridization. From statistical analysis, a greater number of alterations were observed in ALH compared to LCIS. Alterations common to ALH include gain at 2p11.2 and loss at 7p11.2-p11.1 and 22q11.1. Alterations common to LCIS include gain at 20q13.13 and loss at 19q13.2-q13.31. In both ALH and LCIS, we observed loss of 16q21-q23.1, an altered region previously identified in lobular neoplasia and invasive carcinoma. The validation of select alterations reinforces the genomic signature. This study represents the first whole-genome investigation of lobular neoplastic breast lesions using clinical archival specimens. The identified genomic signature includes copy number alterations not previously identified for lobular neoplasia. This genomic signature, common to ALH and LCIS, suggests a role for the acquisition of novel genomic alterations in the aberrant cellular proliferation that defines lobular neoplasia. Keywords: comparative genomic hybridization, high resolution analysis of atypical lobular hyperplasia (ALH) and lobular carcinoma in situ (LCIS) human archival breast lesions by whole genome tiling path array CGH
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Project description:CDH1 and PIK3CA are the two most frequently mutated genes in Invasive Lobular Carcinoma (ILC) of the breast. Transcription profiling has identified molecular subtypes for ILC, one of which - Immune-Related (IR) - is associated with gene expression linked to lymphocyte and macrophage infiltration. Here we report that homozygous deletion of Cdh1 together with mutational activation of Pik3ca in mammary epithelium of genetically modified mice leads to rapid formation of IR-ILC-like tumors with immune cell infiltration, as well as gene expression signatures linked to TRegulatory (Treg) cell signaling and immune checkpoint inhibitor pathway activation. Interestingly, these tumors show enhanced Oct4-, Hif1á-, YAP-, Shh-, Rac- and Notch-dependent transcription/signaling, features in common with human IR-ILC and therefore potential targets for therapy. Gene expression profiling reveals immune infiltration and similarities to a subtype of human Invasive Lobular carcinoma.
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Project description:The identification of lobular caricnoma in situ (LCIS) in a patient's specimen confers and appreciable increased risk of development of future invasive mammary carcinoma. However the study of LCIS presents a challenge as it is usually only recognized in fixed specimens and no good in vivo or in vitro models currently exist. Recent advances in high throughput genomics have made possible comprehensive copy number analysis of lesions such as this. We have characterized LCIS on microdissected cases of archival patient samples using aCGH. We used 4 cases of LCIS with adjacent ILC.
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Project description:aCGH study of lobular carcinoma in situ (LCIS) and invasive lobular carcinoma (ILC)
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Project description:Gene expression array analysis on a series of ten different histological special types of invasive breast carcinomas (tubular, micropapillary, mucinous A, mucinous B, endocrine, apocrine, metaplastic, medullary, adenoid cystic, invasive ductal carcinoma with osteoclastic giant cells) and invasive lobular carcinoma.<br><br>Note: this experiment was reloaded into ArrayExpress in August 2010 to include mappings between raw and processed data files. It now includes additional dye-swap combined normalized data files.
2010-08-20 | E-NCMF-3 | biostudies-arrayexpress
Project description:We identified MDC1 as a putative novel transcriptional co-regulator of estrogen receptor alpha (ER) in models of invasive lobular carcinoma. In this study, our goal was to define the contribution of MDC1 to regulation of the ER transcriptome in ILC cell lines versus invasive ductal carcinoma cells.
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Project description:<p>This study comprises prospectively accrued, microdissected fresh frozen samples of multifocal lobular carcinoma <i>in situ</i> (LCIS), ductal carcinoma <i>in situ</i> (DCIS), invasive lobular carcinoma and invasive ductal carcinoma from patients undergoing prophylactic or therapeutic mastectomies after a diagnosis on LCIS diagnosed and managed at Memorial Sloan Kettering Cancer Center (MSKCC). Microdissected samples were subjected to paired-end whole exome sequencing on an Illumina HiSeq 2000. The data generated were used to define the landscape of somatic genetic alterations of LCIS, DCIS, invasive lobular carcinoma and invasive ductal carcinoma, to define clonal relatedness of these lesions and to investigate the clonal shifts in the progression from <i>in situ</i> to invasive breast cancer.</p>
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Project description:The GATA-type zinc-finger transcription factor TRPS1 has been implicated in breast cancer. However, its precise role remains unclear, as both amplifications and inactivating mutations in TRPS1 have been reported. Here, we used in vitro and in vivo loss-of-function approaches to dissect the role of TRPS1 in mammary gland development and invasive lobular breast carcinoma, which is hallmarked by functional loss of E-cadherin. We show that TRPS1 is essential in mammary epithelial cells, since TRPS1-mediated suppression of interferon signaling promotes in vitro proliferation and lactogenic differentiation. Similarly, TRPS1 expression is indispensable for proliferation of mammary organoids and in vivo survival of luminal epithelial cells during mammary gland development. However, the consequences of TRPS1 loss are dependent on E-cadherin status, as combined inactivation of E-cadherin and TRPS1 causes persistent proliferation of mammary organoids and accelerated mammary tumor formation in mice. Together, our results demonstrate that TRPS1 can function as a context-dependent tumor suppressor in breast cancer, whilst being essential for growth and differentiation of normal mammary epithelial cells.
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