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Polarity gene alterations in pure invasive micropapillary carcinomas of the breast

ABSTRACT: In this study we have identified a new morphological pattern in IMPC defined by the presence of numerous bi-nucleated cells, related to abnormal expression of genes involved in regulation of mitosis. We also demonstrated that IMPC presented tight and adherens junctions proteins expression modifications that could participate to their clinical behavior. We showed that IMPC was associated with a specific genomic profile compared to ER+ grade-matched IDC consisting of gains of 17q, high rates of 17q23 and 17q12 ERBB2 amplifications, losses of heterozygosity of 6q. The putative role of the genes located in this 6q LOH should be further investigated in order to determine if they could play a role in the presence of numerous bi-nucleated cells and inverted polarity of IMPC cells. In addition, we identified two genomic IMPC subsets: the first characterized by numerous amplicons with frequently near-tetraploid cells and the second, associated with different complex gains and losses in addition to 8q gains and 16q losses, and predominantly composed of near-diploïd cells. The observation of two genomic subsets within the IMPC entity suggests the existence of two possible oncogenic mechanisms leading to the development of a single disease.

ORGANISM(S): Homo sapiens

PROVIDER: GSE37035 | GEO | 2014/04/01

SECONDARY ACCESSION(S): PRJNA158289

REPOSITORIES: GEO

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Polarity gene alterations in pure invasive micropapillary carcinomas of the breast

Project description:In this study we have identified a new morphological pattern in IMPC defined by the presence of numerous bi-nucleated cells, related to abnormal expression of genes involved in regulation of mitosis. We also demonstrated that IMPC presented tight and adherens junctions proteins expression modifications that could participate to their clinical behavior. We showed that IMPC was associated with a specific genomic profile compared to ER+ grade-matched IDC consisting of gains of 17q, high rates of 17q23 and 17q12 ERBB2 amplifications, losses of heterozygosity of 6q. The putative role of the genes located in this 6q LOH should be further investigated in order to determine if they could play a role in the presence of numerous bi-nucleated cells and inverted polarity of IMPC cells. In addition, we identified two genomic IMPC subsets: the first characterized by numerous amplicons with frequently near-tetraploid cells and the second, associated with different complex gains and losses in addition to 8q gains and 16q losses, and predominantly composed of near-diploïd cells. The observation of two genomic subsets within the IMPC entity suggests the existence of two possible oncogenic mechanisms leading to the development of a single disease. Phenotypical analysis was combined with copy number, genotyping (SNP6.0 Affymetrix) and transcriptomic analyses in a series of 39 pure IMPC. The results were compared to those of 27 ER and grade-matched invasive ductal carcinomas (IDC).

2014-04-01 | E-GEOD-37035 | biostudies-arrayexpress

BAC CGH array profiling using Phi29-amplified colon mucosa of microdissected samples from APC and MYH mutation carriers.

Project description:Details of the series are available in the publication Cardoso J. et al., âChromosomal instability in MYH- and APC-mutant adenomatous polypsâ, Cancer Research, accepted for publication. Abstract of the publication: âThe vast majority of colorectal cancers display genetic instability, either in the chromosomal (CIN) or microsatellite (MIN) forms. While CIN tumors are per definition aneuploid, MIN colorectal cancers, caused by loss of mismatch repair function, are usually near-diploid. Recently, bi-allelic germline mutations in the MYH gene, were found to be responsible for MAP (MYH associated polyposis), an autosomal recessive predisposition to multiple colorectal polyps, often indistinguishable from the dominant FAP (familial adenomatous polyposis) syndrome caused by inherited APC mutations. Here, we analyzed MYH- and APC-mutant polyps by combining laser-capture microdissection, isothermal genomic DNA amplification, and array-CGH (comparative genomic hybridization). Smoothed quantile regression methods were applied to the MAP and FAP genomic profiles to discriminate chromosomes predominantly affected by gains and losses. Up to 80% of the MAP polyps showed aneuploid changes, which is significantly higher than the 60% found among FAP polyps. Both MAP and FAP adenomas were characterized by frequent losses at chromosome 1p, 17, 19 and 22, and gains affecting chromosome 7 and 13. The observation that aneuploidy is already detectable at early stages of MYH-driven tumorigenesis raises the possibility that CIN may contribute significantly to accelerated tumor progression, increased cancer risk, and poor prognosis in MAP.â Details of the series are available in the publication Cardoso J. et al., âChromosomal instability in MYH- and APC-mutant adenomatous polypsâ, Cancer Research, accepted for publication.

2010-06-30 | E-GEOD-3898 | biostudies-arrayexpress

BAC CGH array profiling using Phi29-amplified colon mucosa of microdissected samples from APC and MYH mutation carriers.

Project description:Details of the series are available in the publication Cardoso J. et al., “Chromosomal instability in MYH- and APC-mutant adenomatous polyps”, Cancer Research, accepted for publication. Abstract of the publication: “The vast majority of colorectal cancers display genetic instability, either in the chromosomal (CIN) or microsatellite (MIN) forms. While CIN tumors are per definition aneuploid, MIN colorectal cancers, caused by loss of mismatch repair function, are usually near-diploid. Recently, bi-allelic germline mutations in the MYH gene, were found to be responsible for MAP (MYH associated polyposis), an autosomal recessive predisposition to multiple colorectal polyps, often indistinguishable from the dominant FAP (familial adenomatous polyposis) syndrome caused by inherited APC mutations. Here, we analyzed MYH- and APC-mutant polyps by combining laser-capture microdissection, isothermal genomic DNA amplification, and array-CGH (comparative genomic hybridization). Smoothed quantile regression methods were applied to the MAP and FAP genomic profiles to discriminate chromosomes predominantly affected by gains and losses. Up to 80% of the MAP polyps showed aneuploid changes, which is significantly higher than the 60% found among FAP polyps. Both MAP and FAP adenomas were characterized by frequent losses at chromosome 1p, 17, 19 and 22, and gains affecting chromosome 7 and 13. The observation that aneuploidy is already detectable at early stages of MYH-driven tumorigenesis raises the possibility that CIN may contribute significantly to accelerated tumor progression, increased cancer risk, and poor prognosis in MAP.” Keywords: repeat, BAC, CGH

2005-12-25 | GSE3898 | GEO

Array comparative genomic hybridization data from 313 CLL specimens to study outcome associations

Project description:This study investigates genomic imbalance in chronic lymphocytic leukemia (CLL) and aims to identify genomic gains and losses with prognostic significance.

2013-09-07 | GSE40834 | GEO

Frequent occurrence of deletions in primary mediastinal B-cell lymphoma

Project description:Primary mediastinal B-cell lymphoma (PMBCL) is a distinct subtype of diffuse large B-cell lymphoma. PMBCL has been previously studied with a variety of genomic techniques resulting in frequent detection of chromosomal gains; however, chromosomal losses have been rarely reported. This finding contrasts many other types of lymphoma, in which deletions are common. We hypothesize that segmental losses do exist but may have escaped detection by methods used in the previous studies. Using array comparative genomic hybridization to a tiling-resolution microarray encompassing the entire human genome, PMBCL samples were analyzed for genomic copy number alterations. Both gains and losses of chromosomal material were detected throughout the genome. These DNA copy number alterations were confirmed by quantitative real-time PCR. Recurrent chromosomal losses include a novel event at 1p13.1-p13.2 present in 42% of cases analyzed. We conclude that losses are present in the PMBCL genome. Given the similar frequency of losses to that of segmental gains of DNA, they are likely to play an important role in the pathogenesis of PMBCL. Keywords: array CGH, PMBCL

2007-08-15 | GSE7383 | GEO

Array comparative genomic hybridization (CGH) analysis of ameloblastoma tumor

Project description:To investigate the minimal genomic alterations in ameloblastoma, we have employed high-resolution CGH as a discovery platform to identify somatic genomic gains and losses in ameloblastoma tumors.

2019-06-11 | GSE132473 | GEO

Frequent occurrence of deletions in primary mediastinal B-cell lymphoma

2007-08-15 | E-GEOD-7383 | biostudies-arrayexpress

Genome-wide profiling of copy-number alteration in monoclonal gammopathy of undetermined significance

Project description:Monoclonal gammopathy of undetermined significance (MGUS) is a benign condition with an approximate 1% annual risk of symptomatic plasma cell disorder development, mostly to multiple myeloma (MM). We performed genome-wide screening of copy-number alterations (CNAs) in 90 MGUS and 33 MM patients using high-density DNA microarrays. We identified CNAs in a smaller proportion of MGUS (65.6%) than in MM (100.0%, p=1.31×10-5) and showed median number of CNAs is lower in MGUS (3, range 0-22) than in MM (13, range 4-38, p=1.82×10-10). In the MGUS cohort, the most frequent losses were located at 1p (5.6%), 6q (6.7%), 13q (30.0%), 14q (14.4%), 16q (8.9%), 21q (5.6%) and gains at 1q (23.3%), 2p (6.7%), 6p (13.3%) and Xq (7.8%). Hyperdiploidy was detected in 38.9% of MGUS cases and the most frequent whole chromosome gains were 3 (25.6%), 5 (23.3%), 9 (37.8%), 15 (23.3%) and 19 (32.2%). We also identified CNAs such as 1p, 6q, 8p, 12p, 13q, 16q losses, 1q gain and hypodiploidy, which are potentially associated with an adverse prognosis in MGUS. In summary, we showed that MGUS is similar to MM in that it is a genetically heterogeneous disorder, but overall cytogenetic instability is lower than in MM, which confirms that genetic abnormalities play important role in monoclonal gammopathies.

2016-02-18 | GSE77975 | GEO

SHED: control vs Hepatocyte-like cells

Project description:Profiling of chromosomal gains and losses in a genomic complement of stem cells from human exfoliated deciduous teeth comparing control undifferentieated SHED with hepatocyte differentiated SHED.

2018-02-01 | GSE102974 | GEO

Identification of novel candidate target genes at 3q26.2-q29 in squamous cell carcinoma of the lung

Project description:High-resolution array-CGH was performed to identify differences in the patterns of genomic imbalances between SCC and AC of non-small cell lung cancer (NSCLC). On a genome-wide profile, SCCs showed higher frequency of gains than ACs (p = 0.067). More specifically, statistically significant differences were observed across the histologic subtypes for gains at 2q14.2, 3q26.2-q29, 12p13.2-p13.33, and 19p13.3, as well as losses at 3p26.2-p26.3, 16p13.11, and 17p11.2 in SCC, and gains at 7q22.1 and losses at 15q22.2-q25.2 occurred in AC (P < 0.05). The most striking difference between SCC and AC was gains at 3q26.2-q29, occurring in 86% (19/22) of SCCs, but in only 21% (3/14) of ACs.

2009-06-19 | GSE16597 | GEO

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