Expression of E-cadherin in 230 infiltrating ductal breast carcinoma

Gamallo, Carlos; Palacios, José; Benito, N; Limeres, María J.; Pizarro, Ángel; Suarez, Arturo; Pastrana, Francisco Gómez; Cano, Amparo; Calero, Francisco Calero

doi:10.3892/ijo.9.6.1207

Cited by 15 publications

(16 citation statements)

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“…Since no mutations in the E-cadherin gene have been detected in tumours in the breast of the ductal histological type (Berx et al, 1996), this provides the clearest evidence of molecular difference in the two main histological types of breast carcinomas. Nonetheless, reduced expression of E-cadherin has been found in both lobular and ductal breast cancers (Oka et al, 1993;Gamallo et al, 1996) and detection of chromosome 16q22.1 is the highest documental loss of a chromosome region in sporadic breast cancers of both histological types (Skirnisdottir et al, 1995; this study). Two explanations of this difference are possible, either: (1) a gene other than the E-cadherin gene is the target of the 16q22.1 deletion in ductal compared to lobular carcinomas of breast cancer; or (2) the progression of ductal carcinomas is more sensitive to loss of one copy of the E-cadherin gene, and corresponding reduction of expression, than lobular breast carcinomas, where both copies need to be eliminated for further progression to malignant invasive growth.…”

Section: Discussionmentioning

confidence: 51%

Chromosome alterations and E-cadherin gene mutations in human lobular breast cancer

et al. 1999

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We have studied a set of 40 human lobular breast cancers for loss of heterozygosity (LOH) at various chromosome locations and for mutations in the coding region plus flanking intron sequences of the E-cadherin gene. We found a high frequency of LOH (100%, 31/31) at 16q21–q22.1. A significantly higher level of LOH was detected in ductal breast tumours at chromosome arms 1p, 3p, 9p, 11q, 13q and 18q compared to lobular breast tumours. Furthermore, we found a significant association between LOH at 16 q containing the E-cadherin locus and lobular histological type. Six different somatic mutations were detected in the E-cadherin gene, of which three were insertions, two deletions and one splice site mutation. Mutations were found in combination with LOH of the wild type E-cadherin locus and loss of or reduced E-cadherin expression detected by immunohistochemistry. The mutations described here have not previously been reported. We compared LOH at different chromosome regions with E-cadherin gene mutations and found a significant association between LOH at 13 q and E-cadherin gene mutations. A significant association was also detected between LOH at 13q and LOH at 7q and 11q. Moreover, we found a significant association between LOH at 3 p and high S phase, LOH at 9p and low ER and PgR content, LOH at 17p and aneuploidy. We conclude that LOH at 16q is the most frequent chromosome alteration and E-cadherin is a typical tumour suppressor gene in lobular breast cancer. © 1999 Cancer Research Campaign

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Section: Discussionmentioning

confidence: 51%

Chromosome alterations and E-cadherin gene mutations in human lobular breast cancer

et al. 1999

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“…Dynamic expression is supported by the frequently observed re-expression of E-cadherin in secondary metastatic foci and even in some lymph node metastasis (Takeichi, 1993;Gamallo et al, 1996;Christofori and Semb, 1999;Graff et al, 2000). Dynamic regulation of E-cadherin expression is a tightly regulated process during embryonic development in which Ecadherin is lost when EMTs occur but is re-expressed in the reverse situation: the establishment of epithelial lineages from mesoderm layers (Takeichi, 1995;Huber et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

The transcription factor Slug repressesE-cadherinexpression and induces epithelial to mesenchymal transitions: a comparison with Snail and E47 repressors

Bolós

Peinado

Pérez-Moreno

et al. 2003

Journal of Cell Science

1,020

746

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There was an error published in J. Cell Sci. 116, 499-511.For the GST-Snail band-shift assay (right-hand panel) shown in Fig. 2, the incorrect data was inadvertently shown to represent the results of the competition with the 1000-fold unlabeled E-pal wild-type (wt) probe experiment (first lane on the left). Additionally, the indication of the removal of lanes was omitted in the original figure. The correct Fig. 2 is presented below. There are no changes to the figure legend, which is accurate. This error does not affect the conclusions of the study.The authors apologise to the readers for any confusion that this error might have caused. 1283

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“…It is well known that a HCC tumor subtypes. As no significant E-CD or catenin immunostaining often consists of multiple histological types 21 ; therefore, the heterogeneity was seen in any histological tumor lesion, the 41 HCCs were classified into the following 67 histologically composite score, which has recently been adopted for precise defined tumor lesions: 29 thin trabecular (TnT)-, 14 pseudo-evaluation of E-CD immunostaining, 25 was not used in the glandular (PG)-, 23 thick trabecular (TkT)-, and 1 compact-current study. type, according to the World Health Organization.…”

Section: Methodsmentioning

confidence: 99%

Expression of Epithelial Cadherin and α– and β–Catenins in Nontumoral Livers and Hepatocellular Carcinomas

et al. 1996

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Expression of the cell adhesion molecule, epithelial nism. 2,3 The transmembrane linker glycoprotein that cadherin (E-CD) and its binding proteins, a-and b-caten-mediates this adhesion is thought to be epithelial cadins, in normal liver, chronic liver diseases, and hepato-herin (E-CD), the homophilic interaction of which links cellular carcinomas (HCCs) was investigated immuno-adjacent cells.4 E-CD is a member of the cadherin famhistologically. In normal liver, weak immunostaining of ily that is involved in Ca 2/ -dependent cell-cell adhesion E-CD and catenins was observed at the lateral mem-in vertebrate tissues.4,5 Regulated E-CD expression fabranes of the hepatocytes, whereas at the interlobular cilitates several epithelial morphogenetic events, in- 3,4 In rat livers, it is suggested that Eas well as Hering canals and proliferating ductules, CD may be a fundamental factor in hepatocyte polarity showed markedly increased molecular expression. Anal-formation and in shaping hepatic plates during embryysis of 66 HCC lesions revealed that the majority (64.3-onic development.6 However, the physiological roles 96.6%) of thin trabecular-and pseudoglandular-type tu-and distribution of E-CD in human liver are still poorly mors preserved or overexpressed E-CD and catenins, understood. whereas thick trabecular-type HCCs frequently showedRecent studies have shown that the full adhesive low E-CD and a-catenin expression (56.5-65.2% reducfunction of E-CD is expressed only when it is complexed tion), suggesting that the thick trabecular histology represented diffuse tumor cell growth. Likewise, the E-CD via a specific cytoplasmic binding domain with three and catenin expression levels correlated with the HCC cytosolic proteins, termed a-, b-, and g-catenins.7,8 Cacell differentiation grades. These collective results indi-tenins mediate connection of E-CD to the actin filament cate that intercellular adhesion mediated by the E-CD-network and link E-CD to other transmembrane procatenin system plays a role in morphological changes in teins, such as Na Furthermore, b-catenin was shown to be the common target for signal transduction pathways mediated by Tight cell-cell binding is an essential phenomenon the proto-oncogenes src and wnt-1 10 and for a-and bthat characterizes the epithelial cellular phenotype, catenins bound to a protein product of the tumor supwhich is achieved primarily by the adherens junctions pressor gene APC (adenomatous polyposis coli). 11,12 present on the cell membranes.1 In normal epithelium, These findings suggest that, in addition to regulating the junctions form a continuous adhesion belt around E-CD activity, catenins play a role in controlling tumoreach interacting cell; those in adjacent epithelial cells igenic cell growth. are directly apposed to them, and the interacting memIt has been known for some time that intercellular branes are held together by a Ca 2/ -dependent mechaadhesion becomes weakened morphologically in carcinomas. Indeed, certain types of carcinoma, such as signet ring cell and und...

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Expression of E-cadherin in 230 infiltrating ductal breast carcinoma

Cited by 15 publications

References 0 publications

Chromosome alterations and E-cadherin gene mutations in human lobular breast cancer

Chromosome alterations and E-cadherin gene mutations in human lobular breast cancer

The transcription factor Slug repressesE-cadherinexpression and induces epithelial to mesenchymal transitions: a comparison with Snail and E47 repressors

Expression of Epithelial Cadherin and α– and β–Catenins in Nontumoral Livers and Hepatocellular Carcinomas

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