E‐cadherin deregulation in breast cancer

Corso, Giovanni; Figueiredo, Joana; Angelis, Simone Pietro De; Corso, Federica; Girardi, Antonia; Pereira, Joana; Seruca, Raquel; Bonanni, Bernardo; Carneiro, Patrı́cia; Pravettoni, Gabriella; Guerini-Rocco, Elena; Veronesi, Giulia; Montagna, Giacomo; Sacchini, Virgilio; Gandini, Sara

doi:10.1111/jcmm.15140

Cited by 83 publications

(62 citation statements)

References 49 publications

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“…However, both histological subtypes have shown a frequent 16q-loss, independently by the presence of inactivating point mutations of CDH1, and the invasive lobular carcinomas have shown a reduced expression of CDH1 at both the mRNA and protein level [ 45 , 48 , 59 , 62 , 63 ]. Indeed, other mechanisms for the reduced expression or function of E-cadherin, such as transcriptional downregulation, promoter methylation of CDH1, and post-translational modifications of E-cadherin, have been detected in breast cancer [ 61 , 64 , 65 , 66 , 67 , 68 ]. It is well-known that E-cadherin antigen, detected by immunohistochemistry analysis, is mainly expressed in ductal carcinomas and absent in lobular ones [ 66 , 69 , 70 , 71 ].…”

Section: Discussionmentioning

confidence: 99%

Aberrations of Chromosomes 1 and 16 in Breast Cancer: A Framework for Cooperation of Transcriptionally Dysregulated Genes

Privitera

Barresi

Condorelli

2021

Cancers

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Derivative chromosome der(1;16), isochromosome 1q, and deleted 16q—producing arm-level 1q-gain and/or 16q-loss—are recurrent cytogenetic abnormalities in breast cancer, but their exact role in determining the malignant phenotype is still largely unknown. We exploited The Cancer Genome Atlas (TCGA) data to generate and analyze groups of breast invasive carcinomas, called 1,16-chromogroups, that are characterized by a pattern of arm-level somatic copy number aberrations congruent with known cytogenetic aberrations of chromosome 1 and 16. Substantial differences were found among 1,16-chromogroups in terms of other chromosomal aberrations, aneuploidy scores, transcriptomic data, single-point mutations, histotypes, and molecular subtypes. Breast cancers with a co-occurrence of 1q-gain and 16q-loss can be distinguished in a “low aneuploidy score” group, congruent to der(1;16), and a “high aneuploidy score” group, congruent to the co-occurrence of isochromosome 1q and deleted 16q. Another three groups are formed by cancers showing separately 1q-gain or 16q-loss or no aberrations of 1q and 16q. Transcriptome comparisons among the 1,16-chromogroups, integrated with functional pathway analysis, suggested the cooperation of overexpressed 1q genes and underexpressed 16q genes in the genesis of both ductal and lobular carcinomas, thus highlighting the putative role of genes encoding gamma-secretase subunits (APH1A, PSEN2, and NCSTN) and Wnt enhanceosome components (BCL9 and PYGO2) in 1q, and the glycoprotein E-cadherin (CDH1), the E3 ubiquitin-protein ligase WWP2, the deubiquitinating enzyme CYLD, and the transcription factor CBFB in 16q. The analysis of 1,16-chromogroups is a strategy with far-reaching implications for the selection of cancer cell models and novel experimental therapies.

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Section: Discussionmentioning

confidence: 99%

Aberrations of Chromosomes 1 and 16 in Breast Cancer: A Framework for Cooperation of Transcriptionally Dysregulated Genes

Privitera

Barresi

Condorelli

2021

Cancers

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“…In normal human mammary tissue, E-cadherin is expressed in luminal epithelial cells, while P-cadherin is found in myoepithelial cells ( 245 ). In HBC, E-cadherin is known to be an inhibitor of metastasis, and its downregulation or inactivation leads to aggressive forms of breast cancer, EMT, lymphovascular invasion and metastasis ( 246 , 247 ), as well as higher histological grade ( 248 ). Likewise, in CMC, reduction of E-cadherin expression has been related to large size and ulceration of mammary tumors ( 249 ), infiltrative growth, high histological grade, and lymph node metastasis ( 250 – 253 ), as well as shorter overall and disease-free survivals ( 254 ).…”

Section: Adjuvant Targeted Therapiesmentioning

confidence: 99%

From Conventional to Precision Therapy in Canine Mammary Cancer: A Comprehensive Review

et al. 2021

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Canine mammary tumors (CMTs) are the most common neoplasm in intact female dogs. Canine mammary cancer (CMC) represents 50% of CMTs, and besides surgery, which is the elective treatment, additional targeted and non-targeted therapies could offer benefits in terms of survival to these patients. Also, CMC is considered a good spontaneous intermediate animal model for the research of human breast cancer (HBC), and therefore, the study of new treatments for CMC is a promising field in comparative oncology. Dogs with CMC have a comparable disease, an intact immune system, and a much shorter life span, which allows the achievement of results in a relatively short time. Besides conventional chemotherapy, innovative therapies have a large niche of opportunities. In this article, a comprehensive review of the current research in adjuvant therapies for CMC is conducted to gather available information and evaluate the perspectives. Firstly, updates are provided on the clinical–pathological approach and the use of conventional therapies, to delve later into precision therapies against therapeutic targets such as hormone receptors, tyrosine kinase receptors, p53 tumor suppressor gene, cyclooxygenases, the signaling pathways involved in epithelial–mesenchymal transition, and immunotherapy in different approaches. A comparison of the different investigations on targeted therapies in HBC is also carried out. In the last years, the increasing number of basic research studies of new promising therapeutic agents on CMC cell lines and CMC mouse xenografts is outstanding. As the main conclusion of this review, the lack of effort to bring the in vitro studies into the field of applied clinical research emerges. There is a great need for well-planned large prospective randomized clinical trials in dogs with CMC to obtain valid results for both species, humans and dogs, on the use of new therapies. Following the One Health concept, human and veterinary oncology will have to join forces to take advantage of both the economic and technological resources that are invested in HBC research, together with the innumerable advantages of dogs with CMC as a spontaneous animal model.

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“…The results demonstrated an enrichment of MAPK and CDH1 signaling pathways in ES-2 cells after over-expression of RALYL ( Figure 5A). Collectively, these findings implied an involvement of RALYL in the OCCC pathogenesis by targeting MAPK and CDH1 signaling pathways, which have been reported to play a key role in the tumorigenesis (13,14). To verify our speculation, western blot was conducted to investigate the expression levels of proteins in the signaling pathways.…”

Section: Ralyl Inhibits Mapk and Cdh1 Signaling Pathways In Occcmentioning

confidence: 55%

Over-expression of RALYL suppresses the progression of ovarian clear cell carcinoma through inhibiting MAPK and CDH1 signaling pathways

Xia

Yang

et al. 2021

Int. J. Med. Sci.

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E‐cadherin deregulation in breast cancer

Cited by 83 publications

References 49 publications

Aberrations of Chromosomes 1 and 16 in Breast Cancer: A Framework for Cooperation of Transcriptionally Dysregulated Genes

Aberrations of Chromosomes 1 and 16 in Breast Cancer: A Framework for Cooperation of Transcriptionally Dysregulated Genes

From Conventional to Precision Therapy in Canine Mammary Cancer: A Comprehensive Review

Over-expression of RALYL suppresses the progression of ovarian clear cell carcinoma through inhibiting MAPK and CDH1 signaling pathways

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