Down-regulation of ANAPC13 and CLTCL1: Early Events in the Progression of Preinvasive Ductal Carcinoma of the Breast


Autoria(s): Sens-Abuazar, Carolina; Napolitano e Ferreira, Elisa; Bueno Toledo Osorio, Cynthia Aparecida; Krepischi, Ana Cristina Victorino; Ricca, Tatiana Iervolino; Castro, Nadia Pereira; da Cunha, Isabela Werneck; Maciel, Maria do Socorro; Rosenberg, Carla; Brentani, Maria Mitzi; Soares, Fernando Augusto; Rocha, Rafael Malagoli; Carraro, Dirce Maria
Contribuinte(s)

UNIVERSIDADE DE SÃO PAULO

Data(s)

01/11/2013

01/11/2013

02/08/2013

Resumo

Alterations in the gene expression profile in epithelial cells during breast ductal carcinoma (DC) progression have been shown to occur mainly between pure ductal carcinoma in situ (DCIS) to the in situ component of a lesion with coexisting invasive ductal carcinoma (DCIS-IDC) implying that the molecular program for invasion is already established in the preinvasive lesion. For assessing early molecular alterations in epithelial cells that trigger tumorigenesis and testing them as prognostic markers for breast ductal carcinoma progression, we analyzed, by reverse transcription-quantitative polymerase chain reaction, eight genes previously identified as differentially expressed between epithelial tumor cells populations captured from preinvasive lesions with distinct malignant potential, pure DCIS and the in situ component of DCIS-IDC. ANAPC13 and CLTCL1 down-regulation revealed to be early events of DC progression that anticipated the invasiveness manifestation. Further down-regulation of ANAPC13 also occurred after invasion appearance and the presence of the protein in invasive tumor samples was associated with higher rates of overall and disease-free survival in breast cancer patients. Furthermore, tumors with low levels of ANAPC13 displayed increased copy number alterations, with significant gains at 1q (1q23.1-1q32.1), 8q, and 17q (17q24.2), regions that display common imbalances in breast tumors, suggesting that down-regulation of ANAPC13 contributes to genomic instability in this disease.

Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (CEPID/FAPESP) [98/14335]

Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (CEPID/FAPESP)

CNPq

CNPq [142790/2008-7]

FAPESP [2009/00669-2, 2009/02457-2]

FAPESP

Identificador

TRANSLATIONAL ONCOLOGY, ANN ARBOR, v. 5, n. 2, supl. 1, Part 6, pp. 113-U105, APR, 2012

1936-5233

http://www.producao.usp.br/handle/BDPI/37432

10.1593/tlo.11280

http://dx.doi.org/10.1593/tlo.11280

Idioma(s)

eng

Publicador

NEOPLASIA PRESS

ANN ARBOR

Relação

TRANSLATIONAL ONCOLOGY

Direitos

openAccess

Copyright NEOPLASIA PRESS

Palavras-Chave #GENE-EXPRESSION PROFILES #IN-SITU DCIS #TUMOR MICROENVIRONMENT #CANCER #CLATHRIN #HETEROGENEITY #MITOSIS #TRANSFORMATION #COMPONENTS #PATTERNS #ONCOLOGY
Tipo

article

original article

publishedVersion