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Pancreatic Neoplasms: HELP
Articles by María González-González
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, María González-González wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Altered interphase fluorescence in situ hybridization profiles of chromosomes 4, 8q24, and 9q34 in pancreatic ductal adenocarcinoma are associated with a poorer patient outcome. 2014

Gutiérrez, María L / Muñoz-Bellvis, Luis / Sarasquete, María E / Hernández-Mejía, David G / Abad, María del Mar / Bengoechea, Oscar / Corchete, Luis / González-González, María / García-García, Jacinto / Gonzalez, Marcos / Mota, Ines / Orfao, Alberto / Sayagues, José M. ·Cytometry General Service-NUCLEUS, Department of Medicine and Cancer Center Research and Institute of Molecular Biology and Cellular Oncology, Institute of Biomedical Research of Salamanca, University of Salamanca, Salamanca, Spain. · Department of General and Digestive Surgery, University Hospital of Salamanca, Salamanca, Spain. · Hematology Service, Institute of Biomedical Research of Salamanca, University Hospital of Salamanca, Cancer Center Research and Institute of Molecular Biology and Cellular Oncology, Salamanca, Spain. · Department of Pathology, University Hospital of Salamanca, Salamanca, Spain. · Cytometry General Service-NUCLEUS, Department of Medicine and Cancer Center Research and Institute of Molecular Biology and Cellular Oncology, Institute of Biomedical Research of Salamanca, University of Salamanca, Salamanca, Spain. Electronic address: orfao@usal.es. ·J Mol Diagn · Pubmed #25157969.

ABSTRACT: Most patients with pancreatic ductal adenocarcinoma (PDAC) die within 6 months of diagnosis. However, 20% to 25% patients undergoing total tumor resection remain alive and disease-free 5 years after diagnostic surgery. Few studies on tumor markers have predicted patient prognosis and/or survival. We evaluated the effect of tumor cytogenetic copy number changes detected by interphase fluorescence in situ hybridization on overall survival (OS) of 55 PDAC patients. The prognostic value of copy number changes showing an effect on OS was validated in an external cohort of 44 surgically resected PDAC patients by comparative genomic hybridization arrays, and the genes coded in altered chromosomes with prognostic value were identified by high-density single-nucleotide polymorphism arrays in 20 cases. Copy number changes of chromosomes 4 and 9q34 with gains of 8q24 were independently associated with shorter OS. On the basis of these three chromosomal alterations, a score is proposed that identifies patients with significantly different (P < 0.001) 5-year OS rates: 60% ± 20%, 16% ± 8%, and 0% ± 0%, respectively. Our results show an association between tumor cytogenetics and OS of PDAC patients and provide the basis for further prognostic stratification of patients undergoing complete tumor resection. Further studies to identify specific genes coded in these chromosomes and their functional consequences are necessary to understand the clinical effect of these changes.

2 Article Association between genetic subgroups of pancreatic ductal adenocarcinoma defined by high density 500 K SNP-arrays and tumor histopathology. 2011

Gutiérrez, María Laura / Muñoz-Bellvis, Luís / Abad, María del Mar / Bengoechea, Oscar / González-González, María / Orfao, Alberto / Sayagués, José María. ·Servicio General de Citometría, Departamento de Medicina and Centro de Investigación del Cáncer (IBMCC-CSIC/USAL), Universidad de Salamanca, Salamanca, Spain. ·PLoS One · Pubmed #21811587.

ABSTRACT: The specific genes and genetic pathways associated with pancreatic ductal adenocarcinoma are still largely unknown partially due to the low resolution of the techniques applied so far to their study. Here we used high-density 500 K single nucleotide polymorphism (SNP)-arrays to define those chromosomal regions which most commonly harbour copy number (CN) alterations and loss of heterozygozity (LOH) in a series of 20 PDAC tumors and we correlated the corresponding genetic profiles with the most relevant clinical and histopathological features of the disease. Overall our results showed that primary PDAC frequently display (>70%) extensive gains of chromosomes 1q, 7q, 8q and 20q, together with losses of chromosomes 1p, 9p, 12q, 17p and 18q, such chromosomal regions harboring multiple cancer- and PDAC-associated genes. Interestingly, these alterations clustered into two distinct genetic profiles characterized by gains of the 2q14.2, 3q22.1, 5q32, 10q26.13, 10q26.3, 11q13.1, 11q13.3, 11q13.4, 16q24.1, 16q24.3, 22q13.1, 22q13.31 and 22q13.32 chromosomal regions (group 1; n = 9) versus gains at 1q21.1 and losses of the 1p36.11, 6q25.2, 9p22.1, 9p24.3, 17p13.3 and Xp22.33 chromosomal regions (group 2; n = 11). From the clinical and histopathological point of view, group 1 cases were associated with smaller and well/moderately-differentiated grade I/II PDAC tumors, whereas and group 2 PDAC displayed a larger size and they mainly consisted of poorly-differentiated grade III carcinomas. These findings confirm the cytogenetic complexity and heterozygozity of PDAC and provide evidence for the association between tumor cytogenetics and its histopathological features. In addition, we also show that the altered regions identified harbor multiple cancer associate genes that deserve further investigation to determine their relevance in the pathogenesis of PDAC.

3 Minor Cytogenetic heterogeneity of pancreatic ductal adenocarcinomas: identification of intratumoral pathways of clonal evolution. 2011

Gutiérrez, María Laura / Sayagués, José María / Abad, María del Mar / Bengoechea, Oscar / González-González, María / Orfao, Alberto / Muñoz-Bellvis, Luís. · ·Histopathology · Pubmed #21323969.

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