Publications by authors named "Angela Schwarz-Cruz Y Celis"

(1) Aim: In the present paper we analyzed the transcriptome of CSCs (Cancer Stem Cells), in order to find defining molecular processes of breast cancer. (2) Methods: We performed RNA-Seq from CSCs isolated from the basal cell line MDA-MB-468. Enriched processes and networks were studied using the IPA (Ingenuity Pathway Analysis) tool.

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Much effort has been made by researchers to elucidate the complex biology of breast cancer stem cells (BCSCs), a small subset of breast tumor cells that display stem cell properties, drive tumor initiation, and growth. In recent years, it has been suggested that BCSCs could be responsible for the process of metastasis and the development of drug resistance. These findings make the need to find the distinguishing blend of markers that can recognize only BCSCs of the utmost importance in order to be able to design new targeted therapies.

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Tissue inhibitor of metalloproteinase-4 (TIMP-4) belongs to a family of extracellular matrix (ECM) metalloproteinases inhibitors that are overexpressed in several cancers. However, the role of TIMP-4 during carcinogenesis is poorly understood. To evaluate TIMP-4 functions in carcinogenesis, stably transfected cells overexpressing this tissue inhibitor were used.

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Article Synopsis
  • Pediatric Ewing sarcoma is primarily characterized by EWS-ETS gene fusions, making it a unique model for studying cancers related to transcription factors.
  • Most Ewing sarcoma tumors exhibit a low mutation rate, with the majority showing only these rearrangements, while about 15% have lost STAG2 expression linked to disease spread.
  • The study emphasizes a lack of mutations in common signaling pathways, indicating a need for novel therapies targeting EWS-ETS fusions.
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To gain insight into the genomic basis of diffuse large B-cell lymphoma (DLBCL), we performed massively parallel whole-exome sequencing of 55 primary tumor samples from patients with DLBCL and matched normal tissue. We identified recurrent mutations in genes that are well known to be functionally relevant in DLBCL, including MYD88, CARD11, EZH2, and CREBBP. We also identified somatic mutations in genes for which a functional role in DLBCL has not been previously suspected.

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There are two hypotheses that explain tumor progression. The first one, the stochastic hypothesis, assumes that any cell within a tumor has the capacity to form and maintain the tumor mass. The second, the so-called hierarchical hypothesis, suggests the existence of a group of cells with a stem phenotype which, like in normal tissues, preserves tumors through a continuous production of progeny.

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