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Histol Histopathol ; 29(7): 913-23, 2014 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-24399516

RESUMO

Disseminated tumour cells (DTCs) in the bone marrow derive from many primary tumours, such as breast cancer. Their mere existence hints to present or future metastasis and implicates a worse prognosis for the patient. DTCs may possess different characteristics in comparison to the primary tumour due to events like Epithelial-Mesenchymal-Transition. Therefore, these cells might be able to survive chemotherapy and cause relapses of the disease at a later point. We aimed to detect and further characterise DTCs by an immunostaining approach with three different antigen markers (Her-2, MUC-1 and TF, also known as CD 176). For that reason, bone marrow of 41 breast cancer patients was obtained during surgery; DTCs were enriched by density gradient centrifugation and cytospins were prepared. After fixation, immunofluorescent double-stainings were carried out with antibodies against CD176 in combination with HER-2 or MUC-1. Cells co-expressing two antigens were found in all staining combinations (Her-2 and CD176: 46.14%; MUC-1 and CD176: 18.15% of all cases). Cells that stained for a single antigen only were also found (Her-2: 36.86%; MUC-1: 34.45%; CD176: 29.65% of all cases). Significant correlations between the stainings of all markers could be shown (p<0,001). In conclusion, Thomsen-Friedenreich Antigen (TF, CD176) is a promising marker in combination with the established marker Her-2 and other markers like MUC-1. These results may serve as a basis for future DTC detection routines and help to individualize medical treatment, reducing side effects and increasing the efficiency of the therapy.


Assuntos
Biomarcadores Tumorais/análise , Neoplasias da Medula Óssea/diagnóstico , Neoplasias da Mama/patologia , Antígenos Glicosídicos Associados a Tumores/análise , Antígenos Glicosídicos Associados a Tumores/biossíntese , Neoplasias da Medula Óssea/secundário , Feminino , Humanos , Imuno-Histoquímica , Mucina-1/análise , Mucina-1/biossíntese , Receptor ErbB-2/análise , Receptor ErbB-2/biossíntese
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