par Chidiac, Mounia 
;Fayyad Kazan, Mohammad ;Daher, Jalil ;Poelvoorde, Philippe ;Bar, Isabelle;Maenhaut, Carine ;Delree, Paul;Badran, Bassam ;Vanhamme, Luc
Référence Pathology, research and practice, 212, 7, page (631-635)
Publication Publié, 2016-07
;Fayyad Kazan, Mohammad ;Daher, Jalil ;Poelvoorde, Philippe ;Bar, Isabelle;Maenhaut, Carine ;Delree, Paul;Badran, Bassam ;Vanhamme, Luc Référence Pathology, research and practice, 212, 7, page (631-635)
Publication Publié, 2016-07
Article révisé par les pairs
| Résumé : | The apolipoprotein L (apoL) family has not yet been ascribed any definite patho-physiological function although the conserved BH3 protein domain suggests a role in programmed cell death. As repression of the regular apoptotic program is considered a hallmark of tumor progression, we investigated apoL expression in cancer. We show that the levels of one member of the family, apolipoprotein L1 (apoL1) is higher in papillary thyroid carcinoma compared to normal tissue. A combination of qRTPCR, immunohistochemistry and in situ hybridization allowed us to ascribe this increase to endogenous overexpression in carcinoma cells. Whether apoL1 plays an instrumental role in refraining cell death is the subject of ongoing molecular biology experiments. |
