AIMS: To compare the morphology and antigenic profile of pulmonary neuroendocrine cells (PNECs) proliferating as a reaction to pulmonary injury with those proliferating in diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) in which carcinoids develop. METHODS AND RESULTS: The morphology and expression of a range of antigens including markers of epithelial differentiation [cytokeratins, thyroid transcription factor (TTF)-1], neuroendocrine antigens [neural cell adhesion molecule (NCAM), chromogranin, protein gene product (PGP) 9.5, neurone-specific enolase (NSE), synaptophysin], peptide products [gastrin-releasing peptide (GRP), calcitonin, calcitonin gene-related peptide (CGRP)] and inactivator [common acute lymphoblastic leukaemia antigen (CALLA)] and antigens involved in cell proliferation and death (p53, p16, p27, Rb, Bcl-2, c-kit, Ki67) were studied in four cases of reactive PNEC proliferation and seven cases of DIPNECH. Proliferation was more florid in DIPNECH. There was no major shift in antigen expression with proliferation in either group apart from CALLA, which was expressed only by proliferating cells and not by solitary PNECs. There were differences between the groups in expression of p53, p16 and Ki67, which were seen more consistently and earlier in proliferation in DIPNECH. CONCLUSIONS: These data suggest that there are early and fundamental differences in cell kinetics between the reactive PNEC proliferation that occurs in response to pulmonary injury and that seen in the pre-neoplastic condition of DIPNECH. 2011 Blackwell Publishing Limited.
AIMS: To compare the morphology and antigenic profile of pulmonary neuroendocrine cells (PNECs) proliferating as a reaction to pulmonary injury with those proliferating in diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) in which carcinoids develop. METHODS AND RESULTS: The morphology and expression of a range of antigens including markers of epithelial differentiation [cytokeratins, thyroid transcription factor (TTF)-1], neuroendocrine antigens [neural cell adhesion molecule (NCAM), chromogranin, protein gene product (PGP) 9.5, neurone-specific enolase (NSE), synaptophysin], peptide products [gastrin-releasing peptide (GRP), calcitonin, calcitonin gene-related peptide (CGRP)] and inactivator [common acute lymphoblastic leukaemia antigen (CALLA)] and antigens involved in cell proliferation and death (p53, p16, p27, Rb, Bcl-2, c-kit, Ki67) were studied in four cases of reactive PNEC proliferation and seven cases of DIPNECH. Proliferation was more florid in DIPNECH. There was no major shift in antigen expression with proliferation in either group apart from CALLA, which was expressed only by proliferating cells and not by solitary PNECs. There were differences between the groups in expression of p53, p16 and Ki67, which were seen more consistently and earlier in proliferation in DIPNECH. CONCLUSIONS: These data suggest that there are early and fundamental differences in cell kinetics between the reactive PNEC proliferation that occurs in response to pulmonary injury and that seen in the pre-neoplastic condition of DIPNECH. 2011 Blackwell Publishing Limited.
Authors: Antonio García Escudero; Enrique Rodríguez Zarco; Juan Carlos Girón Arjona; María José Ríos Moreno; Katherine Gallardo Rodríguez; Ana Vallejo Benítez; Ricardo González Cámpora Journal: Virchows Arch Date: 2016-06-14 Impact factor: 4.064
Authors: Olga Sazonova; Venkata Manem; Chloé Béland; Marc-André Hamel; Yves Lacasse; Marie-Hélène Lévesque; Michèle Orain; David Joubert; Steeve Provencher; David Simonyan; Philippe Joubert Journal: JTO Clin Res Rep Date: 2020-07-24