DCC expression is related to mucinous differentiation but not changes in expression of p21(WAF1/Cip1) and p27Kip1, apoptosis, cell proliferation and human papillomavirus infection in uterine cervical adenocarcinomas.
To clarify possible roles of DCC expression in tumour differentiation and cell kinetics, we immunohistochemically investigated 80 uterine cervical adenocarcinomas (C-ACs), including 31 mucinous (M) and 31 endometrioid (E) lesions, and 18 adenocarcinomas in situ (AIS), along with 39 normal cervical samples. The results were compared with findings for p21(WAF1/Cip1) and p27Kip1 expression, apoptosis, cell proliferation and human papillomavirus (HPV) infection. Nine C-AC cases were also examined using a combination of the reverse transcription-polymerase chain reaction and Southern blot hybridization, as well as Western blot assays. Significantly decreased DCC scores were observed in E-ACs but not M-ACs, as compared to normal cervical glandular epithelia and AIS. Average p21(WAF1/Cip1) and p27Kip1 scores were significantly higher in E-ACs than M-ACs, in line with high apoptotic, mitotic and Ki-67 labelling indices. A concordance of the results for DCC and p21(WAF1/Cip1) expression between mRNA- and protein-based assays was also noted. Change of DCC expression, however, was not related to any of the cell kinetic markers or clinicopathological features in ACs of either type. There was also no association with the HPV status, although infection was significantly linked with high values for cell kinetics. These results suggest that DCC expression in C-ACs is closely associated with mucinous differentiation.
Saegusa
M
M
Department of Pathology, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.
Okayasu
I
I
D000230:Adenocarcinoma / Q000378:metabolism* / Q000473:pathology* / Q000821:virology; D017209:Apoptosis; D015139:Blotting, Southern; D015153:Blotting, Western; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D018797:Cell Cycle Proteins; D002455:Cell Division; D050759:Cyclin-Dependent Kinase Inhibitor p21; D050760:Cyclin-Dependent Kinase Inhibitor p27; D016213:Cyclins / Q000378:metabolism*; D000075389:DCC Receptor; D005260:Female; D016147:Genes, Tumor Suppressor; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000378:metabolism; D008869:Microtubule-Associated Proteins / Q000378:metabolism*; D008940:Mitotic Index; D027383:Papillomaviridae / Q000302:isolation & purification; D030361:Papillomavirus Infections / Q000473:pathology; D011956:Receptors, Cell Surface; D020133:Reverse Transcriptase Polymerase Chain Reaction; D025521:Tumor Suppressor Proteins; D014412:Tumor Virus Infections / Q000473:pathology; D002583:Uterine Cervical Neoplasms / Q000378:metabolism* / Q000473:pathology* / Q000821:virology
C493956:CDKN1A protein, human; D015815:Cell Adhesion Molecules; D018797:Cell Cycle Proteins; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D000075389:DCC Receptor; C501909:DCC protein, human; D019394:Ki-67 Antigen; D008869:Microtubule-Associated Proteins; D011956:Receptors, Cell Surface; D025521:Tumor Suppressor Proteins; D050760:Cyclin-Dependent Kinase Inhibitor p27