Presence of oncogenic HPV DNAs in cervical carcinoma tissues and pelvic lymph nodes associating with proliferating cell nuclear antigen expression.
The presence of oncogenic HPV DNAs (HPV-16/18) in cervical carcinomas and their normal and metastatic pelvic lymph nodes and the expression patterns of proliferating cell nuclear antigen (PCNA) in cervical carcinomas were retrospectively studied to elucidate the possible roles of them in malignant transformation and progression of the disease. HPV-16/18 DNAs were detected by polymerase chain reaction using HPV E6 type-specific primers in 79 patients with cervical cancer. 31 patients who had pelvic lymph node metastasis (group I) and 48 patients without pelvic lymph node metastasis (group II) who were proven by pathologic examination of surgical specimens. HPV-16 or -18 DNAs were detectable in cervical carcinoma tissues in 60 patients from 79 cervical cancer patients (75.9%; HPV-16 was 67.1% and HPV-18 was 8.9%). HPV DNAs were amplified from metastatic pelvic lymph nodes in 13 patients of group I (42%) and from nonmetastatic lymph nodes in 7 group I patients (22.5%). Recurrence was identified in 9 group I patients (29.0%) in 3 years of follow-up. HPV DNAs were amplified from nonmetastatic lymph nodes in 11 group II patients (22.9%). Two group II patients, who had HPV-16 DNA by PCR in nonmetastatic nodes, were recurrent. PCNA was overexpressed in 66.7% of HPV-16- or -18-positive cervical cancers and 16.7% of HPV-16- or -18-negative cervical cancers. However, the expression levels of PCNA in cervical cancers were not influenced by the presence of oncogenic HPV DNA or pathologic metastasis in the pelvic lymph nodes. In conclusion, HPV DNA could be amplified from some metastatic and nonmetastatic pelvic lymph nodes and the detectability of oncogenic HPV DNA in pelvic lymph nodes may represent the poor outcome in the treatment of disease. The expression of PCNA protein which was associated with presence of oncogenic HPV DNAs in cervical cancers, suggesting activation of S phase of cell cycle, may contribute to the malignant progression by HPV-16 or -18.
Park
J S
JS
Department of Obstetrics and Gynecology, Catholic University Medical College, Seoul, Korea.
Rhyu
K S
KS
Kim
C J
CJ
Kim
H S
HS
Han
K T
KT
Ahn
H K
HK
Kim
S J
SJ
Namkoong
S E
SE
D001483:Base Sequence; D002277:Carcinoma / Q000378:metabolism*; D004279:DNA, Viral / Q000378:metabolism*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008198:Lymph Nodes / Q000378:metabolism*; D008875:Middle Aged; D008969:Molecular Sequence Data; D015345:Oligonucleotide Probes / Q000235:genetics; D009857:Oncogenes; D027383:Papillomaviridae / Q000235:genetics*; D010388:Pelvis; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism*; D014018:Tissue Distribution; D002583:Uterine Cervical Neoplasms / Q000378:metabolism*
D004279:DNA, Viral; D015345:Oligonucleotide Probes; D018809:Proliferating Cell Nuclear Antigen