Mirhashemi Ramin, Ganjei-Azar Parvin, Nadji Mehrdad, Lambrou Nicholas, Atamdede Fikret, Averette Hervy E
Harbor-UCLA Medical Center, David Geffen School of Medicine, Department of Obstetrics and Gynecology, Box 3, 1000 W. Carson St., Torrance, CA 90502, USA.
Gynecol Oncol. 2003 Sep;90(3):657-61. doi: 10.1016/s0090-8258(03)00329-9.
The objective was to evaluate the role of human papillomavirus (HPV) in the pathogenesis of papillary squamous cell carcinoma (PSCC) of the cervix and to determine cell proliferative activity and p53 abnormalities in these rare variants of cervical cancer.
Twelve examples of PSCC of the cervix were diagnosed between 1990 and 1999. Formalin-fixed paraffin sections of each tumor were stained by immunoperoxidase method using antibodies to p53 gene product (CM-10) and Ki-67 (MIB-1). In situ hybridization for HPV DNA (ENZO) was used to detect specific sequences of DNA shared by most types of genital HPV, followed by confirmatory PCR analysis. The nuclear staining for Ki-67 was graded as minimal (<10% of cells), moderate (between 10 and 50% of cells), and high (>50% of cells).
Fifty-percent of the tumors showed presence of HPV DNA. Three tumors (25%) showed nuclear accumulation of p53. Moderate and high proliferative activity was observed in four and eight of tumors, respectively. Eight patients presented with stage IB1 tumor (67%), 3 with stage IA1 tumor (25%), and 1 with stage IIIA tumor (8%). Eleven patients (92%) were alive as of last contact with a mean follow-up of 34.2 months (range: 5 days to 84 months).
In this series of patient, PSCC of the uterine cervix had a low rate of HPV DNA in their genome and a low rate of p53 gene abnormality. These genotypic differences may explain the differences between the clinical behavior of PSCC and the common types of squamous cell carcinomas of the cervix.
评估人乳头瘤病毒（HPV）在宫颈乳头状鳞状细胞癌（PSCC）发病机制中的作用，并确定这些罕见宫颈癌变体中的细胞增殖活性和p53异常情况。
1990年至1999年间诊断出12例宫颈PSCC。使用针对p53基因产物（CM-10）和Ki-67（MIB-1）的抗体，通过免疫过氧化物酶法对每个肿瘤的福尔马林固定石蜡切片进行染色。使用HPV DNA原位杂交（ENZO）检测大多数生殖器HPV类型共有的DNA特定序列，随后进行验证性PCR分析。Ki-67的核染色分为轻度（<10%的细胞）、中度（10%至50%的细胞）和高度（>50%的细胞）。
50%的肿瘤显示存在HPV DNA。3个肿瘤（25%）显示p53核聚集。分别在4个和8个肿瘤中观察到中度和高度增殖活性。8例患者表现为IB1期肿瘤（67%），3例为IA1期肿瘤（25%），1例为IIIA期肿瘤（8%）。截至最后一次联系，11例患者（92%）存活，平均随访34.2个月（范围：5天至84个月）。
在这组患者中，宫颈PSCC基因组中HPV DNA的发生率较低，p53基因异常的发生率也较低。这些基因型差异可能解释了PSCC与常见类型宫颈鳞状细胞癌临床行为之间的差异。
