Presence of papillomavirus sequences in condylomatous lesions of the mamillae and in invasive carcinoma of the breast

被引:126
作者
de Villiers, EM [1 ]
Sandstrom, RE
zur Hausen, H
Buck, CE
机构
[1] Deutsch Krebsforschungszentrum, Div Characterizat Tumorviruses, D-6900 Heidelberg, Germany
[2] Lower Columbia Pathologists, Longview, WA USA
关键词
areolar tissue; breast carcinoma; papillomavirus;
D O I
10.1186/bcr940
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background Viruses including Epstein-Barr virus (EBV), a human equivalent of murine mammary tumour virus (MMTV) and human papillomavirus (HPV) have been implicated in the aetiology of human breast cancer. We report the presence of HPV DNA sequences in areolar tissue and tumour tissue samples from female patients with breast carcinoma. The presence of virus in the areolar-nipple complex suggests to us a potential pathogenic mechanism. Methods Polymerase chain reaction (PCR) was undertaken to amplify HPV types in areolar and tumour tissue from breast cancer cases. In situ hybridisation supported the PCR findings and localised the virus in nipple, areolar and tumour tissue. Results Papillomavirus DNA was present in 25 of 29 samples of breast carcinoma and in 20 of 29 samples from the corresponding mamilla. The most prevalent type in both carcinomas and nipples was HPV 11, followed by HPV 6. Other types detected were HPV 16, 23, 27 and 57 (nipples and carcinomas), HPV 20, 21, 32, 37, 38, 66 and GA3-1 (nipples only) and HPV 3, 15, 24, 87 and DL473 (carcinomas only). Multiple types were demonstrated in seven carcinomas and ten nipple samples. Conclusions The data demonstrate the occurrence of HPV in nipple and areolar tissues in patients with breast carcinoma. The authors postulate a retrograde ductular pattern of viral spread that may have pathogenic significance.
引用
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页码:R1 / R11
页数:11
相关论文
共 72 条
[31]  
GISSMANN L, 1982, INT J CANCER, V29, P143, DOI 10.1002/ijc.2910290205
[32]   Absence of human papillomavirus DNA in breast cancer as revealed by polymerase chain reaction [J].
Gopalkrishna, V ;
Singh, UR ;
Sodhani, P ;
Sharma, JK ;
Hedau, ST ;
Mandal, AK ;
Das, BC .
BREAST CANCER RESEARCH AND TREATMENT, 1996, 39 (02) :197-202
[33]   PCR AMPLIFICATION FROM PARAFFIN-EMBEDDED TISSUES - EFFECTS OF FIXATIVE AND FIXATION TIME [J].
GREER, CE ;
PETERSON, SL ;
KIVIAT, NB ;
MANOS, MM .
AMERICAN JOURNAL OF CLINICAL PATHOLOGY, 1991, 95 (02) :117-124
[34]  
GRUSSENDORFCONEN EI, 1987, CANCER, V60, P1832, DOI 10.1002/1097-0142(19871015)60:8<1832::AID-CNCR2820600826>3.0.CO
[35]  
2-2
[36]   Inactivation of both the retinoblastoma tumor suppressor and p21 by the human papillomavirus type 16 E7 oncoprotein is necessary to inhibit cell cycle arrest in human epithelial cells [J].
Helt, AM ;
Funk, JO ;
Galloway, DA .
JOURNAL OF VIROLOGY, 2002, 76 (20) :10559-10568
[37]   Attributable risks for familial breast cancer by proband status and morphology:: A nationwide epidemiologic study from Sweden [J].
Hemminki, K ;
Granström, C ;
Czene, K .
INTERNATIONAL JOURNAL OF CANCER, 2002, 100 (02) :214-219
[38]  
Hennig EM, 1999, J EXP CLIN CANC RES, V18, P369
[39]   Human papillomavirus 16 in breast cancer of women treated for high grade cervical intraepithelial neoplasia (CIN III). [J].
Hennig, EM ;
Suo, ZH ;
Thoresen, S ;
Holm, R ;
Kvinnsland, S ;
Nesland, JM .
BREAST CANCER RESEARCH AND TREATMENT, 1999, 53 (02) :121-135
[40]   Annual report to the nation on the status of cancer (1973 through 1998), featuring cancers with recent increasing trends [J].
Howe, HL ;
Wingo, PA ;
Thun, MJ ;
Ries, LAG ;
Rosenberg, HM ;
Feigal, EG ;
Edwards, BK .
JOURNAL OF THE NATIONAL CANCER INSTITUTE, 2001, 93 (11) :824-842