Human papillomavirus antibody responses among patients with incident cervical carcinoma

Wang, Zhaohui; Kónya, József; Åvall-Lundkvist, Elisabeth; Sapp, Martin; Dillner, Joakim; Dillner, Lena

doi:10.1002/(sici)1096-9071(199708)52:4<436::aid-jmv16>3.0.co;2-e

Cited by 22 publications

(7 citation statements)

References 24 publications

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“…Significant associations for E6 and E7 antibodies for high‐risk types other than HPV16 and 18 extend the findings from other cross‐sectional studies reporting associations between HPV16 E6 and/or HPV16 E7 and risk of cervical and anal cancer . However, many of these studies were not able to stratify by HPV DNA type in the tumor.…”

Section: Discussionsupporting

confidence: 66%

“…The immune response to L1, the main component of the HPV capsid, has been widely studied in cross‐sectional and prospective studies, albeit using different serological assays, and is considered a marker of cumulative exposure to HPV infection, rather than of HPV‐related malignancy. In the present study, HPV16 L1 and HPV18 L1 were both significantly associated with cancer risk.…”

Section: Discussionmentioning

confidence: 99%

“…Sensitivity analysis using lower cut‐off values (defined arbitrarily) had the effect to slightly increase HPV seroprevalence in cases and controls, but did not greatly change the strength of the associations. Studies using a similar or alternative serological assays for E6 and E7 have also reported lack of seroconversion in a substantial fraction of cases …”

Section: Discussionmentioning

confidence: 99%

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Antibodies against high‐risk human papillomavirus proteins as markers for invasive cervical cancer

Combes

Pawlita

Waterboer

et al. 2014

Intl Journal of Cancer

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Different human papillomavirus (HPV) genes are expressed during the various phases of the HPV life cycle and may elicit immune responses in the process towards malignancy. To evaluate their association with cervical cancer, antibodies against proteins from HPV16 (L1, E1, E2, E4, E6 and E7) and HPV18/31/33/35/45/52/58 (L1, E6 and E7) were measured in serum of 307 invasive cervical cancer cases and 327 controls from Algeria and India. Antibody response was evaluated using a glutathione S-transferase-based multiplex serology assay and HPV DNA detected from exfoliated cervical cells using a GP51/61-mediated PCR assay. Among HPV16 DNA-positive cases, seroprevalence of HPV16 antibodies ranged from 16% for HPV16 E1 to 50% for HPV16 E6 and all were significantly higher than controls. Seroprevalence of E6, E7 and L1 antibodies for HPV18 and for at least one of HPV31/33/35/45/52/58 were also higher in cases positive for DNA of the corresponding type (50% and 30% for E6 of HPV18 and HPV31/33/35/45/52/58 combined, respectively). E6 and E7 antibodies were rarely found in controls, but cross-reactivity was evident among cancer cases positive for DNA of closely phylogenetically-related HPV types. E6 or E7 antibodies against any of the eight HPV types were detected in 66.1% of all cervical cancer cases, as compared to 10.1% of controls. E6, and to a lesser extent E7, antibodies appear to be specific markers of HPV-related malignancy. However, even among cases positive for the same type of HPV DNA, approximately one-third of cervical cancer cases show no detectable immune response to either E6 or E7.Twelve types of human papillomavirus (HPV), most notably HPV16 and HPV18, have been declared human carcinogens and their persistent infection in the cervix is established as a necessary cause for cervical cancer. 1 Different HPV genes are expressed during the various phases of the virus life cycle and in the process towards malignancy, and can produce a host immune response. The late protein L1 forms the capsid of the virus, and antibodies against HPV L1 are considered as markers of cumulative exposure to the virus, even though many HPV infected women are known not to seroconvert. 2 The early HPV oncoproteins E6 and E7 interact with cellular proteins involved in cell cycle control and DNA repair, most notably p53 and pRb, and are thus implicated in the induction and maintenance of malignant cellular transformation. Indeed, antibodies against E6 and E7 of HPV16 and 18 have been found to be highly specific markers of cervical cancer in comparison to controls, 3-5 as well as of oropharyngeal cancer. 6-10 To date, little is known about the immune response to other HPV early proteins nor about the immune response to the E6 and E7 proteins of high-risk HPV types other than HPV16 and 18. Hence, we applied a multiplex HPV serology method based on a glutathione S-transferase (GST) capture immunosorbent assay 11 to evaluate antibodies against a broad range of HPV16 (L1, E1, E2, E4, E6 and E7) and HPV18/31/ 33/35/45/52/58 (L1, E6 and E7) protei...

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Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Antibodies against high‐risk human papillomavirus proteins as markers for invasive cervical cancer

Combes

Pawlita

Waterboer

et al. 2014

Intl Journal of Cancer

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“…Several prospective studies have shown that seropositivity for HPV-16 increases the risk for future development of cervical cancer (Lehtinen et al, 1996 ;Shah et al, 1997 ;Dillner et al, 1997 ;Vonka et al, 1999) and other anogenital cancers (Bjo$ rge et al, 1997), and there are also studies that have found seropositivity to HPV-18 and -33 to be associated with invasive cervical cancer (Dillner et al, 1997 ;Wang et al, 1997). However, since the different oncogenic HPV types are similarly transmitted and since seropositivities for the different oncogenic HPV types thus are strongly associated with each other (Dillner et al, 1996), the possibility exists that the excess risks seen may be secondary to the excess risks associated with other HPV types.…”

Section: Introductionmentioning

confidence: 99%

Serological evidence for protection by human papillomavirus (HPV) type 6 infection against HPV type 16 cervical carcinogenesis

Silins

Wang

Lundqvist

et al. 1999

Journal of General Virology

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“…The preponderance of epidemiologic studies implicates a sexually passed agent as the primary risk factor for intraepithelial and invasive neoplasms of the uterine cervix [23][24][25][26][27]. Presently, human papilloma virus (HPV) is the prime suspect, particularly the so-called oncogenic types, including types 16 and 18, and possibly types 31, 35, 45, and other higher types [28][29][30][31][32][33][34][35][36][37]. But other sexually transmissible infections [38][39][40][41][42][43][44][45][46][47] and environmental and hereditary factors, or lack thereof, may ultimately prove to be important for initiation and progression of these neoplasms [48][49][50][51][52][53][54][55].…”

Section: Uterine Cervix Carcinomamentioning

confidence: 99%

Hereditary Factors in Gynecologic Cancer

Lynch¹,

Casey

Shaw³

et al. 1998

The Oncologist

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Cancer predisposition in some families is known to be the result of germ-line mutations. The most noteworthy hereditary gynecologic cancer syndromes include hereditary breast-ovarian cancer (HBOC) syndrome, wherein BRCA1 and BRCA2 germ-line mutations have been identified, and hereditary nonpolyposis colorectal cancer (HNPCC) of the Lynch syndrome II variant, wherein hMSH2, hMLH1, hPMS2, hMSH3, and hMSH6 germ-line mutations have been identified. DNA testing for specific cancer-associated germ-line mutations is now available for HBOC and HNPCC syndrome family members who are in the direct line of inheritance. Genetic counseling is mandatory prior to DNA testing and at the time of disclosure of findings. A patient found to be negative for the family's particular cancer-associated germ-line mutation can revert to general population screening recommendations. When a deleterious mutation is identified, the physician is able to predict a patient's lifetime susceptibility to breast and ovarian carcinomas in the HBOC syndrome or the cancers which characterize the Lynch syndrome II variant of HNPCC, particularly carcinomas of the colon, endometrium, and ovary. Management strategies can be offered which are designed to take advantage of the natural history of that distinct hereditary cancer syndrome. We discuss the unfolding developments concerning familial and heritable susceptibilities, molecular genetics, and possible carcinogenic co-factors of the three most common gynecologic cancers: carcinomas of the uterine cervix, endometrium, and ovary. We offer rationales for management based on current epidemiologic and clinical data and emerging technologies.

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Human papillomavirus antibody responses among patients with incident cervical carcinoma

Cited by 22 publications

References 24 publications

Antibodies against high‐risk human papillomavirus proteins as markers for invasive cervical cancer

Antibodies against high‐risk human papillomavirus proteins as markers for invasive cervical cancer

Serological evidence for protection by human papillomavirus (HPV) type 6 infection against HPV type 16 cervical carcinogenesis

Hereditary Factors in Gynecologic Cancer

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