Human papillomavirus infection and cervical intraepithelial neoplasia in women with renal allografts.

Alloub, M.; Barr, B. B.; McLaren, K M; Smith, I. P.; Bunney, Mary H.; Smart, G. E.

doi:10.1136/bmj.298.6667.153

Cited by 205 publications

(101 citation statements)

References 14 publications

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“…Unknown HPV subtypes are hypothesised to play a role in the aetiology of nonmelanoma skin cancer (Blohme and Brynger, 1985;Barr et al, 1989;Bouwes Bavinck et al, 1997) and defined oncogenic types are clearly causally related to cancer of the cervix (IARC, 1995), anus (Frisch et al, 1997), vulva and vagina (Blohme and Brynger, 1985;Alloub et al, 1989). Although controversial, HPV has also been proposed as a risk factor for oesophageal cancer (Galloway and Daling, 1996) as well as for head and neck cancers (Mork et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Cancer risk following organ transplantation: a nationwide cohort study in Sweden

et al. 2003

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A substantial excess risk of lymphomas and nonmelanoma skin cancer has been demonstrated following organ transplantation. Large sample size and long follow-up time may, however, allow more accurate risk estimates and detailed understanding of long-term cancer risk. The objective of the study was to assess the risk of cancer following organ transplantation. A nationwide cohort study comprising 5931 patients who underwent transplantation of kidney, liver or other organs during 1970 -1997 in Sweden was conducted. Complete follow-up was accomplished through linkage to nationwide databases. We used comparisons with the entire Swedish population to calculate standardised incidence ratios (SIRs), and Poisson regression for multivariate internal analyses of relative risks (RRs) with 95% confidence intervals (CI). Overall, we observed 692 incident first cancers vs 171 expected (SIR 4.0; 95% CI 3.7 -4.4). We confirmed marked excesses of nonmelanoma skin cancer (SIR 56.2; 95% CI 49.8 -63.2), lip cancer (SIR 53.3; 95% CI 38.0 -72.5) and of non-Hodgkin's lymphoma (NHL) (SIR 6.0; 95% CI 4.4 -8.0). Compared with patients who underwent kidney transplantation, those who received other organs were at substantially higher risk of NHL (RR 8.4; 95% CI 4.3 -16). Besides, we found, significantly, about 20-fold excess risk of cancer of the vulva and vagina, 10-fold of anal cancer, and five-fold of oral cavity and kidney cancer, as well as two-to four-fold excesses of cancer in the oesophagus, stomach, large bowel, urinary bladder, lung and thyroid gland. In conclusion, organ transplantation entails a persistent, about four-fold increased overall cancer risk. The complex pattern of excess risk at many sites challenges current understanding of oncogenic infections that might become activated by immunologic alterations.

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Section: Discussionmentioning

confidence: 99%

Cancer risk following organ transplantation: a nationwide cohort study in Sweden

et al. 2003

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“…Some authors have suggested that cytology is plagued with an increase in inadequate specimens from inflammation in this group (87), and studies on immunosuppressed renal transplant recipients show high false-negative rates with cytology as well (88,89). In one small study, cytology and colposcopy were performed on 32 seropositive women, demonstrating cervical SILs in 41%, with only 7.7% of them detected cytologically (90).…”

Section: Lower Genital Tract Neoplasiasmentioning

confidence: 99%

Gynecologic issues in the HIV-infected woman

Cejtin

2003

Obstetrics and Gynecology Clinics of North America

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“…4 Approximately 95% of HPV infections of the anogenital tract resolve spontaneously because of immune responses, 5 and the risk of cervical cancer is markedly increased in patients with immunodeficiency. [6][7][8] These findings suggest that the immune system plays a pivotal role in preventing development and progression of cervical cancer.Two HPV oncoproteins, E6 and E7, which can inhibit the tumor suppressors, p53 and RB respectively, are constitutively expressed in cervical cancer cells and appear to be required to maintain their malignant growth. 9 These viral oncoproteins, which are not present in normal cells, have been considered to be attractive targets for specific immunotherapy against cervical cancer, and identification and characterization of cytotoxic T lymphocyte (CTL) epitopes for HPV have facilitated the development of peptide vaccines against cervical cancer.…”

mentioning

confidence: 90%

Identification of an HLA‐A24‐restricted cytotoxic T lymphocyte epitope from human papillomavirus type‐16 E6: The combined effects of bortezomib and interferon‐γ on the presentation of a cryptic epitope

Akatsuka

Nawa

Kondo

et al. 2006

Intl Journal of Cancer

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About 50% of cervical cancers are associated with human papillomavirus type 16 (HPV-16), and since the HPV-16 E6 and E7 oncoproteins are constitutively expressed in the tumor cells, they are attractive targets for cytotoxic T lymphocyte (CTL)-mediated immunotherapy. Nevertheless, only a limited number of HPV-16 E6 epitopes have been identified to date. Using reverse immunological methods, we have generated a CTL clone against the HPV-16 E6 49-57 epitope restricted by HLA-A*2402, which is the most common allele in Japan and relatively frequent worldwide, capable of lysing 293T cells transduced with HLA-A*2402 and HPV-16 E6. Although it was unable to recognize the SiHa cervical cancer cell line positive for HPV-16 and HLA-A*2402, the cells became susceptible to lysis when transduced with E6-E7 genes, which was unexpectedly offset by pretreatment with interferon (IFN)-c alone. Interestingly, however, combined pretreatment with a proteasome inhibitor, bortezomib and IFN-c fully restored CTL-mediated lysis of the original SiHa cells. Furthermore, such intervention of 2 of 4 other cervical cancer cell lines expressing HPV-16 E6 and HLA-A*2402 was found to induce IFN-c production by specific CTLs. Tetramer analysis further revealed that induction of E6 49-57 -specific T cells was possible in 5 of 7 patients with HPV-16-positive high grade cervical intraepithelial neoplasia or cervical cancer by in vitro stimulation with E6 49-57 peptide. Thus, these findings together indicate that E6 49-57 is a candidate epitope for immunotherapy and immunological monitoring of such patients. ' 2006 Wiley-Liss, Inc.Key words: cytotoxic T lymphocyte; tumor immunity; epitope, cervical neoplasm; bortezomib Cervical cancer, the second most common cancer in women worldwide, with 250,000 new cases diagnosed each year, 1 is causally linked with human papillomavirus (HPV), the first proposed necessary cause of a human cancer as assessed by the World Health Organization. 2 High-risk HPV-16 is the most common type in all countries, with an overall prevalence of more than 50% in cervical cancers, 3 and 42.4% in Japanese patients. 4 Approximately 95% of HPV infections of the anogenital tract resolve spontaneously because of immune responses, 5 and the risk of cervical cancer is markedly increased in patients with immunodeficiency. [6][7][8] These findings suggest that the immune system plays a pivotal role in preventing development and progression of cervical cancer.Two HPV oncoproteins, E6 and E7, which can inhibit the tumor suppressors, p53 and RB respectively, are constitutively expressed in cervical cancer cells and appear to be required to maintain their malignant growth. 9 These viral oncoproteins, which are not present in normal cells, have been considered to be attractive targets for specific immunotherapy against cervical cancer, and identification and characterization of cytotoxic T lymphocyte (CTL) epitopes for HPV have facilitated the development of peptide vaccines against cervical cancer. Most of the CTL epitopes identified to date ...

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Human papillomavirus infection and cervical intraepithelial neoplasia in women with renal allografts.

Cited by 205 publications

References 14 publications

Cancer risk following organ transplantation: a nationwide cohort study in Sweden

Cancer risk following organ transplantation: a nationwide cohort study in Sweden

Gynecologic issues in the HIV-infected woman

Identification of an HLA‐A24‐restricted cytotoxic T lymphocyte epitope from human papillomavirus type‐16 E6: The combined effects of bortezomib and interferon‐γ on the presentation of a cryptic epitope

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