Human papillomaviruses cause cervical cancer

The International Agency for Research on Cancer

Volume 64, Human Papillomaviruses. Summary of Data Reported and Evaluation. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, 1995. International Agency for Research on Cancer. Last updated 08/13/1997.

"5.5 Evaluation There is sufficient evidence in humans for the carcinogenicity of human papillomavirus (HPV) types 16 and 18. There is evidence suggesting lack of carcinogenicity to the cervix in humans of HPV types 6 and 11. There is limited evidence in humans for the carcinogenicity of some other HPV types. HPVs cannot infect animals. Some animal papillomaviruses cause cancer in their natural hosts."

"Overall Evaluation HPV types 16 and 18 are carcinogenic to humans (Group 1). HPV types 31 and 33 are probably carcinogenic to humans (Group 2A). Some HPV types other than 16, 18, 31 and 33 are possibly carcinogenic to humans (Group 2B). The carcinogenicity of types 16 and 18 is supported by experimental evidence that proteins of these viruses interfere with the functions of cellular regulatory pathways."

The National Institutes of Health Consensus Statement

Cervical Cancer. NIH Consensus Statement 1996 April 1-3. "A strong causal relationship between HPV and cervical cancer and its precursors has been established. The evidence for this statement is as follows:

• HPV DNA is present in virtually all cases (93 percent) of cervical cancer and its precursor lesions. [Actually, HPV has been found in 99.7 percent of cervical cancers -cast.]

• Multiple epidemiological studies indicate that HPV infection is the major risk factor for squamous intraepithelial lesions (SIL) and invasive cervical carcinoma.

• Studies have demonstrated that the HPV genes E6 and E7 are integrated into the host genome and that the transforming proteins encoded by these genes are tumorigenic."

Evidently in order to make it acceptable to the powerful anti-smoking establishment, they listing smoking among "factors under investigation."

"A recent report that 93 percent of invasive cervical cancers worldwide contain human papillomavirus (HPV) may be an understatement," due to underdetection. On reanalysis of the specimens, HPV was found in most supposedly HPV-negative cases, and "the worldwide HPV prevalence in cervical carcinomas is 99.7 percent." (Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. JM Walboomers et al. J Pathol 1999 Sep;189(1):12-19).

The causal relation between human papillomavirus and cervical cancer. FX Bosch, A Lorincz, N Muñoz, CJLM Meijer, KV Shah. J Clin Pathol 2002 Apr;55(4):244-265. Review. "The causal role of human papillomavirus infections in cervical cancer has been documented beyond reasonable doubt. The association is present in virtually all cervical cancer cases worldwide... This association has been evaluated under all proposed sets of causality criteria and endorsed by the scientific community and major review institutes. The finding is universally consistent, and to date there are no documented alternative hypotheses for the aetiology of cervical cancer." [The ritual invocations of "carcinogenic chemicals" notwithstanding. -cast] "The role of men as possible vectors of HPV was measured in the early epidemiological studies by questionnaires that asked about the sexual behaviour of the husbands or sexual partners of patients with cervical cancer and controls. In addition, more recent studies had the ability to measure HPV DNA in exfoliated cells from the penile shaft, the coronal sulcus, and the distal urethra. These and other studies consistently showed that the risk of cervical cancer for a given woman can be predicted by the sexual behaviour of her husband as much as her own sexual behaviour. In populations where female monogamy is dominant, the population of female sex workers plays an important role in the maintenance and transmission of HPV infections. Moreover, the probability that a woman is an HPV carrier and her risk of developing cervical cancer have been shown to be related to the presence of HPV DNA in the penis or the urethra of her husband or sexual partner." Then, these authors promptly forget this and lie that studies which simplistically compare HPV positive women are sufficient to demonstrate a supposed consistent risk from smoking, instead of that they reflect confounding by their failure to measure exposure from male partners. This consistent convenient forgetfulness is proof of conspiracy to falsely blame smoking. And, their reference to the Surgeon General is despicable, because the Surgeon General is not an esteemed scientist, but a politicized hack fronting for the corrupt, health fascist Lasker Lobby that has controlled the politicians and the health establishment for six decades.

Worldwide human papillomavirus etiology of cervical adenocarcinoma and its cofactors: implications for screening and prevention. X Castellsague, M Diaz, S de Sanjose, N Munoz, R Herrero, S Franceschi, RW Peeling, R Ashley, JS Smith, PJ Snijders, CJ Meijer, FX Bosch; International Agency for Research on Cancer Multicenter Cervical Cancer Study Group. J Natl Cancer Inst 2006 Mar 1;98(5):303-315.

As of July 27 and 31, 2006, only 58% of U.S. adults (70% of women and 47% of men) have heard of HPV. Of those who had, 70% supported the use of vaccine. (Seventy Percent of U.S. Adults Support Use of the Human Papillomavirus (HPV) Vaccine, According to New Wall Street Journal Online/Harris Interactive Health-Care Poll. Harris Interactive News Release, August 18, 2006.)

Human papillomavirus genotypes and the cumulative 2-year risk of cervical precancer. CM Wheeler, WC Hunt, M Schiffman, PE Castle; Atypical Squamous Cells of Undetermined Significance/Low-Grade Squamous Intraepithelial Lesions Triage Study Group. J Infect Dis 2006 Nov 1;194(9):1291-1299. "The most common HPV genotypes detected at baseline, in descending order of prevalence, were 16, 52, 51, 31, 18, 53, 39, 56, 62, 59, and 58. When detected as a single-type HPV infection, HPV-16 had a 2-year cumulative risk of 50.6% (95% confidence interval [CI], 44.1%-57.2%) for > or =CIN2 and 39.1% (95% CI, 32.9%-45.7%) for > or =CIN3. For other singly detected carcinogenic HPV types, the risk of > or =CIN2 ranged from 4.7% (for HPV-59) to 29.5% (for HPV-31), and the risk of > or =CIN3 ranged from 0.0% (for HPV-59) to 14.8% (for HPV-31). Multiple infections with HPV genotypes of different risk classes resulted in a risk that was similar to, and not significantly different from, the risk observed for the HPV genotype of the highest risk class."

High human papillomavirus oncogene mRNA expression and not viral DNA load is associated with poor prognosis in cervical cancer patients. MA de Boer, ES Jordanova, CG Kenter, AA Peters, WE Corver, JB Trimbos, GJ Fleuren. Clin Cancer Res 2007 Jan 1;13(1):132-138. "We studied the number of viral DNA copies and the level of HPV E6/E7 mRNA expression in 75 HPV 16-positive or HPV 18-positive International Federation of Gynecology and Obstetrics stage Ib and IIa cervical cancer patients. Measurements were done with quantitative PCR. DNA copy number analysis was done on pure tumor cell samples enriched with flow sorting. mRNA expression data were compensated for the percentage of tumor cells included. RESULTS: The number of viral DNA copies was not predictive of survival in cervical cancer patients. In contrast, high HPV E6/E7 mRNA expression was strongly related to an unfavorable prognosis (P = 0.006). In a multivariate Cox model for overall survival, including all known prognostic variables and stratified for HPV type, the level of E6/E7 mRNA expression was an independent prognostic indicator, second only to lymph node status. No correlation was observed between DNA copy number and the level of HPV E6/E7 mRNA expression, which reflects that not all DNA copies are equally transcriptionally active." [Ordonez 2004 reported that Asian American strains of HPV E2 had less repression of E6/E7.]

"The sexual behavior of men... can influence the risk of cervical cancer"

Detection of human papillomavirus infections in the male sexual partners of women attending an STD clinic in Bologna. S Costa, S Syrjanen, C Vendra, F Chang, G Guida, A Tervahauta, M Hippelainen, K Syrjanen. Int J STD AIDS 1992 Sep-Oct;3(5):338-346. "HPV was never present in men with only a single sexual partner, but increased significantly when the number of partners was increased, being highest (27.3%, 3 of 11) in those reporting 11-20 partners.

Papillomavirus research update: Highlights of the Barcelona HPV 2000 international papillomavirus conference. FX Bosch, T Rohan, A Schneider, I Frazer, H Pfister, X Castellsague, S de Sanjose, V Moreno, LM Puig-Tintore, PG Smith, N Munoz, H zur Hausen. J Clin Pathol 2001;54(3):163-175. "One phenomenon of interest in relation to risk of cervical cancer is the so-called male factor. Essentially, this is taken to mean that the sexual behavior of men (for example, the number of sexual partners that they have had) can influence the risk of cervical cancer in their female sexual partners. In this regard, Bleeker et al. presented data showing that 80% of the male sexual partners of women with CIN had penile lesions, of which a substantial portion were infected with HPV, and they speculated that penile lesions in sexual partners of women with CIN are probably productive and that they might play an important role in influencing the course of cervical lesions in these women by continuously reinfecting them with HPV."

The male role in cervical cancer. X Castellsague, FX Bosch, N Munoz. Salud Publica Mex 2003;45 Suppl 3:S345-353. "Acting both as "carriers" and "vectors" of oncogenic HPVs male partners may markedly contribute to the risk of developing cervical cancer in their female partners. Thus, in the absence of screening programs, a woman's risk of cervical cancer may depend less on her own sexual behavior than on that of her husband or other male partners."

Human papillomavirus DNA detection in male sexual partners of women with genital human papillomavirus infection. SM Nicolau, CG Camargo, JN Stavale, A Castelo, GB Dores, A Lorincz, GR de Lima. Urology 2005 Feb;65(2):251-255. "Fifty male, stable sexual partners of women positive for HPV DNA by the Hybrid Capture 2 (hc2) test had material brushed from six different anogenital areas for hc2 testing. One week later, patients underwent classic peniscopy, and the lesions were biopsied for histologic analysis and hc2 testing. RESULTS: The brushings were HPV DNA positive in 35 (70%) of the 50 men: 32% in the high-risk HPV group, 14% in the low-risk HPV group, and 24% in both groups. HPV detection per anatomic site was 24% in the glans, 44% in the prepuce internal surface, 30% in the distal urethra, 24% in the prepuce external surface, 12% in the scrotum, and 8% in the anus. Acetowhite lesions were seen in 44 (88%) of the 50 patients. Overall, HPV DNA was detected in 27 (26%) of the 104 biopsy specimens, but histologic examination showed evidence of HPV infection in only 14 (13.5%) of 104 biopsy specimens. In 3 (6%) of 50 patients, hc2 was positive only in the histologic examination. Overall, the prevalence of detectable high-risk HPV DNA among male partners was 60% (30 of 50). CONCLUSIONS: Of the 50 male partners studied, 76% were HPV DNA positive. Histologic examination was an inaccurate method to diagnose HPV DNA infection in men; however, brushings detected HPV in 92.1% of the infected men."

Penile carcinoma

Clinicopathological features and human papillomavirus dna prevalence of warty and squamous cell carcinoma of the penis. AL Bezerra, A Lopes, G Landman, GN Alencar, H Torloni, LL Villa. Am J Surg Pathol 2001 May;25(5):673-678. "HPV deoxyribonucleic acid was more likely to be associated with WC (five of 11, 45.5%) than SCC (16 of 60, 26.7%), although significance was not reached (p = 0.209)."

Human papillomavirus hpv-16 DNA as an epitheliotropic virus that induces hyperproliferation in squamous penile tissue. EL Salazar, E Mercado, L Calzada. Arch Androl 2005 Jul-Aug;51(4):327-334. "Thirty-eight biopsies were HPV-16DNA positive. This determination was correlated with cellular differentiation and growth pattern. Our data corroborates that squamous cell carcinoma was invariably associated with HPV-16DNA."

Detection of mucosal human papilloma virus DNA in bowenoid papulosis, Bowen's disease and squamous cell carcinoma of the skin. N Hama, T Ohtsuka, S Yamazaki. J Dermatol 2006 May;33(5):331-337. "[W]e detected HPV DNA in none of the 17 normal controls, two of the three BP (66.7%), one of the 21 BD (4.8%), and six of the 26 SCC of the skin samples (23.0%). The occurrence rates of HPV in BP and SCC were significantly elevated compared to that of normal controls (P < 0.01 and P < 0.01, respectively). In addition, the occurrence rate of HPV in BP was significantly elevated compared to that of BD (P < 0.05). The reproducibility was confirmed with a polymerase chain reaction (PCR) with another primer pair. Of the two cases of BP with positive HPV DNA, one case showed HPV 31 and the other case HPV 16. The case of BD with positive HPV DNA showed HPV 31. Of the six cases of SCC with positive HPV DNA, one case showed HPV 16, another case HPV 34, and the other four cases HPV 31. These results showed that mucosal HPV, including HPV 31 and 16, could be detected in SSC of the skin. Mucosal HPV, not only the epidermodysplasia verruciformis type, appear to induce malignant skin tumors."

Expression of p16 and hTERT protein is associated with the presence of high-risk human papillomavirus in Bowenoid papulosis. H Liu, K Urabe, Y Moroi, S Yasumoto, H Kokuba, S Imafuku, T Koga, T Masuda, H Aburatani, M Furue, Y Tu. J Cutan Pathol 2006 Aug;33(8):551-558. "Among the 26 biopsy specimens, in situ hybridization using DNA probes for HPV 16/18 revealed positivity in 18 specimens (69.2%), one of which also showed positivity with the probes for HPV 6/11. HPV 31/33/35 was found in three specimens (11.5%). Two specimens (7.7%) were positive for unclassified HPV."

The prevalence of human papillomavirus genotypes in penile cancers from northern Thailand. M Senba, A Kumatori, S Fujita, P Jutavijittum, A Yousukh, T Moriuchi, T Nakamura, K Toriyama. J Med Virol 2006 Oct;78(10):1341-1346. By PCR, HPV DNA was found in 81.5% of cases. High-risk HPV-18 was found in 55.4% of 65 cases (32.3% single and 23.1% multiple infection) followed by the low-risk HPV-6, found in 43.1% of the cases (24.6% single and 18.5% multiple infection).

High prevalence of human papillomavirus 16 in penile carcinoma. A Pascual, M Pariente, JM Godinez, R Sanchez-Prieto, M Atienzar, M Segura, E Poblet. Histol Histopathol 2007 Feb;22(2):177-183. "38 of the 49 cases were positive for HPV (77,5%). HPV16 appeared in 32 (84,2 %) of the 38 positive cases and HPV18 in 4 (10,5%)."

Demographic and pathologic differences in the incidence of invasive penile cancer in the United States, 1995-2003. MT Goodman, BY Hernandez, YB Shvetsov. Cancer Epidemiol Biomarkers Prev 2007 Sep;16(9):1833-1839. 6,539 penile cancers in 29 US population-based registries, 1995-2003. "Squamous cell carcinomas were the most common histologic type of penile cancer, representing 93% of all malignancies. Hispanic men had the highest age-adjusted incidence rates per million for penile cancer (6.58 per million), followed by Blacks (4.02 per million), Whites (3.90 per million), American Indians (2.81 per million), and Asian-Pacific Islanders (2.40 per million).... The incidence of penile cancer was highest in the South (4.42 per million) and lowest in the West (3.28 per million) of the United States. The highest age-adjusted incidence rate was found among Black men in the South (4.77 per million) and the lowest rate among Asian-Pacific Islanders in the West (1.84 per million)."

Human papillomavirus-16 is the predominant type etiologically involved in penile squamous cell carcinoma. DA Heideman, T Waterboer, M Pawlita, P Delis-van Diemen, I Nindl, JA Leijte, JM Bonfrer, S Horenblas, CJ Meijer, PJ Snijders. J Clin Oncol 2007 Oct 10;25(29):4550-4556. "HPV DNA of mucosal and/or cutaneous types was found in 46 of 83 (55%) penile SCCs. HPV16 was the predominant type, appearing in 24 (52%) of 46 of penile SCCs. The majority of HPV16 DNA-positive SCCs (18 of 24; 75%) demonstrated E6 transcriptional activity and a high viral load."

Human papillomavirus-associated penile sarcomatoid carcinoma. E Poblet, A Pascual, JM Godínez, M Pariente-Martín, E Escario, DC García-Olmo. J Cutan Pathol 2008 Jun;35(6):559-565. HPV16 and HPV 18 were found in two cases.

Systematic review of human papillomavirus prevalence in invasive penile cancer. DM Backes, RJ Kurman, JM Pimenta, JS Smith. Cancer Causes Control 2008 Dec 11. [Epub ahead of print]. Review of 1,266 squamous cell carcinomas from 30 studies. "HPV prevalence was 47.9%, ranging from 22.4% in verrucous SCC to 66.3% for the basaloid/warty subtypes. HPV16 (30.8%), HPV6 (6.7%) and HPV18 (6.6%) were the most prevalent types. HPV16 and/or HPV 18 prevalence was 36.7%."

Different strains in different populations

Worldwide distribution of human papillomavirus types in cytologically normal women in the International Agency for Research on Cancer HPV prevalence surveys: a pooled analysis. Clifford GM, Gallus S, Herrero R, Munoz N, Snijders PJ, Vaccarella S, Anh PT, Ferreccio C, Hieu NT, Matos E, Molano M, Rajkumar R, Ronco G, de Sanjose S, Shin HR, Sukvirach S, Thomas JO, Tunsakul S, Meijer CJ, Franceschi S; IARC HPV Prevalence Surveys Study Group. Lancet 2005 Sep 17-23;366(9490):991-998. "Women were randomly selected from the general population of 13 areas from 11 countries (Nigeria, India, Vietnam, Thailand, Korea, Colombia, Argentina, Chile, the Netherlands, Italy, and Spain)," total 15,613. "HPV prevalence varied nearly 20 times between populations, from 1.4% (95% CI 0.5-2.2) in Spain to 25.6% (22.4-28.8) in Nigeria. Although both overall HPV prevalence and HPV16 prevalence were highest in sub-Saharan Africa, HPV-positive women in Europe were significantly more likely to be infected with HPV16 than were those in sub-Saharan Africa (OR 2.64, p=0.0002), and were significantly less likely to be infected with high-risk HPV types other than HPV16 (OR 0.57, p=0.004) and/or low-risk HPV types (OR 0.44. p=0.0002). Women from South America had HPV-type distribution in between those from sub-Saharan Africa and Europe. Heterogeneity between areas of Asia was significant."

Prevalence of cervical human papillomavirus in Taiwanese women. CJ Jeng, Phdl, ML Ko, QD Ling, J Shen, HW Lin, CR Tzeng, CM Ho, TY Chien, SC Chen. Clin Invest Med 2005 Oct;28(5):261-266. "The overall HPV positivity was 19.85% and multiple infections were found in 35.84% of the infected group, 7.92% of the whole study population. The younger the subject, the higher was the infection rate and multiple infection rates. The most common HPV types were 16, 18, 58, 52, 51 and 56, which is different from the western world."

High prevalence of high-risk oncogenic human papillomaviruses harboring atypical distribution in women of childbearing age living in Libreville, Gabon. A Si-Mohamed, A Ndjoyi-Mbiguino, K Cuschieri, IN Onas, I Colombet, F Ozouaki, JL Goff, H Cubie, L Belec. J Med Virol 2005 Nov;77(3):430-438. "A total of 90 women (55%) harbored high-risk (HR) genotypes, with the most common being HPV-53 (19; 12%), HPV-58 (17; 11%), and HPV-16 (16; 10%). Low-risk genotypes were found in 36 (22%) women with HPV-54 and HPV-70 being the most frequently detected (17; 11% and 10; 6%, respectively). Finally 37 women (23%) tested positive for genotypes of unknown oncogenic risk, the most common in this category being HPV-83 (20; 12%). Multiple infections were detected in 35 (21%) women."

Oncogenic Human Papillomavirus (HPV) Type Distribution and HPV Type 16 E6 Variants in Two Spanish Population Groups with Different Levels of HPV Infection Risk. M Ortiz, M Torres, L Munoz, E Fernandez-Garcia, J Canals, AI Cabornero, E Aguilar, J Ballesteros, J del Amo, A Garcia-Saiz. J Clin Microbiol 2006 Apr;44(4):1428-1434. HPV types 16 and 31 were the most common in both sex workers/ imprisoned women and the general population, but the next most common strains differed between the two groups. Types 58, 66, 56, and 18 were the nest most frequent in the former group, and types 52, 68, 51, and 53 in the latter.

Human Papillomavirus Infections with Multiple Types and Risk of Cervical Neoplasia. H Trottier, S Mahmud, MC Costa, JP Sobrinho, E Duarte-Franco, TE. Rohan, A Ferenczy, LL Villa, EL Franco. Cancer Epidemiol Biomark Prevent 2006 Jul;15:1274-1280. "HSIL risk markedly increased with the number of types [odds ratio (OR), 41.5; 95% confidence interval (95% CI), 5.3-323.2 for single-type infections; OR, 91.7; 95% CI, 11.6-728.1 for two to three types; and OR, 424.0; 95% CI, 31.8-5651.8 for four to six types, relative to women consistently HPV-negative during the first year of follow-up]. The excess risks for multiple-type infections remained after exclusion of women infected with HPV-16, with high-risk HPV types, or persistent infections, particularly for any-grade SIL. Coinfections involving HPV-16 and HPV-58 seemed particularly prone to increase risk." And: Higher Risk for Cervical Cancer Seen Among Women Infected With Multiple HPV Types. DG News, July 10, 2006. Re Trottier et al, Cancer Epidemiology, Biomarkers & Prevention 2006 July. "'Women who harbor multiple infections are at higher risk for cervical lesions than those ever infected with one type only and should be followed more closely,' said Eduardo L. Franco, DrPH, leader of the study and professor of epidemiology and oncology, and director, division of cancer epidemiology at McGill University." "Both HPV 58 and 16 'seemed particularly prone to increase risk' for pre-cancerous lesions in the cervix, said Helen Trottier, PhD, the first author of the research paper." The most common types were 16, 53, 51, 31 and 18, with HPV 16 in 9 of single and 14% of multiple infections.

Comparison of DNA sequencing and Roche Linear array in human papillomavirus (HPV) genotyping. L Giuliani, A Coletti, K Syrjanen, C Favalli, M Ciotti. Anticancer Res 2006 Sep-Oct;26(5B):3939-3941. "The sequence analysis [by PCR] revealed the presence of 80 single high-risk types and 22 single low-risk types. With the Linear array, single infections were found in 46 cases, double infections in 37 cases, triple infections in 12 cases, and more than three in 6 cases. One case positive by sequencing gave a negative result by Linear array."

Sociodemographic factors associated with high-risk human papillomavirus infection. JA Kahn, D Lan, RS Kahn. Obstet Gynecol 2007 Jul;110(1):87-95. 1,921 women aged 14-59, data from NHANES. "High-risk HPV infection was present in 15.6% (95% confidence interval [CI] 12.6-18.6%) of participants, corresponding to a population prevalence of 12,028,293 U.S. women. Women living below the poverty line, compared with those living three or more times above it, were more likely to be positive for high-risk HPV (23% versus 12%, P = .03). Among participants living below the poverty line, only Mexican-American ethnicity (odds ratio [OR] 0.4, 95% CI 0.2-0.9) and unmarried status (OR 3.3, 95% CI 1.2-8.9) were associated with HPV prevalence. In contrast, several factors were associated with HPV among participants living above the poverty line, including black race (OR 1.4, 95% CI 1.0-2.0), income (OR 0.92, 95% CI 0.84-0.99), unmarried status (OR 2.0, 95% CI 1.3-3.0), and age (OR for 22-25 year olds 2.4, 95% CI 1.4-4.0). "

Prevalence of human papillomavirus types 6, 11, 16, 18, 31, and 33 in a cohort of Greek women. E Panotopoulou, A Tserkezoglou, M Kouvousi, I Tsiaousi, G Chatzieleftheriou, D Daskalopoulou, G Magiakos. J Med Virol 2007 Dec;79(12):1898-1905. "HPV was detected in 62.9% of 256 ASCUS smears, 89.3% of 516 LSIL, 86.7% of 60 HSIL and 47.3% of 165 with cervical carcinoma. Overall, HPV 11 was the most common type (13.4%), followed by 18 (10.3%), 6 (7.2%), 16 (6.4%), 31 (3.4%) and 33 (3.4%). Multiple infections with two (11.3%) or more types, primarily 11 and 18 (4.8%), were also identified.... Multiple infections were detected in 2.2% of normal and 31.7% of HSIL. HPV prevalence was 75.4% in abnormal and 24.6% in normal cervical smears. HPV 16 and 18 were the most common types in cancer. Single infection with type 11 and multiple infections with 11 and 18 were more frequent."

Homogeneous Amplification of Genital Human Alpha Papillomaviruses by Novel Broad Spectrum BSGP5+/6+ PCR. M Schmitt, B Dondog, T Waterboer, M Pawlita. J Clin Microbiol 2008 Mar;46(3):1050-9. New broad-spectrum (BS) primers improve detection of 14 genital HPV types and add 5 probes for low-risk types. "BSGP5+/6+ was significantly more sensitive than GP5+/6+ for detection of HPV 30,39,42,44,51,52,53,68,73 and 82, detecting 212 additional HPV infections and increasing the proportion of multiple infections from 17.2 to 26.9% in cancer patients."

Evaluation of Different Techniques for Identification of Human Papillomavirus Types of Low Prevalence. I Sabol, M Salakova, J Smahelova, M Pawlita, M Schmitt, NM Gasperov, M Grce, R Tachezy. J Clin Microbiol 2008 May;46(5):1606-1613. "Interassay agreement was moderate in cases of single HPV infections and poor in cases of multiple HPV infections. The LA [Roche Diagnostics linear array] and the BS-based RLB [broad spectrum noncommercial reverse line blot] assays found a higher rate of cases positive for multiple HPV types than LiPA [Innogenetics INNO-LiPA (line probe assay)] and the GP-based RLB assay. The weakest capability in detecting multiple HPV infections was observed for LiPA."

Comparison of GP5ﾯPCR and SPF10-Line Blot Assays for Detection of High-Risk Human Papillomavirus in Samples from Women with Normal Cytology Results Who Develop Grade 3 Cervical Intraepithelial Neoplasia. AT Hesselink, MAPC van Ham, DAM Heideman, ZMA Groothuismink, L Rozendaal, J Berkhof, FJ van Kemenade, LAFG Massuger, WJG Melchers, CJLM Meijer, PJF Snijders. J Clin Microbiol 2008 Oct;46(10):3215-3221. SPF10 scored significantly more controls as hrHPV positive than did GP5ﾯPCR; "Consequently, women with normal cytology results and an hrHPV GP5ﾯPCR-positive test exhibited a risk of CIN 3 that was 4.5 times higher (odds ratio [OR], 65; 95% confidence interval [95%CI], 24 to 178) than that seen for women with an hrHPV-positive SPF10 test (OR, 14; 95%CI, 5 to 38)).... Our data indicate that GP5ﾯPCR has a better clinical performance than SPF10 for women who are diagnosed with CIN 3 after prior normal cytology results. The extra positivity scored by SPF10 mainly involved infections characterized by low viral loads that do not result in CIN 3."

HPV-Associated Cancers and Socioeconomic Class

For cervical cancer, "About 10 out of every 100,000 women who live in counties in which fewer than 10% of residents have an income below the federal poverty level are diagnosed with cervical cancer each year. The rate climbs to about 13 women per 100,000 in counties in which 10% to less than 20% of residents are below poverty level, and peaks at about 19 per 100,000 [women] in poorer counties." For penile cancer, "About 1 out of every 100,000 men who live in counties in which fewer than 10% of residents have an income below the federal poverty level is diagnosed with penile cancer each year. The rate climbs to about 1.3 men per 100,000 in counties in which 10% to less than 20% of residents are below poverty level, and peaks at about 1.6 per 100,000 men in poorer counties." (HPV-Associated Cancers and Poverty Levels, Centers for Disease Control and Prevention. Page last updated: November 5, 2008.)

Sex Workers Are at Higher Risk of HPV Infection

The prevalence of the human papillomavirus in cervix and vagina in low-risk and high-risk populations. M Baay, V Verhoeven, K Wouters, F Lardon, P Van Damme, D Avonts, E Van Marck, P Van Royen, JB Vermorken. Scand J Infect Dis 2004;36(6-7):456-459. In 96 women visiting their general practitioner, and 63 sex workers visiting a STI clinic, "The overall HPV prevalence was 22.8%; 14.3% in the general population (14.3% in the cervix, 11.9% in the vagina), compared with 34.4% in sex workers (31.1% in the cervix, 27.9% in the vagina)."

Mechanisms

HPV is Both a Necessary and a Sufficient Cause of Cervical Cancer

The human papillomavirus type 16 E6 gene alone is sufficient to induce carcinomas in transgenic animals. S Song, HC Pitot, PF Lambert. J Virol 1999 Jul;73(7):5887-5893. "We generated K14E6 transgenic mice in which the HPV16 E6 gene was expressed in the basal layer of epithelia, using the hK14 promoter. Expression of E6 increased cell proliferation and induced epidermal hyperplasia. Skin tumors developed in adult K14E6 mice with an incidence of about 7% at 1 year of age. In contrast to the tumors derived from K14E7 transgenic mice, which were primarily benign, tumors derived from K14E6 transgenic mice were mostly malignant, indicating that E6 alone not only is sufficient to induce tumors but may contribute to the development of malignancy in animals." "Inactivation of p53, however, may not be the only mechanism for E6-induced carcinogenesis. The K14E6 mice that developed tumors also displayed hyperplastic changes in the epidermis, a property that, as discussed above, cannot be ascribed to E6's inactivation of p53. It is likely that the hyperproliferation induced by E6 is important for its carcinogenesis. Another activity that may contribute to E6-associated carcinogenesis is its apparent inhibition of cellular differentiation. Cancer cells usually lack the ability to terminally differentiate. In this study, we found that the suprabasal compartment of the K14E6 transgenic epidermis stained for K14, indicating that E6 may also perturb cellular differentiation; this perturbation was caused by p53-independent activities of E6."

Enhanced oncogenicity of Asian-American human papillomavirus 16 is associated with impaired E2 repression of E6/E7 oncogene transcription. RM Ordonez, AM Espinosa, DJ Sanchez-Gonzalez, J Armendariz-Borunda, J Berumen. J Gen Virol 2004 Jun;85(Pt 6):1433-1444. "AA variants confer a nine times higher risk than E variants for cervical cancer... The low repression activity of E2 suggests that increased expression of E6/E7 oncogenes may occur much earlier in AA tumours. Therefore, the time period between viral infection and the emergence of a frankly invasive cancer may be decreased. This hypothesis could explain the association of the AA-c variant with patients 11 years younger than those with E variants (Berumen et al., 2001)." [de Boer 2007 reported decreased survival with increased expression of E6/E7 oncogenes.]

Epstein-Barr virus may be involved in early stages of cervical carcinogenesis
Epstein-Barr virus and p16INK4A methylation in squamous cell carcinoma and precancerous lesions of the cervix uteri. NR Kim, Z Lin, KR Kim, HY Cho, I Kim. J Korean Med Sci 2005 Aug;20(4):636-642. "p16-methylation and p16-immunoreactivities were higher in the EBV-positive group (p=0.009, p<0.001) than in the EBV-negative group.... The p16 gene is one of the cell cycle regulating genes and encodes a nuclear protein, p16 which inhibits the D-type cyclin/cyclin-dependent kinase complexes that phosphorylate the retinoblastoma gene product (pRb), thus blocking G1-S cycle progression. The inactivation of p16 tumor suppressor gene promotes cell proliferation, and is found in many different types of carcinomas such as gastric carcinoma, bladder tumor, glioma, breast cancer and head and neck tumors. There is compelling evidence that the inactivation of p16 is an important genetic event in immortalization of keratinocytes. In previous studies of the p16 in cervical carcinomas, methylation specific polymerase chain reaction (PCR) has shown a high level of methylation, concordant with reports that the p16 gene is frequently inactivated through methylation rather than mutation or deletion.... Non-neoplastic cervices showed unmethylation in all the cases, but 40% (12/30) of cervical intraepithelial neoplasms and 61% of invasive squamous cell carcinomas (25/41) showed p16 methylation (p=0.003, Fig. 1, Table 1).... Non-neoplastic cervices were immunonegative for p16 protein except for basal cells that are known to normally express p16 protein, but 53% of cervical intraepithelial neoplasm (16/30 cases) and 68.3% of invasive squamous cell carcinomas (28/41) expressed p16 protein. These results were significantly different among the four groups (p=0.001, Table 1, Fig. 2).... EBV was detected by EBNA-1 PCR in 9.1% of non-neoplastic cervical tissue (1/11), 36.7% of cervical intraepithelial neoplasm (11/30) and 36.6% of invasive squamous cell carcinomas (15/41) (Fig. 3).... Recent development of molecular genetics for carcinogenesis and virus, methylation of CpG islands possessing p16 is induced by the integration of viral DNA into host cells."

HPV and EGFR

Human papillomavirus type 16 E6 and E7 cooperate to increase epidermal growth factor receptor (EGFR) mRNA levels, overcoming mechanisms by which excessive EGFR signaling shortens the life span of normal human keratinocytes. GS Akerman, WH Tolleson, KL Brown, LL Zyzak, E Mourateva, TS Engin, A Basaraba, AL Coker, KE Creek, L Pirisi. Cancer Res 2001 May 1;61(9):3837-3843. "[A]lthough HKc strains expressing relatively low basal EGFR levels grew poorly and tolerated the infection protocol with difficulty, they responded to E6 with an increase in EGFR mRNA and protein and with robust proliferation. However, those HKc strains expressing high basal EGFR levels grew well, but did not respond to E6 with increased EGFR levels or with proliferation. Immunostaining of paraffin-embedded foreskin tissue for the EGFR confirmed that there is an intrinsic interindividual variability of EGFR expression in HKC... We conclude that both E6 and E7 contribute to increasing EGFR levels, but with different mechanisms: although E6 can increase EGFR levels, it cannot overcome the resistance of normal HKc to excessive EGFR signaling. On the other hand E7, which alone does not acutely increase EGFR mRNA or protein, allows for EGFR overexpression in normal HKC."

Requirement of epidermal growth factor receptor for hyperplasia induced by E5, a high-risk human papillomavirus oncogene. SM Genther Williams, GL Disbrow, R Schlegel, D Lee, DW Threadgill, PF Lambert. Cancer Res 2005 Aug 1;65(15):6534-6542. "Cervical cancer is a progressive disease that takes on average one to two decades to develop. During that period, the HPV genome is maintained as a nuclear plasmid in the infected cervical epithelium, and early genes, including E5, are expressed. Thus, E5 has the potential to contribute to the HPV-associated carcinogenic process. In cervical cancer itself, however, HPV genomes commonly are found integrated into the host cellular genome, and this occurs such that the E6 and E7 ORFs remain intact, but E5 is lost or, if present, underexpressed compared with E6 and E7 (39–41). This suggests that E5 may play a critical role in the genesis of cervical cancer but less of a role in its persistence or progression.... Our K14E5 mice provide an opportunity to assess directly the role of E5 in cervical carcinogenesis. In the original HPV transgenic mouse model for cervical cancer, estrogen was found to synergize with the early region of HPV16 present in K14HPV16 mice, including the E5, E6, and E7 oncogenes, to induce cervical cancer that bore histopathologic features very similar to that seen in human cervical cancer (42). More recently, the individual roles of E6 and E7 oncogenes have been elucidated using our previously generated K14E6 and K14E7 mice that express the HPV16 E6 and E7 oncogenes individually (43). It is interesting to note that the estrogen-treated K14E6/K14E7 doubly transgenic mice had lower mean numbers of cancers per mouse than seen with the K14HPV16 mice expressing all three oncogenes (43). This difference in tumor number could be due to a difference in the expression level of the two transgenes or due to the participation of another early viral protein, such as E5, in the genesis of cervical cancer. What is striking about our initial studies reported here is that the early age of onset and high penetrance of spontaneous skin tumors arising in our K4E5 mice indicates that HPV16 E5 is far more potent an oncogene than we have observed for either HPV16 E6 or E7 in our existing K14E6 and K14E7 mouse models."

Lies About Smoking and Cervical Cancer

The Lie That Smoking Interacts With HPV Infection

This latest and "greatest" piece of disinformation purports that "Women who smoke and also carry high levels of the virus associated with cervical cancer are up to 27 times more likely to develop the most common form of cervical cancer compared with uninfected women who also smoke." In point of fact, virtually ALL cervical cancer patients (~99.7%) are actually infected with HPV, and it is likewise for its precursor lesions. Worst of all, they considered only HPV-16, when there are several other types which are known to cause cervical cancer. We can be certain that all of the cases were infected by HPV, and these sleasy "investigators" (propagandists) simply failed to detect the other types. In the actual study, they attempt to weasel: "Another limitation of our study relates to a lack of information on infection with other HPV types than HPV-16 in the smears. This potentially prevents us from adjusting completely for HPV in the analyses of smoking as a main effect." This is a lie, it absolutely prevents them from doing so, not just "potentially." "However, we do adjust for number of sexual partners, which could be regarded as a good proxy for acquiring an HPV infection." This is a lie, because this proxy variable has been proven to be inadequate to prevent confounding. Another deception: "'Clearly, both exposures need to be present at the same time for there to be interaction,' Gunnell said." Well, duh, that is self-evident. But merely noting that both are present does not demonstrate an interaction. The clear intent is to create the false impression that this study found one, when it did not. In addition, the newspaper article lies that smoking and HPVs "are both known to contribute to the disease on their own," when this is true only for HPV. (Smoking increases risk of cervical cancer. By Lee Bowman. Scripps Howard News Service, Nov. 18, 2006. Re: Synergy between Cigarette Smoking and Human Papillomavirus Type 16 in Cervical Cancer In situ Development. AS Gunnell, TN Tran, A Torrang, PW Dickman, P Sparen, J Palmgren, N Ylitalo. Cancer Epidemiol Biomarkers Prev 2006 Nov;15(11):2141-2147.)

A clumsy anti-smoker fraud

The Cigarette Smoke Carcinogen Benzo[a]pyrene Enhances Human Papillomavirus Synthesis. S Alam, MJ Conway, H-S Chen, Craig Meyers. Journal of Virology 2008 Jan;82(2):1053-1058. This one has all the hallmarks of a fraud deliberately concocted for the use of the anti-smokers: "Epidemiological studies suggest that cigarette smoke carcinogens are cofactors which synergize with human papillomavirus (HPV) to increase the risk of cervical cancer progression. Benzo[a]pyrene (BaP), a major carcinogen in cigarette smoke, is detected in the cervical mucus and may interact with HPV. Exposure of cervical cells to high concentrations of BaP resulted in a 10-fold increase in HPV type 31 (HPV31) viral titers, whereas treatment with low concentrations of BaP resulted in an increased number of HPV genome copies but not an increase in virion morphogenesis. BaP exposure also increased HPV16 and HPV18 viral titers. Overall, BaP modulation of the HPV life cycle could potentially enhance viral persistence, host tissue carcinogenesis, and permissiveness for cancer progression."

One thing wrong with their story is that increased viral titers indicate a productive infection, which are the kind that kill the cells, thus removing the chance that they will become cancers. Another is their hysteria about Benzo[a]pyrene (BaP), a supposed major carcinogen in cigarette smoke. Smoking is actually a minor source of it compared to dietary sources. "[T]he food chain is the dominant pathway of human exposure, accounting for about 97% of the total daily intake of BaP. Inhalation and consumption of contaminated water are only minor pathways of human exposure [2% from air, and 1% from water]. The long-term average daily intake of BaP by the general population is estimated to be 2.2 micrograms (ug) per day. Cigarette smoking and indoor activities do not substantially increase human exposure to BaP relative to background levels of BaP present in the environment." And, "[A]verage smokers (i.e., individuals who smoke 20 cigarettes a day) are taking in an additional 780 ng of BaP daily, which means that smokers get an additional 16% BaP from smoking" [based on pre-1979 cigarettes, which contained about twice the quantity of BaP as newer low-tar cigarettes]. Also, the exposure from cooked beef (0.2 -24.1 ug/kg) is less than the exposure from leafy vegetables (7.0 - 48 ug/kg). (Benzo-a-pyrene: Environmental partitioning and human exposure. H.A. Hattemer-Frey, C.C. Travis. Toxicology and Industrial Health 1991;7(3):141-157.) Nobody smokes through their vagina, so they cannot pretend that local levels of BaP there are higher due to direct exposure to smoke. Anybody who was really concerned about the effect of BaP, as opposed to merely manufacturing deceitful propaganda, would would have taken actual human exposure to it into account.

Exposed: The lie that smoking supposedly suppresses immunity by reducing the number of cervical Langerhans cells

It is the E6 protein of human papillomavirus which reduces the number of Langerhans cells

Depletion of Langerhans cells in human papillomavirus type-16 infected skin is associated with E6-mediated down regulation of E-cadherin. K Matthews, CM Leong, L Baxter, E Inglis, K Yun, BT Backstrom, J Doorbar, M Hibma. J Virology 2003 Aug;77(15):8378-8385. "Adhesion between keratinocytes (KC) and LC [Langerhans cells], mediated by E-cadherin, is important in the retention of LC in the skin. Cell surface E-cadherin is reduced on HPV16-infected basal KC, and this is directly asociated with the reduction in numbers of LC in infected epidermis. Expression of a single viral early protein, HPV16 E6, in KC reduces levels of cell surface E-cadherin thereby interfering with E-cadherin-mediated adhesion." This reduces the presentation of antigen by the Langerhans cells, and helps prevent the initiation of a cell-mediated immune response.

Decreased migration of Langerhans Precursor-Like Cells in response to human keratinocytes expressing human papillomavirus Type 16 E6/E7 is related to reduced Macrophage Inflammatory Protein-3{alpha} Production. JC Guess, DJ McCance J Virol. 2005 Dec;79(23):14852-14862. "[F]ollowing proinflammatory stimulus, HPV-16 E6 and E7 inhibit MIP-3alpha transcription, resulting in suppression of the migration of immature Langerhans precursor-like cells. Interestingly, the E6 and E7 proteins from the low-risk HPV types also inhibited MIP-3-alpha transcription. These results suggest that one mechanism by which HPV-infected cells suppress the immune response may be through the inhibition of a vital alert signal, thus contributing to the persistence of HPV infection."

Exposed: The lie that smoking causes mutations of the Fragile Histidine Triad gene

The National Cancer Institute (e.g., Popescu and DiPaulo) have known for over a decade that HPV causes these mutations.

Regional chromosome localization of human papillomavirus integration sites near fragile sites, oncogenes, and cancer chromosome breakpoints. LA Cannizzaro, M Durst, MJ Mendez, BK Hecht, F Hecht. Cancer Genet Cytogenet 1988 Jul 1;33(1):93-98.

Integration of human papillomavirus 16 DNA and genomic rearrangements in immortalized human keratinocyte lines. NC Popescu, JA DiPaolo. Cancer Res 1990 Feb 15;50(4):1316-1323.

FRA3B extends over a broad region and contains a spontaneous HPV16 integration site: Direct evidence for the coincidence of viral integration sites and fragile sites. CM Wilke, BK Hall, A Hoge, W Paradee, DI Smith, TW Glover. Hum Mol Genet 1996;5:187–195.

Common fragile sites are preferential targets for HPV16 integrations in cervical tumors. EC Thorland, SL Myers, BS Gostout, DI Smith. Oncogene 2003 Feb 27;22(8):1225-1237. "Our data demonstrate that 11/23 HPV16 integrations in cervical tumors occurred within CFSs (P&<0.001). In addition, we show that deletions and complex rearrangements frequently occur in the cellular sequences targeted by the integrations and that integrations cluster in FRA13C (13q22), FRA3B (3p14.2), and FRA17B (17q23). Finally, our data suggest that cellular genes, such as Notch 1, are disrupted by the HPV16 integrations, which may contribute to the malignant phenotype."

Systematic review of genomic integration sites of human papillomavirus genomes in epithelial dysplasia and invasive cancer of the female lower genital tract. N Wentzensen, S Vinokurova, MvK Doeberitz. Cancer Res 2004 Jun 1;64(11):3878-3884. "Up to now, in total, 192 individual HPV integration sites have been described in primary tumor samples and cell lines. Here, we summarize all available data on chromosomal HPV integration sites. The data suggest that integration of HR-HPV genomes occurs relatively late in the progression of high-grade cervical dysplasia. It appears that integration of HR-HPV genomes is a consequence of an overall destabilization process of the chromosomal integrity in replicating epithelial stem cells that express the viral E6-E7 oncogenes. The consequences of the structural alterations of the viral genome and the impact of cellular sequences on its transcriptional regulation seem to be more important than functional alteration of specific cellular genes by the integrated viral sequences."

The liars ignore the fact that smokers are more likely to be exposed to HPV, which they have exploited to falsely blame smoking for cervical cancer from the very beginning.

The fragile histidine triad gene: a molecular link between cigarette smoking and cervical cancer. CH Holschneider, RL Baldwin, K Tumber, C Aoyama, BY Karlan. Clin Cancer Res 2005 Aug 15;11(16):5756-5763.

The American Cancer Society

The American Cancer Society still lies that smoking causes cervical cancer. (Smoking May Double Cervical Cancer Risk. American Cancer Society, 2004/01/19.) They use a defective study that ignores the infections in the women's sexual partners, which is contrary to accepted practice in regard to other sexually transmitted diseases, and enables them to exploit higher rates of HPV infection in the sexual partners of women smokers. (Smoking and cervical cancer: pooled analysis of the IARC multi-centric case-control study. M Plummer, R Herrero, S Franceschi, CJLM Meijer, P Snijders, FX Bosch, S de Sanjose, N Munoz. Cancer Causes and Control 2003 Nov;14(9):805-814.) Note that Bosch, de Sanjose, and Munoz were authors of the letter to Phillips and Smith in the International Journal of Epidemiology 1994, in which they admitted that the results of their past studies had been confounded by undetected HPV infection, and that when HPV infection was taken into account, there was no increased risk of cervical cancer in smokers. These people do not need to be told that sexual partners are a key factor in sexual transmitted diseases, it is axiomatic. And this study demonstrates that, instead of recognizing the potential for confounding and avoiding it, they exploited as a new mechanism for manufacturing anti-smoking hate propaganda.

"Only a small percentage of women with certain types of abnormal cells resulting from HPV infection will develop cancer if these cells are not removed and destroyed. Studies suggest that whether a person will develop cancer depends on a variety of factors that act together with HPVs. These factors include smoking, decreased resistance to infection, and infection with other viruses, such as human immunodeficiency virus (HIV)." (Human Papillomavirus (HPV). ACS, revised 03-06-2000.)

The ACS lies again that "Smoking is another risk factor for cervical cancer. Tobacco smoke can produce chemicals that may damage the DNA in cells of the cervix and make cancer more likely to develop. Women who smoke are about twice as likely as non-smokers to get cervical cancer." From: "Cervical Cancer - Overview." ACS, revised 03-16-2000.

"Smoking exposes the body to many cancer-causing chemicals that affect more than the lungs. These harmful substances are absorbed by the lungs and carried in the bloodstream throughout the body. Tobacco by-products have been found in the cervical mucus of women who smoke. Researchers believe that these substances damage the DNA of cells in the cervix and may contribute to the development of cervical cancer. Women who smoke are about twice as likely as nonsmokers to get cervical cancer." They also lie that "Not smoking is another way to reduce the risk of cervical cancer and precancer." (Pap Test. American Cancer Society, 12-03; What Are the Risk Factors for Cervical Cancer, 8-04.) This is the stereotypical deceitful format of health fascist "scary chemicals" propaganda. FACT: Even active smokers are exposed to only 16% more of the combustion product benzo(a)pyrene than nonsmokers; 97% of exposure to it comes from ordinary food, including vegetables. FACT: With modern analytical equipment, trace amounts of anything can be found practically anywhere. FACT: The "researchers" who blame smoking are corrupt hacks whom the Cancer Society nurtures in order to further their health fascist political agenda. And, even after decades of trying, they still haven't identified any mechanism of carcinogenesis. FACT: The lie that smokers are twice as likely to get cervical cancer is based on deliberately falsely blaming smoking for cervical cancer that is actually caused by HPV infection.

As usual, the ACS uses defective studies that failed to detect all HPV and failed to measure the amount of exposure to it, in order to falsely blame smoking. And, here is the truth regarding the dubious role of chemical carcinogens: "Attempts to determine the importance of cofactors utilizing in vitro models with human cells and recombinant HPV have been frustrating. In general, there is a marked contrast between the effects of a carcinogen on rodent and human cells. Whereas a number of chemical and physical viral agents are effective in transforming normal rodent cells to the malignant state, they are for the most part ineffective when applied to human cells. The same can be said for cells that have been immortalized with HPV-16 or -18. The addition of diverse chemical carcinogens to HPV-16 immortalized cells has consistently failed to induce malignancy; however, evidence of effects has been obtained as reflected by new chromosomal arrangements." (Immortalization of human keratinocytes by human papillomaviruses. CD Woodworth, JA DiPaolo. In: DNA tumor viruses. Oncogenic mechanisms. G Barbanti-Brodano, M Bendinelli, H Friedman, eds. Plenum Press, 1995, Ch 6, pp 91-109.)

Co-author DiPaolo is an old mouse painter from the 1950s, and is cited in the 1964 Surgeon General report (Effect on mice of oral painting of cigarette smoke condensates. DiPaolo JA, Moore GE. J Nat Cancer Inst 1959;23:529-534). For more than 40 years, enormous resources have been devoted to fruitless efforts to find some mechanism of chemical carcinogenesis by which to blame smoking. It is certainly not for lack of trying that they have failed. Lacking such a discovery, they resort to pretending that the long-sought discovery is imminent (Introduction of sister chromatid exchanges by tobacco-specific nitrosamine 4-(methylnitrosoamino)-1-(3-pyridyl)-1-butanone in human and hamster cells. D Zimonjic, NC Popescu, JA DiPaolo. Carcinogenesis 1989 Apr;10(4):753-755. The poor man must indeed have had a frustrating life, but not nearly as frustrating as those who have been the targets of this propaganda.

The National Cancer Institute

The National Cancer Institute continues to officially lie about smoking and cervical cancer. From their previous lie that "Cigarette smoking may be associated with an increased risk of cervical cancer. Many studies have shown an association while other studies have not," they have now escalated their lie: "Cigarette smoking is associated with an increased risk of cervical cancer." (Cervical Cancer (PDQ) Prevention - Patients. National Cancer Institute, 7/13/2005.)

The NCI lies even more floridly to health professionals. Their old lie: "Cigarette smoking by women is associated with an increased risk for squamous cell carcinoma. This risk increases with longer duration and intensity of smoking and may be present with exposure to environmental tobacco smoke as well, being as high as 3 times that of women who are nonsmokers and are not exposed to environmental tobacco smoking. Some studies demonstrate an increased risk for current smoking only as opposed to former smokers, suggesting that carcinogens in cigarette smoke exert a late stage effect on carcinogenesis." Their new lie: "Based on solid evidence, cigarette smoking, both active and passive, increases the risk of cervical cancer." "Magnitude of Effects on Health Outcomes: Among HPV-infected women, current and former smokers have approximately 2 to 3 times the incidence of high-grade cervical intraepithelial neoplasia or invasive cancer. Passive smoking is also associated with increased risk, but to a lesser extent." (Cervical Cancer (PDQ) Prevention, Health Professional Version. National Cancer Institute, 7/20/2005.)

Meanwhile, on their General Information page, NCI admits that "Epidemiologic studies convincingly demonstrate that the major risk factor for development of preinvasive or invasive carcinoma of the cervix is HPV infection, which far outweighs other known risk factors such as high parity, increasing number of sexual partners, young age at first intercourse, low socioeconomic status, and positive smoking history." What they don't admit is that studies which ignore HPV falsely blame non-causal "risk factors," including smoking and passive smoking. And, even in studies which do consider it, there may be residual confounding due to false negatives, and to different amounts of exposure to the virus from infected versus uninfected male partners. (General Information. Cervical Cancer (PDQ®): Treatment. Last Modified: 05/18/2006.)

The Cancer Research Campaign

The Cancer Research Campaign in the UK also lies. Their old lie: "Smoking also increases the risk of cancer of the cervix, although it is not clear exactly how or why. The risk increases with the number of cigarettes a woman smokes each day and with the number of years she has smoked." Their updated lie: "Research shows that smoking increases the risk of developing cervical cancer, possibly because smoking weakens the immune system's ability to eliminate HPV." (Cervical Cancer. Cancer Research Campaign, 20/12/2004.)

Health Canada

"In some studies, cigarette smoking has been found to increase the risk." This is weaseling. The studies that find these alleged risks are the ones with residual confounding by HPV infection (or which ignore it entirely). (Screening for cervical cancer. Health Canada, 2005-08-09.)

The Johns Hopkins University

This claim from Dr. Anthony J. Alberg of Johns Hopkins University is deliberate, willful, reckless, knowing, SCIENTIFIC FRAUD, because the confounding effect of failure to fully detect exposure to human papillomavirus is thoroughly documented, and there is no excuse for ignoring it. This study is nothing but a lifestyle questionnaire, deliberately exploiting the different rates of exposure of smokers and passive smokers versus non-smokers, in order to fraudulently claim, for hate propaganda purposes, that secondhand smoke causes cervical cancer. Their study design is inherently defective for its pretended purpose; its results are entirely due to different rates of exposure to HPV; and their facile line that smoking depresses immunity is nothing but a smokescreen. (Active and passive cigarette smoking and the risk of cervical neoplasia. CL Trimble, JM Genkinger, AE Burke, SC Hoffman, KJ Helzlsouer, M Diener-West, GW Comstock, AJ Alberg. Obstetrics and Gynecology 2005 Feb 1;105:174-181.)

And then they spew their poisonous lies for mass consumption: Passive Smoking Linked to Cervical Cancer. By Anthony J. Brown, MD. ReutersHealth, Jan. 21, 2005; Cervical Cancer Tied to Secondhand Smoke. By Katrina Woznicki. WomensENews Jan. 25, 2005.

See also:

cast 02-08-09