Penile cancer, cervical cancer, and circumcision


The alleged relationship between "lack of circumcision" and genital cancers formerly implicated smegma or smegma-borne pathogens as the causative agent. Only two histologic studies of human smegma ever have been conducted, both of which found it to be perfectly harmless. Smegma is composed of secretions of ectopic sebaceous glands in the prepuce mixed with secretions of the prostate, seminal vesicles, mucin from the urethral glands, and desquamated epithelial cells.10,12, 64

The hypothesis that human male smegma is carcinogenic was first formulated in 1932 by circumcision promoter Abraham L. Wolbarst, M.D.1. Wolbarst also believed that circumcision prevented epilepsy. (In the early part of the 20th Century, the paroxysm of masturbation in children was often misidentified as an epileptic seizure.) Wolbarst wrote: "[Circumcision] diminishes the tendency to masturbation, convulsions and other reflex phenomena of local irritation." Wolbarst's beliefs about circumcision were shared by other writers, such as Peter Remondino and Abraham Ravich.

No laboratory or clinical research had been done on the subject at the time. Regardless, Wolbarst's hypothesis about smegma and cancer found its way into early medical textbooks. In the 1950s a few experiments were done to test the hypothesis by injecting horse smegma into wounds made in the backs of mice. There were clinical studies that attempted to induce cancer by introducing smegma subcutaneously and intravaginally: No carcinomas could be induced.

The smegma hypothesis was finally disproven by an exhaustive study by Reddy2 in 1963. His results were: "The conviction that human smegma is a carcinogen could not be substantiated."

Preston established quite clearly that there was little evidence to support a relationship between lack of circumcision and penile cancer, cervical cancer, or cancer of the prostate in 1970 but he was unable to identify the causative agent at that time,6 while Leitch7 did the same in Australia.

Gellis (1978) said there are more deaths from circumcision than from cancer of the penis.8

Boczko et al. found numerous reports of penile cancer in circumcised men, thus conclusively disproving Wolbarst's false claims of protection from penile cancer by circumcision.9

In "Circumcision: An American Health Fallacy," Edward Wallerstein writes14: "If infant circumcision reduces penile cancer we could expect to see proportionately less penile cancer in circumcising nations as compared to noncircumcising ones. No such difference is found." Wallerstein reports that, for various years between 1966 and 1972, the annual rate of new cases of penile cancer was 0.8 for the United States (which circumcises), and 0.5 for Finland, 0.9 for Denmark and 1.1 for both Norway and Sweden (all of which do not). None of these differences is statistically significant. Further, within the same time frame, both France and the United States had the same rate, 0.3, of deaths due to penile cancer.12

The link between the presence of human papillovirus (HPV) and genital cancer was established in the 1980s.15,17,18,19,20,21 Hellberg et al. (1986) identified tobacco use as another risk factor for cancer of the penis. Poland identified the human papilloma virus (HPV) types 16 and 18 as the cause of penile and cervical cancers in 1990. Cervical cancer has epidemiologic similarities to venereal disease. The human papilloma virus is spread by sexual contact.29 DNA sequences from HPV have been identified in more than 50 percent of cervical cancers tested by 1989.26

In February 1996, representatives of the American Cancer Society stated in a letter to the American Academy of Pediatrics:

The American Cancer Society does not consider routine circumcision to be a valid or effective measure to prevent such [genital] cancers. Research suggesting a pattern in the circumcision status of partners of women with cervical cancer is methodologically flawed, outdated and has not been taken seriously in the medical community for decades."

Penile cancer

In 1993, Christopher Maden, Ph.D., et al. reported a study 29 in which 110 men with penile cancer, diagnosed from January 1979, to July, 1990, were interviewed. Of these 110 men, 22 had been circumcised at birth, 19 later in life, and 69 never. The majority of the men interviewed were intact, 37% were circumcised, and 20% had been circumcised as infants. In circumcised men, the cancer usually occurs along the line of the circumcision scar. Finland, where circumcision is extremely rare, has a low incidence of penile cancer.48

It is thus categorically not true that circumcision eliminates the risk of penile cancer, although that assertion has been made nonchalantly in a number of papers by Schoen, Wiswell, and Weiss. In fact, the data indicate that only other factors -- among them cigarette smoking,22,30 genital warts, and 30 or more sexual partners -- contribute to the risk of penile carcinoma.27

To paraphrase Dr. George Denniston: Cancer of the penis is very rare, with a lifetime risk of between 1/600 and 1/1300. It strikes mostly older men. Even if circumcision could prevent it completely (which it does not), about a thousand foreskin amputations would be necessary to prevent one cancer of the penis. A thousand infants would be mutilated, and several would die to prevent that one case of cancer. Who could scientifically advocate foreskin amputation for this reason?

In its 1996 Statement, the Canadian Paediatric Society noted:

Cadman, Gafni and McNamee... calculated that the cost of circumcising 100,000 male infants is $3.8 million and that this maneuver would prevent only two cases of cancer of the penis. ... they estimated that the cost of prevention would be 100 times the cost of treatment.12

There are many documented cases of penile cancer in circumcised men. To reduce the risk of penile cancer, men are best advised simply to use reasonable hygiene, practice responsible sexual behavior, and to avoid handling tobacco.

The history of the penile cancer myth was published by Fleiss and Hodges in the British Medical Journal32.

Post-circumcision cancer may occur at the circumcision scar.16,23 The cause is unknown. One may hypothesize that the circumcision scar tissue is less resistant to penetration of HPV which then transfers DNA to the human cell and starting the growth of the neoplasm. More research is needed to determine the etiology of post-circumcision cancer.

American Cancer Society. The American Cancer Society issued a five part advisory statement on penile cancer in June 1999. Circumcision is not considered to be beneficial in preventing or reducing the risk of penile cancer. The ACS indentifies HPV, smoking, and phimosis as risk factors. Sexually active adult males with a non-retractable foreskin should have the phimotic condition treated. (See phimosis for conservative treatment options. Circumcision is outmoded as a treatment for phimosis.)

The ACS states that penile cancer is extremely rare in Europe and North America. The cancer only occurs in 1 in 100,000 men. Penile cancer usually occurs well beyond age 50, although it can occur earlier.

Vaccine. A newly developed human papillomavirus (HPV) bi-valent vaccine is expected to offer protection against all forms of ano-genital cancer, including penile cancer, when it becomes available.59

Circumcision does not provide protection against penile cancer. Even if it did, it would no longer be necessary due to the expected availability of a HPV vaccine.

Cervical cancer in partners

The hypothesis that cervical cancer is caused by smegma of the male foreskin was invented in 1954 by Wynder. His study was found to be invalid, because most of the cervical cancer patients in his study incorrectly reported that their husbands were uncircumcised. These women had no idea whether their husbands were circumcised or not. They gave the answer they thought the doctor wanted to hear. Wynder later recognized and admitted the error in 1960.3 This hypothesis was formally and scientifically disproven in 1962 by Stern.4

Stern and Neely examined some of the early research on this subject:4

"Since the recommendation had been made that circumcision should be used as a preventative measure against cancer of the cervix, we sought further confirmation of this hypothesis. An almost ideal population was that of the well women attending a cancer detection facility, where the population was split almost equally between women whose husbands were circumcised and those whose husbands were not. The discovery rate for cancer of the cervix among non-Jewish women whose marital partners were circumcised was no different from the rate among non-Jewish women with noncircumcised husbands. Further, the use of a sheath contraceptive by the marital partner, which has an effect equivalent to circumcision in that the cervix is protected from contact with the smegma, was found not to be associated with rate differences for cancer of the cervix."

This study, more than the others, exposed the myth that the presence of a foreskin or smegma had any association with the incidence of cancer of the cervix. See also 37-39.

Ho et al. 36 have established that co-factors such as cigaratte smoking may be necessary to advance HPV infected cervical epithelial cells toward a cancerous condition. Ho et al.37 have also suggested that high levels of antioxidants in the blood serum may provide some protection, although more study is needed.

Walboomers reported that HPV DNA is found in more than 99.7 percent of cervical cancer cells in 1999. HPV infection is a necessary condition for cervical cancer.48

The known etiologies of cervical cancer are: early onset of sexual activity, number of sexual partners, smoking, and the presence of HPV.27 Based on currently available evidence, it would be mistaken to suggest an association between cervical cancer and the presence of the foreskin in the male partner.

The New England Journal of Medicine published an article by Castelsagué and others in 2002. That article purported to show that circumcision reduced the risk of infection to the wives of circumcised men. This article has experienced severe and unrelenting criticism due to numerous methodological flaws, its conflict with other published research, and other research by the same authors that showed that different types of HPV were found in husbands and wives.51 52 53 54 55 56 Editorial problems previously had been reported at the New England Journal of Medicine. The publication of this flawed article may have been the result of those editorial problems.

See the NOCIRC position statement for more information on cervical cancer and circumcision.54

Menczer reports that genetics, not male circumcision, limits the incidence of cervical cancer in Jewish women.57 The argument that Jewish women have a lower incidence of cervical cancer because their husbands are circumcised appears to be destroyed by this finding.

Vaccine. Infection with human papillomavirus (HPV) is a necessary condition for the formation of cervical cancer.48 A bi-valent vaccine that offers substantial protection from infection with HPV has been successfully tested.60 It is expected that approval of this vaccine will receive approval from regulatory authorities and that when it will greatly reduce the incidence of HPV infection, cervical cancer, and death when vaccination against HPV becomes widespread.61 Male circumcision has never been proved to offer any real protection against HPV infection in the female partner, but even if it did, it still would not be necessary because the vaccine will offer protection.63

See also: Cervical cancer: the real causes and the real cure


It is now clear that the major risk factors for both penile cancer and cervical cancer are the use of tobacco,22,31 which spreads carcinogens throughout the body via the bloodstream, and the presence of the human papillomavirus,35 which is communicated through sexual activity.

Abraham Wolbarst's promotional claims that circumcision prevented penile cancer were false and mislead the medical community for decades.34 Circumcision does not prevent penile cancer in men and it does not prevent cervical cancer in the female partner.

However, phimosis, or a non-retractile foreskin, is a risk factor in adult males who are sexually active, because a non-retractile foreskin is more difficult to clean. There are many non-traumatic, non-distructive methods for conservative effective treatment of phimosis available to the male with phimosis. Circumcision is neither required nor recommended to treat phimosis. Cancer may form on the circumcision scar.16,24

A new human papillomavirus (HPV) vaccine offers protection against both penile and cervical cancers.64 Fear of cancer cannot be used to support the practice of male circumcision.

Library holdings

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  2. D.G. Reddy; I.K. Baruah. "Carcinogenic Action of Human Smegma," Archives of Pathology, vol. 75, no. 4 (April 1963): pp. 414-420.
  3. Ernest L. Wynder; Samuel D. Licklider. "The Question of Circumcision," Cancer, vol. 13, no. 3 (May-June 1960): pp. 442-445.
  4. Elizabeth Stern; Peter M. Neely. "Cancer of the Cervix in Reference to Circumcision and Marital History," Journal of the American Medical Women's Association, vol. 17, no. 9 (September 1962): pp. 739-740.
  5. Aitken-Swan J, Baird D. Circumcision and cancer of the cervix. Brit J Cancer 1965;XIX(2):217-226.
  6. Preston EN. Whither the foreskin. JAMA 1970; 213(11):1853-1858.
  7. Leitch IOW. Circumcision - a continuing enigma. Aust Paediatr J 1970;6:59-65.
  8. Gellis SS. Circumcision. Am J Dis Child 1978; 132: 1168-9.
  9. Boczko S, Freed S. Penile carcinoma in circumcised males. N Y State J Med 1979; 79(12):1903-1904.
  10. Parkash S, et al. Sub-Preputial Wetness - Its Nature. Ann Nat Med Sci (India) 1982;18(3):109-112.
  11. Annals of the National Medical Sciences, vol. 18, no. 3 (July-September 1982): pp. 109-112.
  12. Hyman AB; Brownstein MH. Tyson's "Glands," Archives of Dermatology, vol. 99, no. 1 (January 1969): pp. 31-37.
  13. Cadman D, Gafni A, McNamee J: Newborn circumcision: an economic perspective. Can Med Assoc J 1984; 131: 1353-1355.
  14. Wallerstein, Edward. Circumcision: An American Health Fallacy. Springer-Verlag, New York, 1980.
  15. zur Hausen H. Genital papillomavirus infections. Prog Med Virol 1985;32:15-21.
  16. Bissada NK, Morcos RR, el-Senoussi M. Post-circumcision carcinoma of the penis. I. Clinical aspects. J Urol 1986 Feb;135(2):283-5.
  17. Kaufman RH, Adam E: Herpes simplex virus and human papilloma virus in the development of cervical carcinoma. Clin Obstet Gynecol 1986; 3: 678-692
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  27. Brinton LA, Reeves WC, Brenes MM, et al. The male factor in the etiology of cervical cancer among sexually monogamous women. Int J Cancer 1989;44(2):199-203.
  28. Denniston GC. First, do no harm. The Truth Seeker 1989 [Proceedings of the First International Symposium on Circumcision]; 1(3):37.
  29. Poland R. The question of routine neonatal circumcision. New Engl J Med 1990; 322(18):1312-1314.
  30. Maden C et al. History of Circumcision, Medical Conditions, and Sexual Activity and Risk of Penile Cancer. Journal of the National Cancer Institute, vol. 85, no. 1., January 6, 1993, pp. 19-24.
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  33. Frisch M et al. Falling incidence of penis cancer in an uncircumcised population (Denmark 1943-90). British Medical Journal (London), vol. 311, no. 7018 (December 2, 1995): pg. 1471.
  34. Fleiss P, Hodges F. Neonatal circumcision does not protect against cancer (letter). British Medical Journal, (London) Vol. 312 no 7033 (March 23, 1996): pp. 779-780.
  35. Shingleton H, Heath Jr CW. Letter to Peter Rappo, M.D., February 16, 1996.
  36. Cold CJ, Storms MR, Van Howe RS. Carcinoma in situ of the penis in a 76-year-old circumcised man. J Fam Pract 44(4), April 1997, pp. 407-410. [Demonstrates: Circumcision has no statistically-significant effect on the rate of penile cancer, when Maden's data are properly adjusted for age.]
  37. American Cancer Society. Dispelling Miscommunications: Statement on Penile Cancer. ACS News Today, Atlanta, (1998).
  38. Ho GY, Kadish AS, Burk RD, et al. HPV 16 and cigarette smoking as risk factors for high-grade cervical intra-epithelial neoplasia. Int J Cancer 1998;78(3):281-5.
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  41. Circumcision and cancer of the cervix. University of Aberdeen, Dept. of Obstetrics and Gynaecology. British Journal of Cancer, Vol. XIX, Jun, 1965, No. 2:
    "These results do not support the theory that women whose husbands are circumcised will be less likely to develop cervical cancer than those whose husbands are uncircumcised. In this the study agrees with the findings of Jones et al (1958), Dunn and Buell (1959), and Boyd and Doll (1964)."
  42. Ernst L. Wynder, M.D. (American Health Foundation). Journal of the American Medical Association, June 2, 1975, p. 961:
    "Additional variables observed to be more frequent and of more import among patients with cervical cancer are early age of first intercourse, multiple sexual parners, and low socioeconomic class. Unless there exist surgical reasons (such as phimosis) indicating circumcision in the husband, the procedure would seem unwarranted."
  43. Terris, Wilson, Nelson. Relation of cirumcision to cancer of the cervix. Am. J. Obstet. Gynecol., Dec. 15, 1973:
    "No differences were found in circumcision status of husbands of cervical dysplasia patients and controls. The findings of this study are consistant with those reported by Aitken-Swan and Baird. They fail to provide evidence that circumcision status is related to invasive carcinoma or the cervix, carcinoma in situ, or cervical dysplasia."
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  49. Aynaud O, Piron D, Bijaoui G, Casanova JM. Developmental factors of urethral human papillomavirus lesions: correlation with circumcision. BJU Int 1999;84(1):57-60.
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  53. Oliver JC, Oliver RT, Ballard RC. Influence of circumcision and sexual behaviour on PSA levels in patients attending a sexually transmitted disease (STD) clinic. Prostate Cancer Prostatic Dis 2001:4(4):228-31.
  54. Milos M. NEJM Cervical Cancer Study Has Fatal Flaws. BMJ 2002 Rapid Response Letter, 27 April 2002.
  55. Travis J. Misuse of the medical literature. BMJ 2002 Rapid Response Letter, 29 April 2002.
  56. Comments on Male Circumcision, Penile Human Papillomavirus Infection, and Cervical Cancer. New Engl J Med 2002;47(18):1448.
  57. National Organization of Circumcision Information Resource Centers. Position Statement on the Use of Male Circumcision to Prevent Cervical Cancer. San Anselmo: National Organization of Circumcision Information Resource Centers, 2002.
  58. Hill G. Evidence sketchy on circumcision and cervical cancer link. Can Fam Physician 2003;49:1591.
  59. Bhimji A, Harrison D. Evidence sketchy on circumcision and cervical cancer link. Can Fam Physician 2003;49:1591.
  60. Menczer J. The low incidence of cervical cancer in Jewish women: Has the puzzle finally been solved? IMAJ 2004;5:120-3.
  61. Harper DM, Franco EL, Wheeler C, et al. Efficacy of a bivalent L1 virus-like particle vaccine in prevention of infection with human papillomavirus types 16 and 18 in young women: a randomised controlled trial. Lancet 2004;364(9447):1757-65.
  62. Lehtinen M, Paavonen J. Vaccination against human papillomaviruses shows great promise. Lancet 2004;364:1731-2.
  63. Crum C, Jones C, Kirkpatrick P. Fresh from the pipeline: Quadrivalent human papillomavirus recombinant vaccine. Nat Rev Drug Discov 2006;5:629-630.
  64. Van Howe RS, Hodges FM. The carcinogenicity of smegma: debunking a myth. J Eur Acad Dermatol Venereol 2006;20(9):1046.
  65. Van Howe RS. Human papillomavirus and circumcision: A meta-analysis. J Infect (2006) Sept 22 (E-pub ahead of print) doi:10.1016/j.jinf.2006.08.005
  66. Hill G. The "foreskin causes cancer" myth. Knol 2008. [Full Text]

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(File revised 6 November 2008)