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Uterine Cervix
Cancer
Louise A. Brinton,
Ph.D.*
The uterine cervix is the small
cylindrical neck that leads from the uterus, or womb, into the vagina. A knob of
the cervix protrudes into the vagina and can be visualized on physical
examination. Cell samples are taken from this part of the cervix for the Pap
smear test, which is used to detect cancer cells or changes in cell structure
that may lead to cancer. The most commonly detected changes are dysplasias,
which are thought to be precursor conditions for carcinoma in situ (CIS) and
invasive cancer of the cervix. However, many dysplasias regress over time, and
the factors that lead to progression are unclear.
In CIS, an outer layer of normal cells has
been replaced by cancer cells. It is about 95 percent treatable and curable. In
invasive cancer of the cervix, the cancer cells have invaded the underlying
tissue of the cervix. CIS occurs most often among women 25 to 34 years of age,
while invasive cervical cancer most often is diagnosed in women over the age of
50.
Both incidence and mortality for invasive
cancer of the uterine cervix have declined steadily in this country over the
past three decades (Devesa et al., 1989). Nevertheless, black women continue to
experience incidence rates that are nearly two times higher than those in
whites. Racial differences are also evident in survival statistics; blacks have
a 56 percent five-year relative survival rate compared with 70 percent for
whites (Ries et al., 1994). The racial differences may be due, in part, to the
association of cervical cancer with the sexual and other behavioral
characteristics of low socioeconomic status.
High rates for cervical cancer are found
in the American South, particularly in Appalachia. The U.S. incidence rates are
generally low, however, compared to other parts of the world, such as India and
South America, which have world standardized rates over 40 per 100,000. The
comparable world standardized rate for U.S. black women is 12 and, for white
women, 7 per 100,000 (Parkin et al., 1992).
Sexual behavior has been identified as the
major risk factor for both CIS and invasive cervical cancer (Brinton and
Fraumeni, 1986). Risk of both conditions is increased in women reporting either
early age at first intercourse or numerous lifetime sexual partners. Early onset
of sexual activity is thought to be associated with high risk because, during
puberty, cervical tissue undergoes a variety of changes that may make the area
more vulnerable. Because early intercourse is usually correlated with the
eventual number of sexual partners, several studies have attempted to
disentangle the two factors. They have found that the greater the number of
sexual partners, the greater the risk of sexually transmitted disease;
consequently, much research has focused on the role of a variety of sexually
transmitted agents. Further supporting sexually transmitted agents in the
etiology of this disease are several studies which indicate that there may be an
important "male factor" to this disease; husbands of cervical cancer
patients report considerably more sexual partners than husbands of unaffected
women (Brinton et al., 1989b; Buckley et al., 1981). Despite early speculation
regarding potential effects, more recent studies do not confirm a role for
circumcision status of the male partner. Frequency of sexual intercourse with
the same male partner also appears unrelated to risk.
Recently, intense interest has focused on
the role of the human papillomaviruses (HPV), which cause genital warts in both
men and women (Koutsky et al., 1988). Abundant laboratory and clinical data
support a role for HPV in the etiology of cervical cancer, but it is unlikely
that the virus is a necessary and sufficient cause (Schiffman et al., 1993). The
role of possible cofactors, including the herpesviruses, hormonal and dietary
factors, and smoking, is also being investigated.
In a number of studies, cigarette smoking
has been found to increase the risk of cervical cancer, especially among
long-term or high-intensity smokers (Winkelstein, 1990). Smoking constituents
have been found in cervical mucus, but the biologic mechanisms underlying the
smoking-cervical cancer relationship have not been identified.
Choice of contraceptive method also
appears to affect the risk of cervical cancer. Barrier mechanisms lower the
risks--probably by decreasing exposure to infectious agents. The reasons for the
increased risk associated with oral contraceptives--especially in long-term
use--may be more complex. Although there has been concern that the link may
merely reflect the correlation of this method with more intensive sexual
activity, a number of studies have shown that the excess risk persists after
adjustment for a variety of socioeconomic and sexual factors (Brinton, 1991).
The role of hormonal factors in the etiology of cervical cancer has been
underscored by recent studies which identify multiple births as independent risk
factors (Brinton et al., 1989a; Parazzini et al., 1989).
There is increasing evidence that
nutritional factors may play a role in cervical disease. Several studies suggest
that low intake of either vitamin C or beta carotene may be associated with
elevations in risk (Brock et al., 1988; Slattery et al., 1990), although this
has not always been found (Ziegler et al., 1990). Deficiency in folacin (one of
the B complex vitamins) has also been proposed as a risk factor, especially
among oral contraceptive users whose stores of this vitamin are depleted.
REFERENCES
Brinton LA: Oral contraceptives and
cervical neoplasia. Contraception 43:581-595, 1991.
Brinton LA and Fraumeni JF Jr:
Epidemiology of uterine cervical cancer. J Chron Dis 39:1051-1065, 1986.
Brinton LA, Reeves WC, Brenes MM, et al.:
Parity as a risk factor for cervical cancer. Am J Epidemiol 130:486-496, 1989a.
Brinton LA, Reeves WC, Brenes MM, et al.:
The male factor in the aetiology of cervical cancer among sexually monogamous
women. Int J Cancer 44:199-203, 1989b.
Brock KE, Berry G, Mock PA, et al.:
Nutrients in diet and plasma and risk of in situ cervical cancer. J Natl Cancer
Inst 80:580-585, 1988.
Buckley JD, Doll R, Harris RWC, et al.:
Case-control study of the husbands of women with dysplasia or carcinoma of the
cervix uteri. Lancet 2:1010-1015, 1981.
Devesa SS, Young JL Jr, Brinton LA, et
al.: Recent trends in cervix uteri cancer. Cancer 64:2184-2190, 1989.
Koutsky LA, Galloway DA and Holmes KK:
Epidemiology of genital human papillomavirus infection. Epidemiol Rev
10:122-163, 1988.
Parazzini F, La Vecchia C, Negri E, et
al.: Reproductive factors and the risk of invasive and intraepithelial cervical
neoplasia. Br J Cancer 59:805-809, 1989.
Parkin DM, Muir CS, Whelan S, et al.,
eds.: Cancer Incidence in Five Continents, vol VI. IARC Publication No. 120.
World Health Organization, IARC Scientific Agency for Research on Cancer, Lyon,
1992.
Ries LAG, Miller BA, Hankey BF, et al.:
SEER Cancer Statistics Review, 1973-1991: Tables and Graphs, National Cancer
Institute. NIH Publ. No. 94-2789, Bethesda, MD, 1994.
Schiffman MH, Bauer HM, Hoover RN, et al.:
Epidemiologic evidence showing that human papillomavirus infection causes most
cervical intraepithelial neoplasia. J Natl Cancer Inst 85:958-964, 1993.
Slattery ML, Abbott TM, Overall JC Jr, et
al.: Dietary vitamins A, C, and E and selenium as risk factors for cervical
cancer. Epidemiology 1:8-15, 1990.
Winkelstein W Jr: Smoking and cervical
cancer--Current status: a review. Am J Epidemiol 131:945-957, 1990.
Ziegler RG, Brinton LA, Hamman RF, et al.:
Diet and the risk of invasive cervical cancer among white women in the United
States. Am J Epidemiol 132:432-445, 1990.
*
From the Environmental Epidemiology Branch, Division of Cancer Etiology,
National Cancer Institute, Bethesda, Maryland
National Cancer Institute
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