Vaginal cancer pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Syed Musadiq Ali M.B.B.S.[2]
Overview
A pre-cancer is a condition where some cells look abnormal. These cell changes are not cancer, but could become cancer over time. Vaginal intraepithelial neoplasia or VAIN means that the changed cells are only found in the innermost surface layer of the vagina.
VAIN is more common in women who have had their uterus removed (hysterectomy) and in those who were treated for cervical cancer or pre-cancer in the past.
There are 3 types of VAIN: VAIN1, VAIN2, and VAIN3. VAIN3 is the closest to a true cancer. In the past, the term dysplasia was used instead of VAIN. The types of dysplasia were referred to as mild, moderate, and severe, based on how close it was to a true cancer. This term is used much less now.
Low-grade VAIN (VAIN1) will sometimes go away on its own, but VAIN can sometimes lead to cancer if not treated. Higher-grade VAIN (VAIN2 or VAIN3) is usually treated right away. On gross pathology, an ulcerating or fungating mass, or an annular constricting lesion is characteristic finding of vaginal cancer.
Pathophysiology
- Vaginal cancer is a rare type of cancer that affects women.
- The vagina is a tube-like organ that connects the cervix (the lower part of the uterus) to the vulva (the outside female genitals).
- The vagina is lined by a layer of flat cells called squamous cells.
- This layer of cells is also called epithelium because it is formed by epithelial cells.
- At birth, a baby passes through the vagina as he or she is born, so the vagina is sometimes also known as the birth canal.
wo etiologies have been proposed to explain the strong association between VaIN and neoplasia elsewhere in the lower genital tract. One possibility is that women who develop VaIN shortly after surgery for cervical intraepithelial neoplasia (CIN) may simply have vaginal extension of cervical disease that was not detected and treated. However, VaIN is frequently multifocal, can occur several years after a hysterectomy for neoplasia, is independent of the amount of vaginal cuff excised, and is often observed de novo in the absence of cervical disease [26]. Thus, it is unlikely that the condition is the result of extension from the cervix in every case.
A second theory is that lower genital tract neoplasias share common etiologic factors, since approximately one-half of VaIN lesions are associated with concomitant cervical or vulvar neoplasia [13,15]. This field effect is based upon the principle that tissues of common embryological origin are susceptible to neoplasia from exposure to similar carcinogenic stimuli. In particular, exposure to human papillomavirus (HPV) appears to induce neoplasms in all three locations of the lower female genital tract (cervix, vagina, vulva) [27].
HPV infection — HPV-associated lesions are often multifocal (originating within several discrete foci at one anatomic site) and multicentric (involving several distinct anatomic sites of the lower genital tract). Although the relationship between HPV infection and intraepithelial neoplasia of the cervix is well known, there are less data available regarding vaginal neoplasia [28]. A review of 232 published VaIN cases reported a high prevalence of HPV in these lesions as detected by either polymerase chain reaction or hybrid capture assays for HPV DNA detection: 92.6 percent in VaIN 2/3, and 98.5 percent in VaIN 1 [29]. A worldwide collaborative found a similarly high prevalence of HPV in 96 percent of VaIN 2/3, with HPV 16 being the most frequently detected type (59 percent) [30].
Several viral subtypes are associated with VaIN (table 1), with HPV 16 and 18 being the most prevalent HPV types [31]. The prevalence of oncogenic HPV subtypes in the vagina is similar in women who have and have not undergone hysterectomy [32]. Thus, presence of the cervix does not appear to be necessary for oncogenic HPV to infect the genital tract. (See "Cervical cancer screening tests: Techniques for cervical cytology and human papillomavirus testing", section on 'HPV testing'.)
The disparity between the relatively high incidence of CIN and rarity of VaIN in women who test positive for HPV may be due to increased susceptibility of the metaplastic transformation zone of the cervix to oncogenic stimuli. By contrast, the mature, stable, squamous epithelium of the vagina may be less vulnerable to the same stimuli [33]. Women who have been exposed to diethylstilbestrol (DES) in utero often have squamous metaplasia of the vagina instead of normal columnar epithelium; this observation may explain the increased incidence of VaIN noted in some studies of these women [34,35].
- Women who have the human papillomavirus (HPV) are more likely than other women to develop this rare cancer.
- Women who have been infected with herpes simplex virus are also at higher risk for vaginal cancer.
- If a woman’s mother took a medicine called diethylstilbestrol (DES) when she was pregnant between 1940 and 1971.
- Women whose mothers took DES – known as DES daughters – develop clear-cell adenocarcinoma of the :*vagina or cervix more often than women in the general population.
- Lesions characteristically arise from the posterior wall of the upper third of the vagina. The common patterns of disease are:
- An ulcerating or fungating mass or
- An annular constricting lesion
- Vaginal squamous cell carcinoma arises from the thin, flat squamous cells that line the vagina.
- Vaginal adenocarcinoma arises from the glandular (secretory) cells in the lining of the vagina that produce some vaginal fluids.