eMedicine Specialties > Obstetrics and Gynecology > Gynecologic Surgery
Surgical Treatment of Vaginal Cancer
Updated: Dec 10, 2007
Introduction
Malignant diseases of the vagina are either primary vaginal cancers or metastatic from adjacent or distant organs. Primary vaginal cancers are defined as arising solely from the vagina with no involvement of the external cervical os superiorly or the vulva inferiorly. The importance of this definition lies in the different clinical approach in the treatment of upper and lower vaginal cancer. According to the International Federation of Gynecology and Obstetrics (FIGO), a vaginal lesion involving the external os of the cervix should be considered cervical cancer and treated as such; a tumor involving both vulva and vagina should be considered vulvar cancer. A patient with history of a preinvasive lesion or an invasive carcinoma arising from the cervix or the vulva requires that 5-10 years of disease-free interval have past before diagnosing a new vaginal lesion as primary vaginal carcinoma. This criterion is required to rule out recurrent cervical or vulvar disease.
About 80% of vaginal cancers are metastatic, primarily from the cervix or endometrium. Metastatic cancer from the vulva, ovaries, choriocarcinoma, rectosigmoid, and bladder are less common. These cancers usually invade the vagina directly. Cancers from distant sites that metastasize to the vagina through the blood or lymphatic system also occur, including colon cancer, renal cell carcinoma, melanoma, and breast cancer.
History of the Procedure
In 1946, Alexander Brunschwig published the first cases of pelvic exenteration. In his first series, 5 of 22 surgical patients died from the operation itself. The original procedure consisted of connecting the ureters to the colostomy. In 1950, Bricker modified the procedure by isolating a loop of ileum, closing one end, anastomosing the ureters to it, and bringing the patent end out as a stoma.1 Since then, several other modifications have improved the outcome of this procedure. Today, with vaginal reconstruction and continent vesicostomy, the procedure is widely accepted as a treatment in selective cases.
Frequency
Primary vaginal carcinoma is rare, constituting only 1-2% of all malignant gynecological tumors. It ranks fifth in frequency behind cancer of the uterus, cervix, ovary, and vulva. The age-adjusted incidence in the United States is 0.6 per 100,000 population. The strict criteria used in defining vaginal carcinoma contribute to this low incidence.
Etiology
The etiology of vaginal cancer has not been identified. Note that vaginal cancer is not histologically homogeneous; several types of lesions exist, each with its own characteristics, age predilection, aggressiveness, and prognosis (see the Table). This suggests that a single etiologic factor is unlikely. Although some histologic types of vaginal cancer have been associated with exposure to certain agents, so far no clear cause-and-effect relationship exists between any of those agents and vaginal carcinoma.
The strongest association is between squamous cell carcinoma and human papilloma virus (HPV) infection, which is similar to cervical carcinoma. HPV subtypes 16 and 18 have the highest oncogenic potential and are most commonly linked to dysplastic changes in the female genital tract. Because HPV is sexually transmitted, this association raises the question as to whether women who engage in high-risk sexual behaviors, such as sex with multiple partners, are at risk for developing vaginal cancer. Other associated infectious agents are herpes simplex virus (HSV) and Trichomonas vaginalis. In 2000, Lee and colleagues reported a case of rapidly progressive vaginal squamous cell carcinoma in a young woman with a 2-year history of human immunodeficiency virus (HIV) infection.2 They suggest that young women infected with both HIV and HPV are at increased risk for a more aggressive and less responsive vaginal cancer.
Another association that strengthens the link between HPV infection and vaginal cancer is the presence of a premalignant lesion in the vagina, known as vaginal intraepithelial neoplasia (VAIN). In 1991, Aho and coworkers reported that 5-9% of patients treated for VAIN progressed to invasive carcinoma.3 This suggests that VAIN may be a precursor to vaginal cancer even though the incidence of VAIN in the United States is 0.2-0.3 per 100,000 women, which is less than the incidence of diagnosed vaginal cancer. This is because of the fact that women with VAIN are usually asymptomatic and that screening for VAIN is not recommended for the general population. Still, the true malignant potential of VAIN needs to be identified.
A previous history of cervical intraepithelial neoplasia (CIN), invasive cervical carcinoma, or invasive vulvar carcinoma has also been associated with vaginal carcinoma. Several studies indicate that up to 30% of patients with primary vaginal carcinoma have a previous history of in situ or invasive carcinoma that was treated at least 5 years before diagnosis.
Long-term pessary use and chronic irritation of vaginal mucosa in women with procidentia have been associated with vaginal cancer. Other predisposing factors include cigarette smoking, immunosuppressive therapy, chemotherapy, and radiation therapy. Approximately 10% of women diagnosed with primary vaginal carcinoma have a previous history of irradiation to the pelvis. In a 2000 report, Carthew and colleagues demonstrated that tamoxifen, a chemotherapeutic drug, induced endometrial and vaginal cancer in rats in the absence of endometrial hyperplasia.4
In 1999, Pukkala and colleagues reported an association between low socioeconomic class in Finland and an increased incidence of cervical, endometrial, and vaginal cancer.5
Diethylstilbestrol (DES), a drug previously used in the first trimester to prevent pregnancy loss, has a strong association with clear cell adenocarcinoma of the vagina. Herbst and colleagues first observed this association in 19716 , which led to the discontinuation of DES that same year. By 1987, the Registry for Hormonal Transplacental Carcinogenesis, established by Herbst and Scully, identified 524 women with clear cell adenocarcinoma, but only 60% had a history of DES exposure. Disease in the other 40% of patients with no history of DES exposure could be explained by recall bias or exposure to other unidentified factors. Women with in utero exposure to DES are at higher risk of developing adenocarcinoma than the general population. The estimated risk in these women is 1 in 1000.
Although 59% of women with vaginal cancer had a prior hysterectomy, in a 1986 report, Herman and colleagues demonstrated that when age and prior cervical cancer are controlled for, risk of vaginal cancer is not increased following hysterectomy for benign disease.7 Note that hysterectomy by itself is not a risk factor, rather women who underwent hysterectomy were poorly monitored.
In a 2004 publication, Hellman et al in Sweden reviewed 341 cases of primary carcinoma of the vagina from 1956-1996 and suggested that the etiology of vaginal cancer may be age related.8 In younger women, the disease occurred in the upper part of the vagina and seemed to be related to cervical dysplasia and HPV infection, while in older patients, the tumors were exophytic. There was significant correlation with late menarche, suggesting hormonal factors and trauma to the vagina as probable etiologies.
Pathophysiology
The presence of different stages of histologic differentiation—VAIN, carcinoma in situ, possible microinvasive carcinoma, and invasive cancer—suggests a continuum of transformation from less malignant to more invasive, which is similar to the continuum described for cervical cancer. As reported by Ikenberg et al in 19909 and Ostraw et al in 198810 , identification of HPV DNA in squamous cell cancer cells by in situ hybridization (21%) and southern blot hybridization (56%) strongly suggests an association with HPV infection and a possible role of HPV in the pathogenesis of squamous cell vaginal carcinoma.
On the other hand, the significant association with a previous history of cervical or vulvar cancer suggests that the entire genital tract is at risk for squamous cell carcinoma once malignancy has occurred anywhere along the tract; this is a phenomenon postulated by Marcus and is known as the field effect. HPV infection could explain this phenomenon because HPV is associated with cervical, vaginal, and vulvar disease. Koyamatsu et al did a comparative analysis of the presence of HPV types 16 and 18 by polymerase chain reaction (PCR) and expression of p53 gene and Ki-67 antigen using immunohistochemistry in cervical, vaginal, and vulvar cancer.11 They suggested that in cervical cancer, HPV 16 and 18 played a common causal role, and in vulvar cancer, p53 gene mutations were the main carcinogenic cause, while vaginal cancer has transitional characteristics between cervical and vulvar cancer. There was no significant difference in overexpression of Ki-67 antigen among the 3 cancers.
Another explanation for this association is that an occult residual disease, such as VAIN, is trapped within the vaginal cuff posthysterectomy and goes unnoticed until it develops into invasive carcinoma. This possibility illustrates the theory of the field effect and HPV infection because HPV has also been linked to VAIN. It also partially explains why women with previous hysterectomy go unnoticed until they present with advanced-stage vaginal carcinoma.
The third possibility is radiation carcinogenesis.
The pathogenesis by which DES might play a role in inducing clear cell adenocarcinoma is unclear. In 1972, Forsberg and colleagues12 proposed the possibility of estrogen-induced maturation arrest of the müllerian ducts, and in 1984 Robboy and colleagues13 suggested that atypical vaginal adenosis and atypical cervical ectropion of the tuboendometrial type might act as the precursors of clear cell adenocarcinoma of the vagina and cervix.
Most vaginal cancers occur in the upper third of the vagina. Reports are contradictory as to whether the anterolateral wall or the posterior wall is the more frequent site. Reports suggesting that the upper posterior wall is the most common site favor the hypothesis that irritating substances, such as vaginal secretions and semen, pool in the posterior fornix and cause chronic irritation, which could lead to induction of a carcinogenic process.
The proximity of the bladder anteriorly and the rectum posteriorly to the vagina predisposes these organs to direct invasion by the tumor. Lymphatic dissemination follows the lymphatic drainage of the vagina. The middle-to-upper vagina communicates superiorly with the lymphatics of cervix and drains into the pelvic obturator node, the internal and external iliac chains, then to the para-aortic nodes. The distal third of vagina drains to the inguinal node then the pelvic node. Posterior wall lymphatics communicate with rectal lymphatics and drain to the inferior gluteal, sacral, and rectal nodes. Hematogenous dissemination to distant sites includes the lungs, liver, bone, and skin. A submucosal lesion suggests that the malignancy is metastatic via the vaginal lymphatics.
Presentation
Duration of symptoms averages 6-12 months before diagnosis, with a range of 0-11 years. Delay in diagnosis of vaginal carcinoma is not uncommon, and this is partially because of disease rarity and delay in relating patient symptoms to a vaginal origin. As expected, the longer the delay, the more advanced the cancer once the diagnosis is made, which results in a poorer outcome.
Painless vaginal bleeding is the most common symptom, accounting for 65-80% of all presentations. Bleeding is postmenopausal in about 70% of patients, which is consistent with the peak age of 60 years for squamous cell carcinoma, the most common type. Menorrhagia, intermenstrual bleeding, and postcoital bleeding have also been reported.
Vaginal discharge occurs in 30% of patients, while 20% of patients report urinary symptoms, which are caused by an anterior lesion compressing or invading the bladder, the urethra, or both. This causes bladder pain, dysuria, urgency, and hematuria.
About 15-30% of patients present with pelvic pain. Posterior lesions compress or invade the rectosigmoid, which causes tenesmus or constipation.
Only 10% of patients report a vaginal mass or vaginal prolapse. In 2000, Eltabbakh and coworkers reported a single patient who presented with a cystic pelvic mass arising from the posterior vaginal wall that mimicked an ovarian neoplasm.14
About 10-27% of patients are asymptomatic; diagnosis is made during routine pelvic examination. These patients tend to be caught at a much earlier stage than those presenting with symptoms, and their prognosis is much better.
Indications
Consensus as to the proper treatment of vaginal carcinoma is lacking, mainly because of the rarity of the disease. The most commonly used treatment modality is radiotherapy. Surgery, with or without concomitant radiation therapy, is indicated in the following conditions:
- Squamous cell carcinoma
- Stage I disease in the upper posterior vagina
- Stage IVa disease, particularly in the presence of a rectovaginal or vesicovaginal fistula
- Central recurrence after radiotherapy
- Ovary transposition in young patients prior to radiotherapy
- Clear cell adenocarcinoma: Although the etiology is different, the presentation may be similar to squamous cell carcinoma.
- Verrucous carcinoma: Because radiation therapy is contraindicated, surgery is the only treatment.
- Other cases
- Melanoma
- Sarcoma
- Embryonal rhabdomyosarcoma
- Endodermal sinus tumor
These indications are discussed in detail in Treatment.
Relevant Anatomy
The vagina is located in the true pelvis, which also contains the rest of the internal genital tract, the rectosigmoid, the bladder, the proximal urethra, and the pelvic portions of the ureters. The pelvic organs are partially covered by the peritoneum. The endopelvic fascia covers these organs and forms their supporting ligaments in conjunction with the pelvic vasculature and musculature.
The pelvic cavity is divided into anterior and posterior compartments by the transversely positioned broad ligament. The uterus is centered within the broad ligament and is attached to the round ligaments, which run anterolaterally within the broad ligament from the uterus to the pelvic wall.
The anterior cul-de-sac, also known as the vesicouterine pouch, is located between the uterus and the bladder. It has small lateral recesses known as the paravesical fossae. This pouch ends where the cervix and the bladder connect and does not extend down to the vagina. The posterior cul-de-sac, known as the rectouterine pouch of Douglas, is located between the uterus posteriorly and the rectum anteriorly. It is continuous with the pararectal fossae and contrary to the anterior pouch. It extends about 1-2 cm down to the vagina, separating the cervix from the rectum.
The vagina is a muscular tube that extends from the cervix to the hymenal ring, penetrating the levator ani and the urogenital diaphragm. These latter structures provide vaginal support inferiorly. From the outermost to the innermost layers, the vagina is composed of an endopelvic fascia, which contains an abundant plexus of vessels, lymphatics, and nerves as well as outer longitudinal and inner circular smooth muscle layers, submucosa, and mucosa. The vagina is attached to the rectum posteriorly by the rectal pillars, while the bladder pillars provide anterior vaginal attachment to the bladder. During vaginal inspection with a speculum, the anterior and posterior sulci provide the anatomic landmark of the site of attachment of these pillars. These are most easily observed in nulliparous women.
The rectal and bladder pillars are paired, parallel, longitudinal, fibrovascular bundles containing extensive vascular and lymphatic networks between the vagina and the rectum and bladder, respectively. They both run the entire length of the vagina. The bladder pillars also contain the paravaginal tissues (paracolpium). As it joins the lower end of the cervix, the upper end of the bladder pillar forms the vesicouterine ligament. This ligament forms a tunnel through which the ureters run inferomedially to reach the inferolateral portion of the bladder. The tunnel divides the vesicouterine ligament into anterior and posterior leaves. This anatomic structure is important during radical hysterectomy when careful dissection of the ligament is needed to mobilize the ureters. The rectal pillars receive the middle rectal arteries from the cardinal ligament.
The cardinal ligaments are wedge-shaped fibrovascular bundles containing the uterine, vaginal, inferior vesical, and middle rectal arteries and veins as well as the lymphatic system. On each side, they run from the lateral aspect of the cervix to the lateral pelvic sidewall, traversing the pelvic plane at a 30º angle from transverse pelvic diameter and dividing the paravesical and paravaginal spaces from the pararectal spaces. On the pelvic wall, they insert on the endopelvic fascia and the hypogastric vasculature. The anterior part of the cardinal ligament is more vascular, while the posterior part is more fibrous and contains the autonomic system of the bladder and rectum. An important landmark is the uterine artery that crosses the anterior-most portion of the cardinal ligament. The ureter enters the upper portion of the ligament beneath this artery (water under the bridge) and 1-2 cm lateral to the isthmus of the uterus. The uterine veins cross below the ureters.
The uterosacral ligaments run from the posterolateral aspect of the cervix to the anterolateral part of the rectum. They are in close contact to the rectal pillars and straddle the posterior cul-de-sac.
Several avascular tissue planes are developed during pelvic surgery. The paravesical space is bordered by the symphysis pubis anteriorly, the cardinal ligaments posteriorly, the obliterated umbilical artery along the bladder medially, and the obturator internus laterally. The pararectal space is bordered by the cardinal ligament anteriorly, sacrum posteriorly, rectum medially, and hypogastric artery laterally. The rectovaginal space is bounded by the vagina anteriorly and the rectum posteriorly, while the rectal pillars form its lateral walls. The vesicovaginal space is limited laterally by the bladder pillars, anteriorly by the bladder, and posteriorly by the vagina. To develop this space, the peritoneal reflection of the anterior cul-de-sac is entered.
The levator ani forms the major support of the pelvic structures and is the major component of the pelvic diaphragm. It is penetrated anteriorly by the rectum, vagina, and urethra. It forms the floor of all the planes discussed above.
The upper part of the vagina receives its blood supply from the uterine and the internal pudendal arteries, from which the vaginal artery arises. The inferior rectal artery and other branches arising from the internal pudendal artery supply the lower vagina. The vaginal venous plexus mainly drains into the pelvic wall through the parametrial veins, and to a lesser degree to the vesical and rectal plexuses.
Crossover of the vaginal lymphatic system is extensive. The middle-to-upper vagina communicates superiorly with the cervical lymphatics and drains into the pelvic obturator node, the internal and external iliac chains, and then the para-aortic nodes. The distal third of the vagina drains to the inguinal then the pelvic nodes. The posterior wall lymphatics communicate with the rectal lymphatics and drain to the inferior gluteal, sacral, and rectal nodes.
The vagina stays in close proximity to the bladder and urethra anteriorly, which increases risk of accidental injury to these structures during surgery. The sigmoid, on the other hand, reflects away from the posterior vaginal wall at its midpoint, facilitating approaching the vagina posteriorly through the posterior cul-de-sac and a developed rectovaginal plane.
Contraindications
Metastasis and extension to pelvic sidewalls are contraindications for exenteration. Microscopic pelvic node involvement is more of a controversy than a contraindication, and patients with positive pelvic nodes and no other poor prognostic factors can be considered candidates for exenteration. Involvement of both the pelvic and para-aortic nodes should warrant aborting the surgery.
More on Surgical Treatment of Vaginal Cancer |
 Overview: Surgical Treatment of Vaginal Cancer |
| Workup: Surgical Treatment of Vaginal Cancer |
| Treatment: Surgical Treatment of Vaginal Cancer |
| Follow-up: Surgical Treatment of Vaginal Cancer |
| References |
| Next Page » |
References
Bricker EM. Bladder substitution after pelvic evisceration. Surg Clin North Am. 1950;30:1511-1521.
Lee YC, Holcomb K, Buhl A. Rapid progression of primary vaginal squamous cell carcinoma in a young HIV-infected woman. Gynecol Oncol. Sep 2000;78(3 Pt 1):380-2. [Medline].
Aho M, Vesterinen E, Meyer B. Natural history of vaginal intraepithelial neoplasia. Cancer. Jul 1 1991;68(1):195-7. [Medline].
Carthew P, Edwards RE, Nolan BM. Tamoxifen induces endometrial and vaginal cancer in rats in the absence of endometrial hyperplasia. Carcinogenesis. Apr 2000;21(4):793-7. [Medline].
Pukkala E, Weiderpass E. Time trends in socio-economic differences in incidence rates of cancers of the breast and female genital organs (Finland, 1971-1995). Int J Cancer. Mar 31 1999;81(1):56-61. [Medline].
Herbst AL, Ulfelder H, Poskanzer DC. Adenocarcinoma of the vagina. Association of maternal stilbestrol therapy with tumor appearance in young women. 1971. Am J Obstet Gynecol. Dec 1999;181(6):1574-5. [Medline].
Herman JM, Homesley HD, Dignan MB. Is hysterectomy a risk factor for vaginal cancer?. JAMA. Aug 1 1986;256(5):601-3. [Medline].
Hellman K, Silfversward C, Nilsson B. Primary carcinoma of the vagina: factors influencing the age at diagnosis. The Radiumhemmet series 1956-96. Int J Gynecol Cancer. May-Jun 2004;14(3):491-501. [Medline].
Ikenberg H, Runge M, Goppinger A. Human papillomavirus DNA in invasive carcinoma of the vagina. Obstet Gynecol. Sep 1990;76(3 Pt 1):432-8. [Medline].
Ostrow RS, Manias DA, Clark BA. The analysis of carcinomas of the vagina for human papillomavirus DNA. Int J Gynecol Pathol. 1988;7(4):308-14. [Medline].
Koyamatsu Y, Yokoyama M, Nakao Y. A comparative analysis of human papillomavirus types 16 and 18 and expression of p53 gene and Ki-67 in cervical, vaginal, and vulvar carcinomas. Gynecol Oncol. Sep 2003;90(3):547-51. [Medline].
Forsberg JG. Estrogen, vaginal cancer, and vaginal development. Am J Obstet Gynecol. May 1 1972;113(1):83-7. [Medline].
Robboy SJ, Young RH, Welch WR. Atypical vaginal adenosis and cervical ectropion. Association with clear cell adenocarcinoma in diethylstilbestrol-exposed offspring. Cancer. Sep 1 1984;54(5):869-75. [Medline].
Eltabbakh GH, Field JM, Trask CE. Primary vaginal squamous cell carcinoma presenting as a cystic pelvic mass. Gynecol Oncol. Feb 2000;76(2):213-7. [Medline].
Manetta A, Gutrecht EL, Berman ML. Primary invasive carcinoma of the vagina. Obstet Gynecol. Oct 1990;76(4):639-42. [Medline].
Videlefsky A, Grossl N, Denniston M. Routine vaginal cuff smear testing in post-hysterectomy patients with benign uterine conditions: when is it indicated?. J Am Board Fam Pract. Jul-Aug 2000;13(4):233-8. [Medline].
Al-Kurdi M, Monaghan JM. Thirty-two years experience in management of primary tumours of the vagina. Br J Obstet Gynaecol. Nov 1981;88(11):1145-50. [Medline].
Plataniotis GA, Kouvaris JR, Sykiotis CA. Dermal metastasis from vaginal squamous cell carcinoma. Br J Dermatol. Sep 1999;141(3):579-80. [Medline].
Tavassoli FA, Norris HJ. Smooth muscle tumors of the vagina. Obstet Gynecol. Jun 1979;53(6):689-93. [Medline].
Oudouxa A, Rousseaub T, Bridjia B. Interest of F-18 fluorodeoxyglucose positron emission tomography in the evaluation of vaginal malignant melanoma. Gynecologic Oncology. 2004;95 (3):765-8. [Medline].
Senekjian EK, Frey KW, Anderson D. Local therapy in stage I clear cell adenocarcinoma of the vagina. Cancer. Sep 15 1987;60(6):1319-24. [Medline].
Matthews CM, Morris M, Burke TW. Pelvic exenteration in the elderly patient. Obstet Gynecol. May 1992;79(5 ( Pt 1)):773-7. [Medline].
Reid GC, Schmidt RW, Roberts JA. Primary melanoma of the vagina: a clinicopathologic analysis. Obstet Gynecol. Aug 1989;74(2):190-9. [Medline].
Buchanan DJ, Schlaerth J, Kurosaki T. Primary vaginal melanoma: thirteen-year disease-free survival after wide local excision and review of recent literature. Am J Obstet Gynecol. Jun 1998;178(6):1177-84. [Medline].
Van Nostrand KM, Lucci JA 3rd, Schell M. Primary vaginal melanoma: improved survival with radical pelvic surgery. Gynecol Oncol. Nov 1994;55(2):234-7. [Medline].
Siu SS, Lo KW, Chan AB. Nodal detection in malignant melanoma of the vagina using laparoscopic ultrasonography. Gynecol Oncol. Mar 2004;92(3):985-8. [Medline].
Rodier JF, Janser JC, David E. Radiopharmaceutical-guided surgery in primary malignant melanoma of the vagina. Gynecol Oncol. Nov 1999;75(2):308-9. [Medline].
Nakagawa S, Koga K, Kugu K. The evaluation of the sentinel node successfully conducted in a case of malignant melanoma of the vagina. Gynecol Oncol. Sep 2002;86(3):387-9. [Medline].
Irvin WP, Bliss SA, Rice LW. Malignant melanoma of the vagina and locoregional control: radical surgery revisited. Gynecol Oncol. Dec 1998;71(3):476-80. [Medline].
Miller B, Morris M, Rutledge F. Aborted exenterative procedures in recurrent cervical cancer. Gynecol Oncol. Jul 1993;50(1):94-9. [Medline].
Andersen BL, Hacker NF. Psychosexual adjustment following pelvic exenteration. Obstet Gynecol. Mar 1983;61(3):331-8. [Medline].
Clarke JS, Condon RE, Bartlett JG. Preoperative oral antibiotics reduce septic complications of colon operations: results of prospective, randomized, double-blind clinical study. Ann Surg. Sep 1977;186(3):251-9. [Medline].
Classen DC, Evans RS, Pestotnik SL. The timing of prophylactic administration of antibiotics and the risk of surgical-wound infection. N Engl J Med. Jan 30 1992;326(5):281-6. [Medline].
Hatch KD. Construction of a neovagina after exenteration using the vulvobulbocavernosus myocutaneous graft. Obstet Gynecol. Jan 1984;63(1):110-4. [Medline].
Jensen JK, Lucci JA, DiSaia PJ. To drain or not to drain: a retrospective study of closed-suction drainage following radical hysterectomy with pelvic lymphadenectomy. Gynecol Oncol. Oct 1993;51(1):46-9. [Medline].
Brunschwig A. What are the indications and results of pelvic exenteration?. JAMA. Oct 18 1965;194(3):274. [Medline].
Morley GW, Hopkins MP, Lindenauer SM. Pelvic exenteration, University of Michigan: 100 patients at 5 years. Obstet Gynecol. Dec 1989;74(6):934-43. [Medline].
Anthopoulos AP, Manetta A, Larson JE. Pelvic exenteration: a morbidity and mortality analysis of a seven-year experience. Gynecol Oncol. Nov 1989;35(2):219-23. [Medline].
Hawighorst-Knapstein S, Schonefussrs G, Hoffmann SO. Pelvic exenteration: effects of surgery on quality of life and body image--a prospective longitudinal study. Gynecol Oncol. Sep 1997;66(3):495-500. [Medline].
Benedet JL, Murphy KJ, Fairey RN. Primary invasive carcinoma of the vagina. Obstet Gynecol. Dec 1983;62(6):715-9. [Medline].
Brunschwig A. Complete excision of pelvic viscera for advanced carcinoma. Cancer. 1948;1:177-183.
Dixit S, Singhal S, Baboo HA. Squamous cell carcinoma of the vagina: a review of 70 cases. Gynecol Oncol. Jan 1993;48(1):80-7. [Medline].
Eddy GL, Marks RD Jr, Miller MC 3rd. Primary invasive vaginal carcinoma. Am J Obstet Gynecol. Aug 1991;165(2):292-6; discussion 296-8. [Medline].
Gallup DG, Talledo OE, Shah KJ. Invasive squamous cell carcinoma of the vagina: a 14-year study. Obstet Gynecol. May 1987;69(5):782-5. [Medline].
Goodman A. Primary vaginal cancer. Surg Oncol Clin N Am. Apr 1998;7(2):347-61. [Medline].
Gupta JC, Arora MM, Jungalwala BN. Primary melanoma of the vagina. J Obstet Gynaecol Br Commonw. Oct 1964;71:801-3. [Medline].
Hatch KD, Gelder MS, Soong SJ. Pelvic exenteration with low rectal anastomosis: survival, complications, and prognostic factors. Gynecol Oncol. Sep 1990;38(3):462-7. [Medline].
HPV (human papillomavirus). U.S. Food and Drug Administration. Available at http://www.fda.gov/womens/getthefacts/hpv.html. Accessed 12/10/07.
Isaacs JH. Verrucous carcinoma of the female genital tract. Gynecol Oncol. Sep 1976;4(3):259-69. [Medline].
Johnston GA Jr, Klotz J, Boutselis JG. Primary invasive carcinoma of the vagina. Surg Gynecol Obstet. Jan 1983;156(1):34-40. [Medline].
Kirkbride P, Fyles A, Rawlings GA. Carcinoma of the vagina--experience at the Princess Margaret Hospital (1974-1989). Gynecol Oncol. Mar 1995;56(3):435-43. [Medline].
Koutsky LA, Ault KA, Wheeler CM. A controlled trial of a human papillomavirus type 16 vaccine. N Engl J Med. Nov 21 2002;347(21):1645-51. [Medline].
Kulasingam SL, Myers ER. Potential health and economic impact of adding a human papillomavirus vaccine to screening programs. JAMA. Aug 13 2003;290(6):781-9. [Medline].
Levitan Z, Gordon AN, Kaplan AL. Primary malignant melanoma of the vagina: report of four cases and review of the literature. Gynecol Oncol. Apr 1989;33(1):85-90. [Medline].
Manetta A, Pinto JL, Larson JE. Primary invasive carcinoma of the vagina. Obstet Gynecol. Jul 1988;72(1):77-81. [Medline].
Manetta A, Podczaski ES, Larson JE. Scalene lymph node biopsy in the preoperative evaluation of patients with recurrent cervical cancer. Gynecol Oncol. Jun 1989;33(3):332-4. [Medline].
Matthews KS, Numnum TM, Conner MG, Barnes M 3rd. Fertility-sparing radical abdominal trachelectomy for clear cell adenocarcinoma of the upper vagina: a case report. Gynecol Oncol. June/2007;105(3):820-2. [Medline]. [Full Text].
Melnick S, Cole P, Anderson D. Rates and risks of diethylstilbestrol-related clear-cell adenocarcinoma of the vagina and cervix. An update. N Engl J Med. Feb 26 1987;316(9):514-6. [Medline].
Perticucci S. Diagnostic, prognostic, and therapeutic considerations in invasive carcinoma of the vagina. Obstet Gynecol. Dec 1972;40(6):843-50. [Medline].
Rutledge F. Cancer of the vagina. Am J Obstet Gynecol. Mar 1 1967;97(5):635-55. [Medline].
Further Reading
Keywords
cervical cancer, vulvar cancer, premalignant disease of the vagina, human papilloma virus, HPV, cervical carcinoma, herpes simplex virus, HSV, Trichomonas vaginalis, T vaginalis, human immunodeficiency virus, HIV, sexually transmitted diseases, STDs, melanoma, exenteration
