Management of the Woman with Genital Tract Cancer

Annekathryn Goodman

Cancers of the genital tract account for about 20% of cancer diagnoses and 10% of cancer deaths in women in the United States. They range from the readily detectable and curable carcinoma of the cervix to the very problematic ovarian carcinoma, with its tendency to remain inconspicuous until very late. Endometrial carcinoma has come to be one of the most common genital cancers of the postmenopausal years. Cervical cancer is associated with sexual exposure to human papillomavirus (HPV) and is therefore of great concern for younger women.

Treatment of the woman with genital tract cancer is usually the province of the oncologist and gynecologist, but the primary physician remains an important part of the collaborative effort. Patient counseling, monitoring, and management of ongoing medical problems are among the important responsibilities.

CARCINOMA OF THE CERVIX (1, 2, 3, 4, 5 and 6)

The incidence of invasive cervical carcinoma peaks between the ages of 48 and 55 years. The peak for carcinoma in situ is between ages 25 and 40 years. Most women with the disease present in their 20s and 30s due to early detection from use of cytologic testing and, more recently, HPV DNA testing (see Chapter 107).

Principles of Management

Diagnosis

Postcoital bleeding should raise suspicion for the diagnosis. In most cases of early disease, the patient is asymptomatic, and as noted, detection is by screening Papanicolaou test and/or HPV DNA testing (see Chapter 107). Diagnosis may be made by biopsy at the time of colposcopy following an abnormal screening test or of a grossly suspicious-looking lesion. In many cases, curative intervention occurs before invasive cancer is diagnosed. Because cervical cancer has a long preinvasive phase, biopsy-confirmed preinvasive disease can be cured by excisional procedures such as Loop Electrosurgical Excision Procedure (LEEP) or cone biopsy or destructive procedures such as carbon dioxide laser ablation or cryotherapy. Immediate excision, or the “see-and-treat” approach, is becoming a mainstay of screening programs in low- and middle-income countries. In resource-rich countries such as the United States, careful evaluation with colposcopy and biopsy can allow the triage of low-grade lesions to observation and close follow-up.

Staging

Clinical staging of cervical cancer is based on findings from biopsy, physical examination, and radiologic study. An estimate of extent of local disease can be made by pelvic examination, carefully palpating to see whether there is lateral extension to the vagina or pelvic wall. Palpating lymph nodes may detect a distant nodal metastasis, but clinical staging for involvement of pelvic nodes and the more distant paraaortic ones requires lymphangiography and/or computed tomography (CT). The latter has been especially helpful in the assessment of paraaortic nodes. Studies of magnetic resonance imaging suggest some usefulness in delineating local extension.

Stage of disease is designated by the TMN (tumor, metastasis, node) system (Table 123-1). FIGO (Federation International Gynecology Obstetrics) staging is the most widely used system worldwide. Stage I cancers are confined to the cervix. Stage II cancers involve either the upper two thirds of the vagina or the inner half of the parametria. A stage III cancer involves the lower third of the vagina, extension of tumor from the cervix to the pelvic side wall, or hydronephrosis. Stage IV cancer involves direct extension into the bladder or rectum or distant spread.

Prognosis worsens with advancing stage of local disease, development of regional and distant nodal metastases (especially paraaortic nodes), and histologic grade. Risk of nodal metastasis is zero for tumors with less than 3-mm invasion. The incidence of nodal spread increases steadily for tumors larger than 3 mm, and survival is directly proportional to number of lymph nodes involved.

Treatment and Prognosis

Early stages of carcinoma of the cervix are curable. Patients sometimes ask the opinion of their primary physician regarding the choices of therapy for early-stage disease. Consequently, these choices are worth reviewing here.

For stage 0 disease, which is preinvasive disease such as severe dysplasia or carcinoma in situ, the long-standing treatment of choice has been cold knife conization. Alternatives excisional approaches include loop electrosurgical excision and laser conization. Ablative methods include cryotherapy, laser ablation, electrofulguration, and cold coagulation. Hysterectomy is reserved for those who have intraepithelial neoplasia at the margins of the excised specimen and for whom future childbearing is not an issue. Cure is greater than 99%.

Stage IA1, microinvasive cancer with less than 3 mm of invasion, is treated with vaginal hysterectomy when childbearing is not an issue. When it is desired, excisional conization and close followup are the alternative if the cone margins are free of tumor. Five-year survival is greater than 90%. There is debate regarding the best approach to stage IA2 disease, which is defined as invasion between 3 and 5 mm with a maximum of 7-mm lateral spread. A cone biopsy, simple hysterectomy, or fertility sparing radical trachelectomy, the removal of the cervix with preservation of the fundus of the uterus, can be considered.

TABLE 123-1 Carcinoma of the Cervix Uteri—Staging

FIGO Stages		TNM Categories
	Primary tumour cannot be assessed	TX
	No evidence of primary tumour	T0
0	Carcinoma in situ (preinvasive carcinoma)	Tis
I	Cervical carcinoma confined to uterus (extension to corpus should be disregarded)	T1
IA	Invasive carcinoma diagnosed only by microscopy. All macroscopically visible lesions—even with superficial invasion— are Stage IB/T1b	T1a
IA1	Stromal invasion no greater than 3.0 mm in depth and 7.0 mm or less in horizontal spread	T1a1
IA2	Stromal invasion more than 3.0 mm and not more than 5.0 mm with a horizontal spread 7.0 mm or less^a	T1a2
IB	Clinically visible lesion confined to the cervix or microscopic lesion greater than IA2/T1a2	T1b
IB1	Clinically visible lesion 4.0 cm or less in greatest dimension	T1b1
IB2	Clinically visible lesion more than 4 cm in greatest dimension	T1b2
II	Tumour invades beyond the uterus but not to pelvic wall or to lower third of the vagina	T2
IIA	Without parametrial invasion	T2a
IIB	With parametrial invasion	T2b
III	Tumour extends to pelvic wall and/or involves lower third of vagina and/or causes hydronephrosis or nonfunctioning kidney	T3
IIIA	Tumour involves lower third of vagina no extension to pelvic wall	T3a
IIIB	Tumour extends to pelvic wall and/or causes hydronephrosis or nonfunctioning kidney	T3b
IVA	Tumour invades mucosa of bladder or rectum and/or extends beyond true pelvis^b	T4
IVB	Distant metastasis	M1
^aThe depth of invasion should not be more than 5 mm taken from the base of the epithelium, either surface or glandular, from which it originates. The depth of invasion is defined as the measurement of the tumour from the epithelialstromal junction of the adjacent most superficial epithelial papilla to the deepest point of invasion. Vascular space involvement, venous or lymphatic, does not affect classification. ^bThe presence of bullous edema is not sufficient to classify a tumour as T4. Reprinted with permission from Benedet JL, Bender H, Jones H III, et al. FIGO staging classifications and clinical practice guidelines in the management of gynecologic cancers. FIGO Committee on Gynecologic Oncology. Int J Gynaecol Obstet 2000;70(2):209-262. Copyright © 1999, Elsevier.

Stages IB and IIA are treated by radical hysterectomy plus pelvic lymphadenectomy or by definitive irradiation. Surgery is preferred in young women because the ovarian function can be spared and the vagina is more pliable than after irradiation. In addition, radiation effects on bowel and other adjacent structures are avoided. Radiation therapy spares the need for an extensive surgical procedure and its attendant complications. With either procedure, 5-year survival is equally good, with rates averaging about 85% for patients with no pelvic node disease. If there is involvement of pelvic nodes, 5-year survival falls to about 50%.

Stages IIB and beyond are treated with irradiation. Five-year survival averages about 60% for patients with IIB disease and falls to about 35% for stage IIIB disease and to 20% for stage IV disease.

Concomitant chemotherapy with cisplatin ±5 fluorouracil and radiation therapy has been shown to increase overall survival and progression-free survival in women with locally advanced cervical cancer compared to treatment with radiation alone and is now considered the standard of care. It also may reduce local and distant recurrence rates. There is an increase in acute treatment toxicity; the effect on long-term side effects has not been well defined.

The high likelihood of nodal metastasis associated with advancing stages of local disease markedly lowers the chances of cure. Clinically unapparent involvement of paraaortic nodes is a particularly difficult problem, leading some to advocate surgical sampling. Prophylactic radiation to the area does not seem to improve survival.

Patient Education

Young patients need to know that carcinoma of the cervix is potentially curable and that early disease can be successfully treated without overly compromising childbearing capacity. Such knowledge ensures that the young woman with precancerous lesions will not refuse timely treatment out of fear. The clinician should, however, carefully explain the risks of preterm delivery and low birth weight that are conferred by conization and similar procedures. Older patients presenting with more-invasive disease can still obtain some comfort from knowing the prognosis remains very favorable for most stages of this disease.

CARCINOMA OF ENDOMETRIUM (7, 8, 9, 10, 11 and 12)

This disease continues to be the most common female genital cancer, accounting for about half of all new cases (about 47,000 per year). While it predominantly strikes postmenopausal women, 25% of new cases are diagnosed in premenopausal women. Peak incidence is between ages 55 and 60 years. Only 5% of cases occur in women younger than the age of 40 years. Risk factors include obesity, nulliparity, late menopause, and prolonged unopposed estrogen stimulation of the uterus (either from replacement therapy or polycystic ovary syndrome; see Chapter 109). Uninterrupted estrogen stimulation in the absence of progestin risks induction of complex atypical hyperplasia, which is considered a premalignant change. Obesity may contribute by the ability of adipose tissue to convert circulating androstenedione into estrogen. Postmenopausal bleeding (defined as uterine bleeding occurring 6 months after the onset of menopause) may be the only early clue to the development of this tumor. Occasionally, a mass is felt on routine pelvic examination.

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