PERSPECTIVE AND PATTERNS OF SPREAD
The staging criteria for gynecologic cancers reflect their oncoanatomy, which can be characterized as variants of both hollow and solid organs.
PERSPECTIVE AND PATTERNS OF SPREAD
The cervix uteri is the anatomic isocenter and an excellent starting point.
Although the incidence of gynecologic cancers is highest during the reproductive years, it does not become a significant kille until menarche. In developing countries, carcinoma of the cervix remains a leading cause of death, often following multiple pregnancies. By contrast, in the Western world, with the introduction of the Papanicolaou smear cytology tests, the cancer can be detected in its early stages. Its incidence remains high; it is the third-most-common gynecologic cancer, largely owing to increases in sexual activity as a result of better contraception, especially among women who have begun at an early age and have multiple sexual partners. According to the most recent Surveillance Epidemiology and End Results figures, uterin cervix, uterine corpus, and ovary account for 10% of all new cases and the same percentage of deaths. This translates into approximately 83,000 diagnoses and 28,000 deaths annually.
Ovarian and uterine cancers often occur during menopause. Although death rates have dramatically declined for cervical and uterine cancers, ovarian cancer survival rates remain the same. Most ovarian cancers are advanced on detection and spread widely. In contrast, uterine cancers usually remain contained within the uterus, and are clinically more evident, as they produce postmenopausal bleeding.
Three of the six sites that give rise to a large variety of neoplasms are discussed in this chapter. The ovary, the fallopian (uterine) tubes, uterus, cervix, vagina, and vulva are each afflicted with neoplastic disease. Adenocarcinomas predominate in the ovary, fallopian tube, and uterus. Squamous cell cancers occur in the cervix, vagina, and vulva. Special germ cell tumors or dysgerminomas, teratomas, and granulosa cell cancers are unique to the ovary. Gestational trophoblastic neoplasms and sarcomas are aggressive malignancies that invade deeply into the uterus. Uterine sarcomas have been emphasized in the seventh edition of the AJCC Cancer Staging Manual and expanded to include four different types, each with its own unique staging system. The patterns of spread of each malignancy determine the outcome: some are invasive; others grow slowly (Fig. 42.1). Each has a different tendency to metastasize.
Figure 42.1 | Patterns of spread. A. Coronal. B. Sagittal. Collage of the four major primary sites color coded to demonstrate T0 (yellow), T1 (green), T2 (blue), T3 (purple), and T4 (red). The concept of visualizing patterns of spread to appreciate the surrounding anatomy is well demonstrated by the six-directional pattern, SIMLAP (Table 42.1).
In summary, the patterns of spread in cervical cancer can act as a compass to female pelvic anatomy (Table 42.1). SIMLAP:
• Superiorly into the uterine fundus
• Inferiorly into the vaginal walls
• Medially into the ureters that run along the floor of the pelvi
• Laterally further into the parametrium via the broad ligament to the sidewalls of the boney pelvis
• Anteriorly into the trigone of the bladder
• Posteriorly into the rectum via the posterior vaginal wall
TNM STAGING CRITERIA
TNM STAGING CRITERIA
At gynecologic sites, the TNM staging criteria have been relatively stable and developed in conjunction with the Fédération Internationale de Gynécologie et d'Obstétrique (FIGO). A variety of primary of cancer sites are illustrated in Fig. 42.2 to provide an overview of gynecologic cancers.
The cervix uteri cancer is a good starting point for comprehension of the oncoanatomy of the female pelvis by understanding spread patterns of cancer of the cervix. Cervical cancers are most often detected by Papanicolaou smear tests when they are localized to the cervix in their in situ phase. The concept of microinvasion was first defined in the cervix as 5.0 depth and then 3.0 mm. Once a cancer forms, it can spread in numerous directions as it invades deeper into the stroma and then adjacent structures. Superficial spread involves the uteru superiorly and the vagina inferiorly. The common infiltratio pattern is laterally into the parametrial ligaments, where the ureter and the uterine branches of the hypogastric or internal iliac artery and veins are present. Surgical dissections require isolation of the uterine artery to avoid ligation of the ureter. As the tumor extends laterally into the cardinal or broad ligaments, it becomes fixed to the sidewall of the pelvis. When thi occurs, the prognosis becomes grave, and leg edema and pelvis pain occur (stage T3). With anteroposterior spread, the bladder and the rectum are invaded, and fistula formation can occu.
Pelvic pain can have many different patterns. It can even be referred to the extremities. As invasion occurs in the sacral and coccygeal plexus areas, zones of hyperesthesia, hypoesthesia, and even anesthesia can occur in and around the perineum, radiating into the thigh and lower limb. Eventually, muscle invasion and bone destruction can be seen in uncontrolled, advanced, and, particularly, recurrent tumors when standard treatment procedures have failed. The borderline between the false and true pelvis is particularly vulnerable because this is the attachment of the lateral cervical ligaments. Erosion of the medial inner cortex of the true pelvis occurs. In the anterior direction, cervical cancer invades into the bladder and can cause bullous edema and eventually erosion of the mucosa, which leads to urinary bleeding and fistula formation. Posteriorl, rectal invasion can lead to bleeding and fistula formation. This complication is rarel found in fundal uterine cancer.
The uterine fundus usually contains the malignant process within itself. This may relate to the fact that the uterus is normally invaded by a more naturally occurring neoplastic process, namely, the placenta of pregnancy. Thus, the first path ways of cancer spread are superficial: inferiorly into the cervi and superiorly and laterally into the fallopian tubes. When deep invasion occurs, it is usually into the myometrium, toward the serosal surface. With cervical invasion, the spread pattern is similar to that of cervical cancer that invades laterally into the parametrium. Vaginal metastases commonly follow lymphatic channels, skip into the distal vagina, and occur as suburethral nodules. In summary, the major tumor spread patterns at this site are into the (i) myometrium, (ii) serosa and peritoneal cavity, (iii) cervix, (iv) vagina, and (v) fallopian tube and ovary.
The ovary is as much a structure of the whole peritoneal cavity as it is of the pelvis. This is particularly true once it has become subject to malignant transformation. The ovary is positioned essentially at the bottom of the peritoneal cavity. Its blood supply reflects its abdominal origin. When cancer form in the ovary, it invades through its capsule and forms excrescences. Tumor cells are released and seed the peritoneal surface, often invading the gynecologic tract in the manner of ovulation and/or filling the cul-de-sac. Because there is no true separatio between the pelvic and abdominal cavities, this cancer often seeds the omentum, mesentery, and intestine serosal surface. The inferior surface of the diaphragm provides the lymphatic drainage of the abdominal cavity. Thus, the diaphragm may act as a “blotter” for these dispersed tumor cells in the peritoneal cavity. Ascites and pleural effusion are common in advanced stages. In summary, ovarian cancer spread patterns are inferiorly and medially into and onto the uterus, laterally to the pelvic wall, posteriorly into the pouch of Douglas (rectouterine), or superiorly seeding into the peritoneal cavity.
TNM STAGING OF UTERINE CERVIX
Uterine cervix cancer is the archetype and prototype for cancer staging (Fig. 42.2C). The League of Nations introduced the concept of cancer classification and staging more than 70 year ago in 1937 in accord with the FIGO. Pierre Denoix in the 1950s introduced the TNM staging system. In the 1970s, the American Joint Cancer Committee (AJCC) and the Union Internationale Contre le Cancer (UICC) developed an active collaboration and became the first to jointly elaborate th TNM system to encompass all gynecologic cancers. For most decades in the twentieth century FIGO published gynecologic cancer survival results from a selected number of institutions that stringently followed the basic ground rules:
• Clinical staging excluded surgical pathologic staging.
• Joint pelvic examination by a gynecologist and radiation oncologist under anesthesia allowed for speculum and coloscopy observation and rectal/vaginal palpation to determine extent of cancer progression. Radiologic procedures were not admissible, to avoid exclusion of hospitals with limited resources.
• Biopsy specimens were eventually required as Papanicolaou smears shifted advanced disease to earlier stages at the time of detection. Surgically resected specimens could not alter the initial clinical stage.
• Microinvasion of cancer in the first site, which introduce the criteria for Tis (in situ) stages.
• Bladder and rectal invasion: T4 could not rely on endoscopic viewing alone but required biopsy confirmation
*When there is doubt, the lesser stage should be assigned to make survival results appear worse and avoid stage migration.
The TNM Staging Matrix is color coded for identification o Stage Group once T and N stages are determined (Table 42.2).
Figure 42.2 | TNM staging diagram. Only the T categories are displayed for (A) ovary, (B) uterine fundus, (C) uterine cervix, and (D) vulva. Color bars are coded for stage: stages 0 and IA, yellow; IB, green; II, blue; III, purple; IV, red; and metastatic disease to viscera and nodes, black.
OVERVIEW OF HISTOGENESIS
The specific normal epithelial cell is paired with the derivativ cancer histopathologic type (Table 42.3). The overview of histogenesis is presented for the six potential sites that constitute the female reproductive organs (Fig. 42.3). The female reproductive system consists of paired ovaries, paired uterine fallopian tubes, and a single uterus, which is pear shaped with thick muscular walls terminating into cervix. The cervix is at the apex of the vagina with its vestibule centered in the vulva. The specialized gonadal cells of the ovary are in sharp contrast to the epithelial surface of the fallopian tube, which is lined by simple columnar ciliated cells projecting into its lumen as folds, and the endometrial lining of the uterus, which has simple columnar cells over a spongy functionalis layer, which is shed during menses. All of these structures give rise to adenocarcinomas. The cervix is the transitional organ, with an endocervical canal rich in mucous secretion and a surface of squamous cells that blend into the vagina as a stratified squamous cell epithelium. The vulva labia mucosa is a mucosal surface that becomes skin in the labia majora, again lined by stratified squamous cells. Squamous cell cancers are the predominant cancer in the lower female genital tract (cervix, vagina, and vulva).
Referring to Fig. 42.3, we can see that there are six gynecologic sites with distinct cytohistologic features; each can give rise to malignancies:
A Ovaries are encapsulated by a simple cuboidal epithelium similar to peritoneal lining cells, which, with repeated microtrauma of oocyte ejection monthly in the adult, can lead to adenocarcinomas that are histologically varied—serous, mucinous, and endometroid.
B Ovary germ cells are highly carried and have the potential to transition into granulosa cell cancers, dysgerminomas, and so on.
C Fallopian tubes are lined by ciliated simple columnar cells and peg cells, preferably giving rise to serous adenocarcinomas.
D Uterine fundus epithelial lining is hormonally activated at puberty, rapidly divides and proliferates monthly, and then sheds during menses. This glandular lining consists of simple columnar cells. These cells at menopause can transition from hyperplasia due to hormonal excess stimuli into neoplasia, leading to adenocarcinomas, which undergo meta-plasia into adenosquamous cell mixtures, each of which can become malignant, giving rise to both squamous cell cancers and adenocarcinomas. Endometriosis is a benign proliferative phase in which foci can disseminate into the peritoneal cavity, as well as in other parts of the female gynecologic system. These deposits can transition into endometroid cancers. The fibrocyte and smooth muscle lieomyocytes commonly give rise to fibromas referred to a fibroids and to leiomyomas, respectively. These mesenchymal cells each can morph into malignant sarcomas, that is, endometrial stromal sarcomas and leiomyosarcomas. In addition, mixed cellular components can both be malignant, giving rise to adenosarcomas intermeshed with adenocarcinomas. The seventh edition of the AJCC Cancer Staging Manual offers separate staging systems for sarcomas, and these are discussed in more detail in Chapter 44.
E Uterine placenta, with its actively mitosing chorionic villi, can be genetically altered to evolve into hydatiform moles and less frequently transform into choriocarcinomas, which are highly invasive and aggressive, resulting in their rapid metastatic dissemination to distant sites.
F Uterine cervix both has a simple columnar epithelium lining the endocervical canal and transitions into a squamous cell lining of the exocervix as it extends to the vaginal fornix. Each cell type can transform into cancers, that is, mucinous adenocarcinomas and squamous cell cancers in varying degrees of differentiation. Cancer in situ is most often discovered at this site.
G Vagina is lined by stratified squamous cells, which can give rise to squamous cell cancer. The exception to this rule can occur in young women exposed to hormones, which can lead to a distinct vaginal adenocarcinoma.
H Vulva, because of its distinct organization of various lining tissues and glandular elements, can give rise to both squamous cell cancers from the mucosal surface of the labia minora and squamous cell cancer from the skin surface of both the labia majora and minora covered by stratified squamous epithelium. Basal cell cancers can occur on its skin surface. The Bartholin glands can transform into adenocarcinomas.
Figure 42.3 | Overview of histogenesis. There are six potential sites for gynecologic cancer, each with a distinctive anatomy and histology. The cancer can be traced to a derivative cell. A. Schematic of female internal sex organs. The anatomic isocenters are displayed for gynecologic primary cancer sites. B. Ovary epithelial neoplasms include the common varieties of adenocarcinoma (serosa, endometrioid, mucinous), (C) Ovary also gives rise to a rich variety of cells leading to germ cell neoplasms. D. The uterine wall undergoes dramatic proliferative change monthly in its glandular epithelium during the menstrual cycle and gives rise to adenocarcinomas. E. The cervix has a simple columnar epithelium and changes to a stratified squamous epithelium, which gives rise to squamous cell cancers. F. The fallopian tube is lined by ciliated columnar epithelium and tends to give rise mainly to serous adenocarcinomas. G. Syncytiotrophoblast gives rise to choriocarcinoma and gestational trophoblast tumors.
T-ONCOANATOMY
ORIENTATION OF THREE-PLANAR ONCOANATOMY
Overview of T-oncoanatomy
The juxtaposition of pelvic and abdominal viscera obscures the fact of their separation by the peritoneum. The entire gynecologic tract is retroperitoneal except for the ovary; the digestive system is intraperitoneal. The isocenters of the six primary gynecologic cancers are shown in their pelvic location and range from S2 to the coccyx (Fig. 42.4).
Table 42.4 lists the six primary sites with their surrounding anatomic structures and viscera, their sentinel lymph nodes, and osseous landmarks. The presentation is in a cephalad-to-caudad fashion and includes relationships to the urinary bladder, urethra, rectum, and anus, which are also extraperitoneal in the true pelvis.
Ovary
The ovaries are a pair of solid, flattened ovoids 2.0 to 4.0 c in diameter. They are connected by a peritoneal fold to the broad ligament and by the suspensory ligament of ovary to the lateral wall of the pelvis. Cancers arise from the mesothelial covering of the ovary rather than its germ cells.
The lymphatic drainage occurs via the ovarian and round ligament trunks and an external iliac accessory route into the following regional nodes: The para-aortic nodes are the major regional nodes, followed by the external iliac, common iliac, hypogastric, lateral sacral, and, rarely, the inguinal nodes. Although the ovary is pelvic in location, its lymphatic drainage recapitulates its abdominal or homologous origin, namely, the para-aortic lymph nodes. Its vestigial relationship via the round ligament to the labia majora reaffirms its similarity t the testes in its intimate scrotal location, which makes drainage to inguinal nodes possible. Ovarian cancers seed and invade the uterus, which drains into pelvic nodes.
Uterus and Fallopian Tubes
Oviducts are paired organs with fimbrae designed to catch a oocyte. The ampulla is characterized by a virtual labyrinth maze of primary, secondary, and tertiary longitudinal folds that narrow at the isthmus as it joins the uterine fundus. The mucosa consists of simple columnar epithelium, which can be ciliated and nonciliated. This can give rise to adenocarcinomas, usually of serous cell variety. The upper two thirds of the uterus above the level of the internal cervical os is called the corpus uteri. The fallopian tubes enter at the upper lateral corners of its pear -shaped body. That portion of the muscular organ positioned above the line joining the tubouterine orifice is called the fundus. Cancers arise mainly from its epithelial columnar lining cells. The relationship of the uterus to other pelvic tissues is important, particularly to the rectum and bladder. The body of the uterus sits in the peritoneal cavity. Although it is juxtaposed to these structures, it is separated by the peritoneal lining, making direct invasion rare.
Cervix
The cervix comprises the lower one third of the uterus. It is roughly cylindrical in shape, projecting into the upper anterior vaginal fornix. It communicates with the vagina through an orifice, namely, the cervical os. Cancer of the cervix may originate on the vaginal surface or in the cervical canal and be either squamous cell or adenocarcinoma. The mesometrium, or broad ligament of the uterus, contains a number of very important structures that determine the course of events in a number of oncologic presentations and complications. The course of the ureter, which is the critical structure, passes from its lateral position in the abdomen to its medial location in the pelvis by moving horizontally to insert into the bladder. It is crossed superiorly and medially by the uterine artery. The long, transverse course of the ureter makes it particularly vulnerable to entrapment by cancer spread from the cervix because it lies juxtaposed to the cervix before its entry to the bladder. Along the sidewall of the pelvis, the obturator nerve and vessel enter into the obturator canal. Cervical cancer tends to invade these structures instead of the body of the uterus; when the rectovaginal or vesicovaginal septum is invaded, the juxtaposition of the vaginal wall directly to the bladder and the rectum makes these organs directly accessible.
Vagina
The vagina is the external os, and the cervix is the internal os. The vagina itself is a fibromuscular tube that extends from the cervix to the vestibule of the external genitalia. It consists of numerous folds of an inner mucosa, a middle muscle layer, and an outer fibrous adventitia. The vagina has no glands and i lubricated by the cervical mucous glands. It is lined by stratified squamous epithelium and has a loose fibroelastic connective tissue and rich vasculature, which comprise the lamina propria, then a smooth muscle layer. The urethra runs anteriorly. The predominant cancer is squamous cell.
Vulva
The vestibule of the vagina is the region between the labia minora and hymen. The labia majora are external and fuse into the mons pubis. The prepuce of the clitoris is like a hood over the clitoris. The underlying musculature consists of three muscles: the bulbospongiosus, the ischiocavernosus, and the transverse perineal superficialis. Deep to this is the perinea membrane and the “urogenital diaphragm” or urethral sphincter.
Figure 42.4 | Orientation of T-oncoanatomy of the female pelvis, which houses all the internal female genital organs. From a cephalad-to-caudad fashion each is presented at a different vertebral level. (A) Coronal and (B)sagittal views with primary sites presented from cephalad to caudad at specific transverse levels related to vertebrae
N-ONCOANATOMY AND M-ONCOANATOMY
N-ONCOANATOMY
To avoid confusion with regard to lymph node drainage and each pelvic site at which a cancer arises, see Table 42.5A for the sentinel nodes as a key to the N-oncoanatomy (Fig. 42.5A). The gynecologic organs lie in the true pelvis and are supplied by the hypogastric or internal iliac artery, which enters the broad ligament artery as the uterine artery. The venous drainage and lymphatics are parallel reentering the internal iliac veins. The obturator node is the sentinel node for the cervix and is located in a plane posterior to the more anterior external iliac nodes (Table 42.5A). This lymph node is in the true pelvis. Occasionally, there is an aberrant channel connecting an internal iliac node to an external iliac node. The external iliac node chain runs with the external iliac artery and vein and is well anterior to the internal iliac node chain. The obturator node, when involved, is often associated with cancer of the cervix infiltrating the broad ligament. Once this occurs retrograde or abnormal flow patterns alter the course of lymphatics, and collateral channels can connect internal and external iliac nodes. The cervix is drained by preuteral, postuteral, and uterosacral lymphatic routes into the following first station nodes: parametrial, hypogastric (obturator), external iliac, presacral, and common iliac. Para-aortic nodes are second station and juxtaregional nodes.
The lymphatic drainage of gynecologic primary sites is displayed in Fig. 42.5B and Table 42.5B. The fundus of the uterus and fallopian tubes may follow lymphatic channels related to the ovarian artery and vein. The major lymphatic trunks are the utero-ovarian (infundibulopelvic), parametrial, and presacral and drain into the hypogastric, external iliac, common iliac, presacral, and para-aortic nodes. The ovaries descend from their retroperitoneal para-aortic location in the fetus by the gubernaculums. Thus, ovarian cancer can spread to nonregional as well as regional nodes, that is, the para-aortic, pelvic, and even inguinal nodes, owing to attachment of the round ligament. The sentinel nodes depend on location of the cancer in the vagina: In the superior portico, it is similar to the cervix; inferiorly, it is similar to the vulva. The distal vagina and vulva can drain into the inguinal and femoral nodes, as well as into the pelvic iliac lymph nodes. The vaginal drainage depends on the location of the primary. Proximal cancers juxtaposed to the cervix will drain into obturator nodes first, then internal an external iliac nodes. Distal cancers will drain to inguinal nodes. The sentinel nodes will vary with location and can be either femoral or inguinal nodes.
Figure 42.5 | A. Orientation of oncoanatomy by sentinal lymph nodes. (1) Renal hilar. (2) Renal pelvis and ureter. (3) Para-aortic and paracaval. (4) Common iliac. (4′) Presacral. (5) External iliac. (6) Internal iliac. (6′) Obturator. (7) Deep inguinal. (8) Superficial inguinal. (9) Femoral B: Orientation of oncoanatomy by lymphatic drainage of primary site.
M-ONCOANATOMY
The internal and external iliac veins drain the female reproductive organs, and metastatic dissemination is via the inferior vena cava to the lung, which is the favored target organ (Fig. 42.6A,B).
• Ovarian cancers arise from the epithelial surface, which during embryogenesis is derived from the coelomic cavity lined by mesothelial cells that became specialized to form a serosal covering of the gonadal ridge. As ovarian cancers shed their cells into the peritoneal cavity, they behave as peritoneal mesotheliomas, studding the omentum, the intestinal tissues, liver, and diaphragm, resulting in ascites.
• Uterine cancers illustrate the difference between circulating cancer cells that are released as a result of the curettage of endometrial cancer to establish the diagnosis compared to the incidence of metastases. The presence of circulating cancer cells is a universal phenomenon compared to the low incidence of pulmonary and other metastases. Unique to uterine cancers is the occurrence of vaginal metastases, which can be synchronous or metachronous. A nodule in the vaginal wall that is an adenocarcinoma in an adult should be considered a signal that there may be a uterine fundal cancer.
• Cervical cancers target the lungs or can present as mediastinal adenopathy if para-aortic nodes are present. Unique to cancer of the cervix is the aggressiveness of bone invasion as a result of extension in broad ligament to obturator nodes located at the lateral brim of the true pelvis wall. In addition, common iliac nodes and para-aortic nodes can massively erode vertebras as well as intervertebral disc, leading to curvature of the lumbar spine.
• Vaginal and vulvar cancers tend to be diagnosed in their localized stages, and lymph node metastases predominate in hematogenous spread to lung.
Figure 42.6A | Pelvic veins and venous plexuses.
Figure 42.6B | Orientation of M-oncoanatomy.
STAGING WORKUP
RULES OF CLASSIFICATION AND STAGING
Clinical Staging and Imaging
The importance of clinical staging by physical examination and standard laboratory and readily available radiologic procedures, such as intravenous pyelography and barium enema, was the essence of its universal adoption. The International Federation of Gynecology and Obstetrics recognized the fact that alternative radiation treatment to surgery never allowed for surgical pathologic staging in cervical cancer. Clinical staging preceded any treatment and could not be changed because of subsequent findings once therapy started. The staging process, however, has been modified to allow colposcop, endocervical curettage, hymenoscopy, cystoscopy, and proctoscopy, and requires suspected bladder and rectal cancer be confirmed by biopsy. Fine-needle aspiration of cytologically palpable nodes may be used to confirm cancer, but laparoscopy or radiologically guided biopsy is not allowed.
Although encouraged, sophisticated imaging, such as computed tomography (CT), magnetic resonance imaging (MRI), positron emission tomography, and ultrasonography (US), are not allowed to alter stage because these technologies are not always available (Table 42.6; Fig. 42.7A,B).
The completely resected specimen, including the primary site and regional lymph nodes, must be thoroughly analyzed and are pTNM designated. Radical hysterectomy and bilateral salpingo-oophorectomy with pelvic lymph node resection is the usual procedure for pathologic evaluation.
The staging has remained unchanged at most gynecologic primary sites; in fact, the rules for classification still do not allow for sophisticated imaging, which includes CT, MRI, and US to alter staging. The multidisciplinary approach to decision making is truly interdisciplinary, most often involving a gynecologic oncologist and a dedicated radiation oncologist. Over the decades, diagnostic and therapeutic protocols in national cooperative groups have provided a scientific basis for intro ducing combined modalities and innovations into clinical practice.
Figure 42.7A | CT transverse axial of female pelvis. 1. Left ovary 2. Physiologic fluid in pelvi (normal in menstruating-age female) 3. Uterine fundus 4. Endometrial cavity 5. Iliopsoas muscle 6. Gluteus minimus muscle 7. Gluteus medius muscle 8. Gluteus maximus muscle.
Figure 42.7B | MRI Sagittal section of female pelvis. 1. Rectus abdominis m. 2. Levator ani (pubococcygeus) m. 3. Sphincter ani externus m. 4. Pubis 5. Vertebral body (L5) 6. Sacrum (S1) 7. Coccyx 8. Urinary bladder 9. Urethra 10. Vagina 11. Posterior fornix of the vagina 12. Fundus uterus 13. Corpus uterus 14. Endometrium 15. Junctional zone 16. Myometrium 17. Internal os cervix 18. Endocervical canal 19. External os cervix 20. Cervical stroma 21. Rectum 22. Anal canal
PROGNOSIS AND CANCER SURVIVAL
CANCER STATISTICS AND SURVIVAL
Female genital system cancers collectively account for 80,000 new cases annually, with uterine corpus exceeding cervix cancer by a factor of four. Both cervical and uterine cancers are highly curable, and deaths are relatively low. The major gynecologic killer is ovarian cancer, with 16,000 annual deaths, which exceeds the other six primary sites combined.
The survival rate gains in both cervix uteri and fundus uteri have been incremental. Given that invasive cancers of the gynecologic tract have had a higher baseline—greater than 50% in the 1950s—the gains for all stages are only 15%, or 2% to 3% per decade. As noted, mortality rates have plummeted owing to early detection, especially of cervical cancer because it is most often detected in its noninvasive stage. Localized uterine cancers are more than 90% curable.
The cancer survival rates indicate the gain in survival for uterine corpus and cervix cancer have been modest (14%) over the last five decades. Howeve, most uterine cervix cancers are detected as cancer in situ, and this is not reflected in the fiures. Ovarian cancer survival has improved by 22% and, as stated, remains lethal because most cases are detected late owing to its insidious onset and the inaccessibility of ovarian cysts and nodules to early diagnosis. On the bright side is the high cure and 5-year survival rates for stage I patients with cervical cancer (92%), uterine corpus cancer (96%), and ovarian cancer (95%) (Fig. 42.8).
The most recent survival rate data is provided in the AJCC 7th Edition for most common gynecologic cancers. As observed survival curves over five years based on large patient popula tions. In Figures 42.9, the five year observed survival is show as a series of bar graphs. Note that early localized stages yield very high survival rates. These survival statistics are confirme in the most recent ACS facts and figures (Table 42.7).
Figure 42.8 | Trajectory of Uterine Cancer Curability.
Figure 42.9 | Five-year observed survival rates for the most common gynecologic cancers. A. Ovary. B. Fallopian tube. C. Uterine fundus. D. Cervix. E. Vagina. (Data from Edge SB, Byrd DR, and Compton CC, et al., AJCC Cancer Staging Manual, 7th edition, New York: Springer; 2010.)
