Gynecology_Novak

Gynecology_Novak. Juvenile granulosa cell tumors of the ovary are rare and constitute less than 5% of ovarian tumors in childhood and adolescence (446). About 90% are diagnosed in stage I, and they have a favorable prognosis. The juvenile subtype behaves less aggressively than the adult type. Only about 10% of juvenile granulosa cell tumors are malignant and late relapse is unusual. Advanced-stage tumors are successfully treated with platinum-based combination chemotherapy (e.g., BEP) (433,440). Sertoli-Leydig Tumors Sertoli-Leydig tumors occur most frequently in the third and fourth decades of life; 75% of these tumors are seen in women younger than 40 years. These neoplasms are extremely rare and account for less than 0.2% of ovarian cancers (2,447,448). Sertoli-Leydig cell tumors are most frequently low-grade malignancies; a poorly differentiated variety may behave more aggressively (Fig. 37.24) (447–449).


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Gynecology_Novak. The tumors typically produce androgens, and clinical virilization is noted in 70% to 85% of patients (449). Signs of virilization include oligomenorrhea followed by amenorrhea, breast atrophy, acne, hirsutism, clitoromegaly, deepening of the voice, and a receding hairline. Measurement of plasma androgens may reveal elevated testosterone and androstenedione, with normal or slightly elevated dehydroepiandrosterone sulphate (2,450). Rarely, the Sertoli-Leydig tumor is associated with manifestations of estrogenization (i.e., isosexual precocity, irregular or post-menopausal bleeding). Because these low-grade lesions are only rarely bilateral (<1%), the usual treatment is unilateral salpingo-oophorectomy and evaluation of the contralateral ovary for patients who are in their reproductive years (3,422). For older patients, hysterectomy and bilateral salpingo-oophorectomy are appropriate (447,448).


Gynecology_Novak

Gynecology_Novak. There are insufficient data to document the utility of radiation or chemotherapy for patients with persistent disease, but some responses in patients with measurable disease were reported with pelvic irradiation and the VAC chemotherapy regimen (3,451–455). The 5-year survival rate is 70% to 90%, and recurrences thereafter are uncommon (3,450– 455). Most fatalities occur in the presence of poorly differentiated tumors. Figure 37.24 Sertoli-Leydig cell tumor of the ovary. Note the aggregates of eosinophilic Leydig cells in the stroma adjacent to Sertoli cell tubules.


Gynecology_Novak

Gynecology_Novak. Figure 37.24 Sertoli-Leydig cell tumor of the ovary. Note the aggregates of eosinophilic Leydig cells in the stroma adjacent to Sertoli cell tubules. Lipoid Cell Tumors Lipoid cell tumors are believed to arise in adrenal cortical rests that reside in the vicinity of the ovary. More than 100 cases were reported, and bilateral disease was noted in only a few (2). Most are associated with virilization and, occasionally, with obesity, hypertension, and glucose intolerance, reﬂecting corticosteroid secretion. Rare cases of estrogen secretion and isosexual precocity were reported. Most of these tumors have benign or low-grade behavior, but about 20%, most of which are initially larger than 8 cm in diameter, are associated with metastatic lesions. Metastases are usually in the peritoneal cavity but can occur at distant sites. The primary treatment is surgical extirpation of the primary lesion. There are no data regarding the effectiveness of radiation or chemotherapy for this disease.


Gynecology_Novak

Gynecology_Novak. Sarcomas Malignant mixed mesodermal tumors (MMMT) of the ovary or carcinosarcomas are uncommon. Clinical, morphologic and molecular data suggest that MMMTs are monoclonal and are metaplastic carcinomas in which the mesenchymal part reﬂects dedifferentiation. Most tumors are heterologous, and 80% occur in postmenopausal women. The signs and symptoms are similar to those of most ovarian malignancies. These tumors are biologically aggressive, and most patients have evidence of metastases at presentation. They are treated either with carboplatin and paclitaxel or iphosphamide and cisplatin, but in general have a poor prognosis. Small Cell Carcinoma, Hypercalcemic Type


Gynecology_Novak

Gynecology_Novak. Small Cell Carcinoma, Hypercalcemic Type This rare tumor occurs at an average age of 24 years (range 2 to 46 years) (456). The tumors are typically unilateral. Approximately two-thirds of the tumors are accompanied by paraendocrine hypercalcemia. This tumor accounts for one-half of all of the cases of hypercalcemia associated with ovarian tumors. About 50% of the tumors have spread beyond the ovaries when they are diagnosed (456). Immunohistochemical stains are helpful to differentiate this tumor from a lymphoma, leukemia, or sarcoma. The management of these malignancies consists of surgery followed by platinum-based chemotherapy or radiation therapy or both. In addition to the primary treatment of the disease, control of the hypercalcemia may require aggressive hydration, loop diuretics, and the use of bisphosphonates or calcitonin. The prognosis tends to be poor, with most patients dying within 2 years of diagnosis in spite of treatment.


Gynecology_Novak

Gynecology_Novak. About 5% to 6% of ovarian tumors are metastatic from other organs, most frequently from the female genital tract, the breast, or the gastrointestinal tract (457–473). The metastases may occur from direct extension of another pelvic neoplasm, by hematogenous or lymphatic spread, or by transcoelomic dissemination, with surface implantation of tumors that spread in the peritoneal cavity.


Gynecology_Novak

Gynecology_Novak. Gynecologic Nonovarian cancers of the genital tract can spread by direct extension or metastasize to the ovaries. Tubal carcinoma involves the ovaries secondarily in 13% of cases, usually by direct extension (2,3). Under some circumstances, it is difficult to know whether the tumor originated in the tube or in the ovary when both are involved. Cervical cancer spreads to the ovary only in rare cases (<1%), and most of these are of an advanced clinical stage or are adenocarcinomas. Adenocarcinoma of the endometrium can spread and implant directly onto the surface of the ovaries in about 5% of cases, but two synchronous primary tumors probably occur with greater frequency (472). In these cases, an endometrioid carcinoma of the ovary is usually associated with the adenocarcinoma of the endometrium.


Gynecology_Novak

Gynecology_Novak. Nongynecologic The frequency of metastatic breast carcinoma to the ovaries varies according to the method of determination, but the phenomenon is common (Fig. 37.25). In autopsy data of women who died of metastatic breast cancer, the ovaries were involved in 24% of cases, and 80% of the involvement was bilateral (457–462). Similarly, when ovaries are removed to palliate Figure 37.25 Metastatic carcinoma in the ovary. Note the linear, single cell pattern found in this metastatic breast carcinoma. advanced breast cancer, about 20% to 30% of the cases reveal ovarian involvement, 60% of those bilaterally. The involvement of ovaries in early-stage breast cancer seems to be considerably lower, but precise figures are not available. In almost all cases, either ovarian involvement is occult or a pelvic mass is discovered after other metastatic disease becomes apparent.


Gynecology_Novak

Gynecology_Novak. Krukenberg Tumor The Krukenberg tumor, which can account for 30% to 40% of metastatic cancers to the ovaries, arises in the ovarian stroma and has characteristic mucin-filled, signet-ring cells (463–465) (Fig. 37.26). The primary tumor is frequently located in the stomach and less commonly in the colon, appendix (so-called goblet cell carcinoid), breast, or biliary tract. Rarely, the cervix or the bladder may be the primary site. Krukenberg tumors can account for about 2% of ovarian cancers at some institutions, and they are usually bilateral. The lesions are usually not discovered until the primary disease is advanced, and, therefore, most patients die of their disease within 1 year. In some cases, a primary tumor is never found.


Gynecology_Novak

Gynecology_Novak. In other cases of metastasis from the gastrointestinal tract to the ovary, the tumor does not have the classic histologic appearance of a Krukenberg tumor; most of these are from the colon and, less commonly, the pancreato-biliary tract, appendix, and small intestine (Fig. 37.27). As many as 1% to 2% of women with intestinal carcinomas will develop metastases to the ovaries during the course of their disease (459). Before exploration for an adnexal tumor in a woman older than 40 years, a barium enema is indicated to exclude a primary gastrointestinal carcinoma with metastases to the ovaries, particularly if there are any gastrointestinal symptoms. Metastatic colon cancer can mimic a mucinous cystadenocarcinoma of the ovary histologically, and the histological distinction between the two can be difficult (458,459,466–470). Lesions that arise in the appendix may be associated with ovarian metastasis and confused with primary ovarian malignancies, especially when associated with


Gynecology_Novak

Gynecology_Novak. two can be difficult (458,459,466–470). Lesions that arise in the appendix may be associated with ovarian metastasis and confused with primary ovarian malignancies, especially when associated with pseudomyxoma peritonei (466,470). It is reasonable to consider the performance of prophylactic bilateral salpingo-oophorectomy at the time of surgery for women with colon cancer (471).


Gynecology_Novak

Gynecology_Novak. Figure 37.26 Krukenberg tumor of the ovary metastatic from a gastric carcinoma. Malignant cells have discrete vacuoles that push nuclei eccentrically, giving a signet-ring appearance. Mucicarmine stain demonstrates the cytoplasmic vacuoles to be mucin. CHAPTER 37 Ovarian, Fallopian Tube, and Peritoneal Cancer Figure 37.27 Metastatic colorectal carcinoma in the ovary often has areas of necrotic debris (so-called dirty necrosis) adjacent to partial gland structures showing a cribriform pattern.


Gynecology_Novak

Gynecology_Novak. Lymphoma and Leukemia Lymphomas and leukemia can involve the ovary. When they do, the involvement is usually bilateral (477–479). About 5% of patients with Hodgkin’s lymphoma will have lymphomatous involvement of the ovaries, but this involvement occurs typically with advanced-stage disease. With Burkitt’s lymphoma, ovarian involvement is very common. Other types of lymphoma involve the ovaries less frequently, and leukemic infiltration of the ovaries is uncommon (479). Sometimes the ovaries can be the only apparent sites of involvement of the abdominal or pelvic viscera with a lymphoma; if this circumstance is found, a careful surgical exploration may be necessary. Intraoperatively, a hematologist-oncologist should be consulted to determine the need for these procedures if frozen section of a solid ovarian mass reveals a lymphoma. Most lymphomas no longer require extensive surgical staging; biopsy of enlarged lymph nodes should be performed. In some cases of Hodgkin’s lymphoma, a


Gynecology_Novak

Gynecology_Novak. of a solid ovarian mass reveals a lymphoma. Most lymphomas no longer require extensive surgical staging; biopsy of enlarged lymph nodes should be performed. In some cases of Hodgkin’s lymphoma, a more extensive evaluation may be necessary. Treatment involves that of the lymphoma or leukemia. Removal of a large ovarian mass may improve patient comfort and facilitate a response to subsequent radiation or chemotherapy.


Gynecology_Novak

Gynecology_Novak. Figure 37.28 Carcinoma of the fallopian tube. This is a high-grade serous carcinoma that has invaded the lamina propria of the tubal mucosa. Most primary fallopian tube carcinomas arise in the distal (fimbria) portion of the fallopian tube. Historically, carcinoma of the fallopian tube accounted for 0.3% of all cancers of the female genital tract (2,3,480–486). Data suggest primary fallopian tube carcinoma may be more common. In histologic features and behavior, fallopian tube carcinoma is similar to ovarian cancer; thus, the evaluation and treatment are essentially the same (Fig 37.28). The fallopian tubes frequently are involved secondarily from other primary sites, most often the ovaries, endometrium, gastrointestinal tract, or breast. They may be involved in primary peritoneal carcinomatosis. Almost all cancers are of epithelial origin, frequently of serous histology. Rarely, sarcomas are reported.


Gynecology_Novak

Gynecology_Novak. As noted above, there is growing evidence to suggest that many high-grade serous carcinomas of the ovary may prove to arise from the fimbrial end of the fallopian tube (5,7). The true incidence of fallopian tube cancer may be historically underestimated because of the convention of assigning many of these as ovarian cancer when the site of origin is unclear. Despite the uncertainty concerning site of origin, all evidence suggests that our evaluation and treatment of these high-grade serous carcinomas should be the same. In recognition of this, many pathologists resorted to diagnosing these tumors as (nonuterine) high-grade serous carcinomas without definite assignment to primary site. (iii) a pelvic mass. This triad is noted in fewer than 15% of patients, and may be less common based on the histopathologic origins of fallopian tube cancers (3).


Gynecology_Novak

Gynecology_Novak. (iii) a pelvic mass. This triad is noted in fewer than 15% of patients, and may be less common based on the histopathologic origins of fallopian tube cancers (3). Vaginal discharge or bleeding is the most common symptom reported by patients with tubal carcinoma and is documented in more than 50% of patients (3,481). Lower abdominal or pelvic pressure and pain are noted in many patients. The symptoms may be rather vague and nonspecific. For perimenopausal and postmenopausal women with unusual, unexplained, or persistent vaginal discharge, in the absence of bleeding, the clinician should be concerned about the possibility of occult tubal cancer. Fallopian tube cancer may be found incidentally in asymptomatic women at the time of abdominal hysterectomy and bilateral salpingo-oophorectomy.


Gynecology_Novak

Gynecology_Novak. On examination, a pelvic mass is present in about 60% of patients, and ascites may be present if advanced disease exists. For patients with tubal carcinoma, the results of dilation and curettage will be negative, although abnormal or adenocarcinomatous cells may be seen in cytologic specimens obtained from the cervix in 10% of patients (483). Spread Pattern Tubal cancers spread in the same manner as epithelial ovarian malignancies, principally by the transcoelomic exfoliation of cells that implant throughout the peritoneal cavity. In about 80% of the patients with advanced disease, metastases are confined to the peritoneal cavity at the time of diagnosis (482). The fallopian tubes are richly permeated with lymphatic channels, as are the ovaries, and spread to the para-aortic and pelvic lymph nodes is common. Metastases to the para-aortic lymph nodes are documented in at least 33% of the patients with all stages of disease (486).


Gynecology_Novak

Gynecology_Novak. Staging Fallopian tube cancer is staged according to FIGO (480,485). The staging is based on the surgical findings at laparotomy (Table 37.9). According to this system, about 20% to 25% of patients have stage I disease, 20% to 25% have stage II disease, 40% to 50% have stage III disease, and 5% to 10% have stage IV disease (480). A somewhat lower incidence of advanced disease is seen in these patients than in patients with epithelial ovarian carcinomas, presumably because of the earlier occurrence of symptoms, particularly vaginal bleeding or unusual vaginal discharge. Findings on transvaginal ultrasonography and CT scan may be suspicious for tubal carcinomas (488).


Gynecology_Novak

Gynecology_Novak. Treatment The treatment of this disease is the same as that of epithelial ovarian cancer (480,483,489– 495). Exploratory laparotomy is necessary to remove the primary tumor, to stage the disease, and to resect metastases. After surgery, the chemotherapy is the same as with epithelial ovarian cancer (i.e., carboplatin and paclitaxel). Surgery Patients with tubal carcinoma should undergo total abdominal hysterectomy and bilateral salpingo-oophorectomy (3). If there is no evidence of gross tumor spread, a staging operation is performed. The retroperitoneal lymph nodes should be adequately evaluated, and peritoneal cytologic studies and biopsies should be performed, along with an infracolic omentectomy.


Gynecology_Novak

Gynecology_Novak. In patients with metastatic disease, an effort should be made to remove as much tumor bulk as possible. The role of cytoreductive surgery in this disease is unclear, but extrapolation from the experience with epithelial ovarian cancer indicates that significant benefit might be expected, particularly if all macroscopic disease can be resected (490).


Gynecology_Novak

Gynecology_Novak. Chemotherapy As with epithelial ovarian cancer, the most active agents are platinum and the taxanes (489,490). The recommended treatment for fallopian tube cancer is the same as that for epithelial ovarian cancer (i.e., platinum and taxane-based chemotherapy). A variety of other chemotherapeutic agents that are effective against recurrent ovarian cancer appear to be active in recurrent or persistent fallopian tube carcinomas. These agents include docetaxel, etoposide, topotecan, gemcitabine, and liposomally encapsulated doxorubicin (491–495). As data on well-staged lesions are scarce, it is unclear whether patients with disease confined to the fallopian tube (i.e., a stage IA, grade 1 or 2 carcinoma) benefit from additional therapy. Table 37.9 FIGO Staging for Carcinoma of the Fallopian Tube


Gynecology_Novak

Gynecology_Novak. Table 37.9 FIGO Staging for Carcinoma of the Fallopian Tube FIGO, International Federation of Gynecology and Obstetrics. From Berek JS, Hacker NF. Berek and Hacker’s Gynecologic Oncology. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2010:494; adapted from FIGO Annual Report. Vol 26, Int J Gynecol Obstet 2006;105:3–4. Prognosis The overall 5-year survival for patients with epithelial tubal carcinomas is about 40%. This number is higher than for patients with ovarian cancer and reﬂects the somewhat higher proportion of patients diagnosed with early-stage disease. These data may reﬂect the fact that some advanced stage tubal cancers were classified as ovarian cancers. The reported 5-year survival rate for patients with stage I disease is only about 65%. The 5-year survival rate for patients with stage II disease is 50% to 60%, but it is only 10% to 20% for patients with stages III and IV disease (480,485).


Gynecology_Novak

Gynecology_Novak. Tubal Sarcomas Tubal sarcomas, particularly malignant mixed mesodermal tumors, are described, but rare. They occur mainly in the sixth decade and typically are advanced at the time of diagnosis. If all gross disease can be resected, platinum-based combination chemotherapy should be tried. Survival is poor, and most patients die of their disease within 2 years (2,450). 1. Siegel R, Ward E, Brawley O, et al. Cancer statistics, 2011. CA Cancer J Clin 2011;61:212–236. http://cacancerjournal.org 2. Scully RE, Young RH, Clement PB. Tumors of the ovary, maldeveloped gonads, fallopian tube, and broad ligament. In: Atlas of tumor pathology. Washington, DC: Armed Forces Institute of Pathology, 1998:Fascicle 23, 3rd series. 3. Berek JS, Friedlander M, Hacker NF. Epithelial ovarian, fallopian tube and peritoneal cancer. In: Berek and Hacker’s gynecologic oncology. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2009:443–508. 4.


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Gynecology_Novak. 4. Kindelberger DW, Lee Y, Miron A, et al. Intraepithelial carcinoma of the fimbria and pelvic serous carcinoma: evidence for a causal relationship. Am J Surg Pathol 2007;31:161–169. 5. Callahan MJ, Crum CP, Medeiros F, et al. Primary fallopian tube malignancies in BRCA-positive women undergoing surgery for ovarian cancer risk reduction. J Clin Oncol 2007;25:3985–3990. 6. Kurman RJ, Shih IeM. Pathogenesis of ovarian cancer: lessons from morphology and molecular biology and their clinical implications [review]. Int J Gynecol Pathol 2008;27:151–160. 7. Crum CP, Drapkin R, Miron A, et al. The distal fallopian tube: a new model for pelvic serous carcinogenesis [review]. Curr Opin Obstet Gynecol 2007;19:3–9. 8. Barnhill DR, Kurman RJ, Brady MF, et al. Preliminary analysis of the behavior of stage I ovarian serous tumors of low malignant potential: a Gynecologic Oncology Group study. J Clin Oncol 1995;13:2752–2756. 9.


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Gynecology_Novak. 9. Seidman JD, Kurman RJ. Subclassification of serous borderline tumors of the ovary into benign and malignant types: a clinicopathologic study of 65 advanced stage cases. Am J Surg Pathol 1996;20:1331–1345. 10. Bell DA, Weinstock MA, Scully RE. Peritoneal implants of ovarian serous borderline tumors: histologic features and prognosis. Cancer 1988;62:2212–2222. 11. Bell DA. Ovarian surface epithelial-stromal tumors. Hum Pathol 1991;22:750–762. 12. Bell DA, Scully RE. Clinical perspectives on borderline tumors of the ovary. In: Greer BE, Berek JS, eds. Gynecologic oncology: treatment rationale and techniques. New York: Elsevier Science, 1991:119–134. 13. McCaughey WT, Kirk ME, Lester W, et al. Peritoneal epithelial lesions associated with proliferative serous tumours of the ovary. Histopathology 1984;8:195–208. 14.


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Gynecology_Novak. 13. McCaughey WT, Kirk ME, Lester W, et al. Peritoneal epithelial lesions associated with proliferative serous tumours of the ovary. Histopathology 1984;8:195–208. 14. Longacre TA, McKenney JK, Tazelaar HD, et al. Ovarian serous tumors of low malignant potential (borderline tumors): outcome-based study of 276 patients with long term (>5 year) follow-up. Am J Surg Pathol 2005;29:707–723. 15. Seidman JD, Kurman RJ. Ovarian serous borderline tumors: a critical review of the literature with emphasis on prognostic indicators. Hum Pathol 2000;31:539–557. 16. Michael H, Roth LM. Invasive and noninvasive implants in ovarian serous tumors of low malignant potential. Cancer 1986;57:1240– 1247. 17. Gershenson DM, Silva EG. Serous ovarian tumors of low malignant potential with peritoneal implants. Cancer 1990;65:578–585. 18. Bell DA, Scully RE. Ovarian serous borderline tumors with stromal microinvasion: a report of 21 cases. Hum Pathol 1990;21:397–403. 19.


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Gynecology_Novak. 18. Bell DA, Scully RE. Ovarian serous borderline tumors with stromal microinvasion: a report of 21 cases. Hum Pathol 1990;21:397–403. 19. Sampson JA. Endometrial carcinoma of the ovary. Arch Surg 1925;10:1. 20. Kurman RJ, Craig JM. Endometrioid and clear cell carcinomas of the ovary. Cancer 1972;29:1653–1664. 21. Roth LM, Dallenbach-Hellweg G, Czernobilsky B. Ovarian Brenner tumors. I. Metaplastic proliferating and of low grade potential. Cancer 1985;56:582–591. 22. Robey SS, Silva EG, Gershenson DM, et al. Transitional cell carcinoma in high-grade stage ovarian carcinoma: an indicator of favorable response to chemotherapy. Cancer 1989;63:839–847. 23. Silva EG, Robey-Cafferty SS, Smith TL, et al. Ovarian carcinomas with transitional cell carcinoma pattern. Am J Clin Pathol 1990;93:457–462. 24. Austin RM, Norris HJ. Malignant Brenner tumor and transitional cell carcinoma of the ovary: a comparison. Int J Gynecol Pathol 1987;6:29–34. 25.


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Gynecology_Novak. 24. Austin RM, Norris HJ. Malignant Brenner tumor and transitional cell carcinoma of the ovary: a comparison. Int J Gynecol Pathol 1987;6:29–34. 25. Piver MS, Jishi MF, Tsukada Y, et al. Primary peritoneal carcinoma after prophylactic oophorectomy in women with a family history of ovarian cancer: a report of the Gilda Radner Familial Ovarian Cancer Registry. Cancer 1993;71:2751–2755. 26. Fowler JM, Nieberg RK, Schooler TA, et al. Peritoneal adenocarcinoma (serous) of m¨ullerian type: a subgroup of women presenting with peritoneal carcinomatosis. Int J Gynecol Cancer 1994;4:43–51. 27. Truong LD, Maccato ML, Awalt H, et al. Serous surface carcinoma of the peritoneum: a clinicopathology study of 22 cases. Hum Pathol 1990;21:99–110. 28. Tobachman JK, Greene MH, Tucker MA, et al. Intraabdominal carcinomatosis after prophylactic oophorectomy in ovarian cancer– prone families. Lancet 1982;2:795–797. 29.


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Gynecology_Novak. 33. Franceschi S, La Vecchia C, Booth M, et al. Pooled analysis of three European case-control studies of epithelial ovarian cancer: II. Age at menarche and menopause. Int J Cancer 1991;49:57–60. 34. Franceschi S, Parazzini F, Negri E, et al. Pooled analysis of three European case-control studies of epithelial ovarian cancer: III. Oral contraceptive use. Int J Cancer 1991;49:61–65. 35. Berek JS, Chalas E, Edelson M, et al. Prophylactic and risk-reducing bilateral salpingo-oophorectomy: recommendations based on risk of ovarian cancer. Obstet Gynecol 2010;116:733–743. 36. Parker WH, Broder MS, Chang E, et al. Ovarian conservation at the time of hysterectomy and long-term health outcomes in the nurses’ health study. Obstet Gynecol 2009;113:1027–1037. 37. Campbell S, Bhan V, Royston P, et al. Transabdominal ultrasound screening for early ovarian cancer. BMJ 1989;299:1363–1367. 38.


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Gynecology_Novak. 37. Campbell S, Bhan V, Royston P, et al. Transabdominal ultrasound screening for early ovarian cancer. BMJ 1989;299:1363–1367. 38. Higgins RV, van Nagell JR Jr, Donaldson ES, et al. Transvaginal sonography as a screening method for ovarian cancer. Gynecol Oncol 1989;34:402–406. 39. van Nagell JR Jr, DePriest PD, Puls LE, et al. Ovarian cancer screening in asymptomatic postmenopausal women by transvaginal sonography. Cancer 1991;68:458–462. 40. Rulin MC, Preston AL. Adnexal masses in postmenopausal women. Obstet Gynecol 1987;70:578–581. 41. Kurjak A, Zalud I, Jurkovic D, et al. Transvaginal color ﬂow Doppler for the assessment of pelvic circulation. Acta Obstet Gynecol Scand 1989;68:131–135. 42. Kurjak A, Zalud I, Alfirevic Z. Evaluation of adnexal masses with transvaginal color ultrasound. J Ultrasound Med 1991;10:295–297. 43. Rustin GJS, van der Burg MEL, Berek JS. Tumor markers. Ann Oncol 1993;4:S71–S77. 44.


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Gynecology_Novak. 43. Rustin GJS, van der Burg MEL, Berek JS. Tumor markers. Ann Oncol 1993;4:S71–S77. 44. Jacobs I, Davies AP, Bridges J, et al. Prevalence screening for ovarian cancer in postmenopausal women by CA 125 measurements and ultrasonography. BMJ 1993;306:1030–1034. 45. Jacobs IJ, Skates S, Davies AP, et al. Risk of diagnosis of ovarian cancer after raised serum CA 125 concentration: a prospective cohort study. BMJ 1996;313:1355–1358. 46. Einhorn N, Sjovall K, Knapp RC, et al. A prospective evaluation of serum CA 125 levels for early detection of ovarian cancer. Obstet Gynecol 1992;80:14–18. 47. Jacobs IJ, Oram DH, Bast RC Jr. Strategies for improving the specificity of screening for ovarian cancer with tumor-associated antigens CA125, CA15–3, and TAG 72.3. Obstet Gynecol 1992;80:396– 399. 48. Berek JS, Bast RC Jr. Ovarian cancer screening: the use of serial complementary tumor markers to improve sensitivity and specificity for early detection. Cancer 1995;76:2092–2096. 49.


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Gynecology_Novak. 48. Berek JS, Bast RC Jr. Ovarian cancer screening: the use of serial complementary tumor markers to improve sensitivity and specificity for early detection. Cancer 1995;76:2092–2096. 49. Skates SJ, Xu FJ, Yu YH, et al. Towards an optimal algorithm for ovarian cancer screening with longitudinal tumour markers. Cancer 1995;76:2004–2010. 50. Jacobs IJ, Skates SJ, MacDonald N, et al. Screening for ovarian cancer: a pilot randomised controlled trial. Lancet 1999;353:1207– 1210. 51. Skates SJ, Menon U, MacDonald N, et al. Calculation of the risk of ovarian cancer from serial CA-125 values for preclinical detection in postmenopausal women. J Clin Oncol 2003;21(Suppl):206–210. 52. Petricoin EF, Ardekani AM, Hitt BA, et al. Use of proteomic patterns in serum to identify ovarian cancer. Lancet 2002;359:572–577. 53.


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Gynecology_Novak. 52. Petricoin EF, Ardekani AM, Hitt BA, et al. Use of proteomic patterns in serum to identify ovarian cancer. Lancet 2002;359:572–577. 53. Zhang Z, Bast RC Jr, Fung E, et al. A panel of serum biomarkers identified through proteomic profiling for the detection of early stage ovarian cancer. Cancer Res 2004;64:5882–5890. 54. American College of Obstetricians and Gynecologists. Genetic risk and screening techniques for epithelial ovarian cancer. ACOG Committee Opinion 117. Washington, DC: ACOG, 1992. 55. Woodward ER, Sleightholme HV, Considine AM, et al. Annual surveillance by CA125 and transvaginal ultrasound for ovarian cancer in both high-risk and population risk women is ineffective. BJOG 2007;114:1500–1509. 56. Hermsen BB, Olivier RI, Verheijen RH, et al. No efficacy of annual gynaecological screening in BRCA1/2 mutation carriers; an observational follow-up study. Br J Cancer 2007;96:1335–1342. 57.


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Gynecology_Novak. 56. Hermsen BB, Olivier RI, Verheijen RH, et al. No efficacy of annual gynaecological screening in BRCA1/2 mutation carriers; an observational follow-up study. Br J Cancer 2007;96:1335–1342. 57. Bourne TH, Campbell S, Reynolds KM, et al. Screening for early familial ovarian cancer with transvaginal ultrasonography and colour blood ﬂow imaging. BMJ 1993;306:1025–1029. 58. Easton DF, Ford D, Bishop DT. Breast Cancer Linkage Consortium: breast and ovarian cancer incidence in BRCA1-mutation carriers. Am J Hum Genet 1995;56:265–271. 59. Whittemore AS, Gong G, Itnyre J. Prevalence and contribution of BRCA1 mutations in breast cancer and ovarian cancer: results from three U.S. population-based case-control studies of ovarian cancer. Am J Hum Genet 1997;60:496–504. 60. Frank TS, Manley SA, Olopade OI, et al. Sequence analysis of BRCA1 and BRCA2: correlation of mutations with family history and ovarian cancer risk. J Clin Oncol 1998;16:2417–2425. 61.


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