MANAGEMENT GUIDELINES GYNECOLOGIC CANCER 1.0 Carcinoma of ...

MANAGEMENT GUIDELINES GYNECOLOGIC CANCER 1.0 Carcinoma of Vulva and Vagina 2.0 Carcinoma of the Cervix (squamous cell carcinoma, adenocarcinoma) 3.0 Carcinoma of the Endometrium (adenocarcinoma, papillary serous carcinoma) 4.0 Uterine/Gynecological Sarcomas (Mixed mullerian sarcoma, leiomyosarcoma) 5.0 Carcinoma of the Fallopian Tube 6.0 Epithelial Carcinoma of the Ovary (borderline, carcinoma) 7.0 Non Epithelial Ovarian Cancer (germ cell, sex cord tumors) 8.0 Trophoblastic Neoplasia (GTN) 9.0 Selected References 10.0 Appendix (Staging) 11.0 Summary (Common Gyn Cancers) 1

1.0 CARCINOMA OF VULVA AND VAGINA • Uncommon • Local/regional disease managed by surgery and/or radiotherapy • No standard role for systemic therapy (chemotherapy) 2.0 CARCINOMA OF THE CERVIX 2.1 Introduction/Background • Common malignancy worldwide (incidence and death rate high in Latin America, Africa, India, and Eastern Europe) although lower in Saudi Arabia (ninth most common malignancy in Saudi females. Second among gyn malignancies behind ovarian cancer). • Histology – primarily squamous cell carcinoma (SCC, 80-90%) and adenocarcinoma (less than 10%). • Follows a relatively orderly pattern of metastatic progression (eg, regional nodes, paraaortic nodes, distant sites – lung, liver, bone). • Prognostic factors: FIGO stage, clinical tumor diameter (greater or less than 4 cm), lymph nodes metastases (regional, paraaortic), histologic features (lymph vascular space invasion, deep stromal invasion, uterine body involvement, SCC better than adenocarcinoma), anemia. 2.2 Staging • FIGO staging most widely accepted (over TNM) – see appendix. • FIGO staging based on careful clinical examination (pelvic, EUA) and specific radiologic studies, (CT abdomen and pelvis, CXR) and procedures (cystoscopy, sigmoidoscopy). MRI and PET scans are not used in routine management, although one recent study (Rose et al, JCO 17:41-45, 1998) suggested that PET scanning may accurately identify nodal metastases. 2.3 Initial Workup/Investigation: • See 2.2 (to establish FIGO state). • No specific markers 2

2.4 Treatment • Stage 1A, 1B1 and early IIA: Surgery (radical hysterectomy and pelvic node dissection). • Stage 1B2 (lesion greater than 4 cm), IIB, III, IVA: Radiotherrapy is the primary modality of treatment. Neoadjuvant chemotherapy (chemotherapy given before radiotherapy) although producing high initial response rates, has not improved survival, (one large study has, in fact, shown a decrease in survival). Concurrent chemotherapy (chemoradiotherapy) does show a survival advantage over XRT alone (cisplatin based, with or without other agents). Based on these data it is recommended that patients with higher risk for relapse (patients with pelvic lymphadenopathy and/or para-aortic lymphadenopathy) should receive concurrent chemotherapy (cis-platin 40 mg/m2 iv q wk x 5 during the course of radiotherapy). Adjuvant chemotherapy following radiotherapy is investigational. • Stage IVB (metastatic) or recurrent disease outside of a radiation field can be given a trial of chemotherapy. Treatment is palliative with the exception of occasional individuals with isolated late pulmonary metastasis, central pelvic recurrences after primary treatment with radiation therapy, or those who develop central pelvic recurrences after radical hysterectomy. In selected circumstances these situations may benefit from local management. • Chemotherapy is for palliative intent for metastatic disease or recurrence outside a radiation field. Therefore only patients with good PS (ECOG 2 or better) symptomatic disease and good renal function to be selected. Local palliative radiotherapy may be utilized to treat symptomatic bony metastases or other soft tissue sites that have not responded to chemotherapy. • Chemotherapy to consist of cisplatin (50 mg/m2 i.v. q 3 wk) as a single agent. Although higher response rates have been reported with platinum combinations (eg, ifosfamide, bleomycin, vinca) toxicity is high with no improvement in survival. Higher than standard doses of cisplatin is also controversial and not recommended outside of a study setting. • The efficacy should be assessed after no more than 3 cycles. If there is no significant response, or improvement in symptomatology, it should be discontinued. Generally if there is a response, chemotherapy can be continued until 2 cycles after the best response or stable disease is obtained, or unacceptable toxicity or quality of life issues intervene. • Small-cell carcinoma of the cervix is uncommon and should be treated with a combination of XRT and chemotherapy (VP-16 and cis-platin). 3

• Investigational Protocols A number of other chemotherapeutic agents have shown some activity (eg 5FU, Taxol, Taxotere, Gemcitabine, Topotecan, Irinotecan, Vinorelbine) but their use should at present be restricted to specific protocols. 2.5 Follow-up Schedule • If no response to palliative chemotherapy patient should be given symptomatic and supportive care (eg, palliative care) and referred to appropriate services or local institution. 3.0 CARCINOMA OF THE ENDOMETRIUM 3.1 Introduction/Background • The most common gynecological cancer in North America, although less common in Saudi Arabia (third in incidence for gynecological cancers behind ovary and cervix). • Predominantly a disease of post-menopausal women. Patients receiving long term unopposed estrogen or tamoxifen (eg. Breast cancer) have an increased risk and may need to be monitored. • Histology: Endometrioid/endometrial adenocarcinomas most common type, and most commonly associated with estrogen exposure or a precursor lesion (endometrial hyperplasia). They are more likely to be hormone responsive. Other less common lesions, (eg. Clear cell, papillary serous) associated with poor prognosis, hormone unresponsiveness, less responsiveness to chemotherapy, and without identifiable precursor lesions. • Progression of disease often by local/lymphatic extension eg. to cervix, spread to local organs (bladder, colon, adnexa), pelvic and para-aortic nodes. Peritoneal extension less common (unlike ovarian carcinoma except for the papillary serous type). Hematogenous metastases also less common. • Prognostic factors: FIGO stage, histology (eg. adenocarcinoma versus papillary serous), tumor grade, depth of myometrial invasion, lymphatic/vasc invasion. Well differentiated (low grade) tumors are more likely to be hormone responsive than high grade tumors. 3.2 Staging • FIGO staging most widely accepted. It is a surgical staging system (FIGO 1988), not a clinical staging system (previously used but often under-staged patients). However, clinical staging is still important for initial evaluation, prior to surgery and still correlates fairly well with prognosis. 4

• See staging Table in Appendix 3.3 Initial Workup/Investigation • Clinical assessment and fractional curettage. • Chest X-ray • Cystoscopy and sigmoidoscopy for locally advanced disease. • CT scan or ultrasound of abdomen or pelvis. • CA-125 occasionally helpful (papillary-serous or peritoneal disease). • No specific markers. 3.4 Treatment • Stage 1A to 3A: surgery (TAH BSO) and/or radiotherapy. • Stage 3B and 3C or gross residual disease (post surgery), or advanced disease unsuitable for surgery or initial radiotherapy, should be considered for chemotherapy or hormonal therapy, with or without subsequent pelvic radiotherapy. Only good performance status patients with assessable/symptomatic disease should be considered for chemotherapy. There is no role for adjuvant chemotherapy. • Stage 4, distant metastases, or recurrence outside a radiation field considered for hormonal or chemotherapy (again patients with good performance status and assessable or symptomatic disease). Localised recurrences might be managed by surgery and/or irradiation alone. Vaginal bleeding secondary to pelvic recurrence may be palliated with radiotherapy. • Hormonal therapy. Well differentiated tumors, and slowly progressive disease are reasonable indicators. Medroxyprogesterone 100 mg po qid or 200 mg po bid(response rate in the range 9-48%), or Megace 160 mg po od. There is no clear dose response noted. Maximum clinical response may not be apparent for at least 3 months. Tamoxifen 20-40 mg per day has demonstrated activity (response rate 5- 46%), but is believed to be inferior to progestogens. Tamoxifen unlikely to be active in patients failing to respond to progesterone and does not improve the response rate when added to progesterone. • Chemotherapy. Active single agents (response rate 20% or better) include doxorubicin, epirubicin, cisplatin, carboplatin, 5-FU, and taxol. At present standard chemotherapy to consist of doxorubicin 50 mg/m2 IV and cisplatin 50 mg/m2 IV every 3 weeks (with assessment after 3-4 cycles). 5

• Papillary-serous carcinoma of the endometrium is more aggressive and stage for stage has a lower survival than the more common adenocarcinoma. Its behaviour is more analogous to epithelial ovarian cancer. Optimal treatment is not clear although pretreatment with chemotherapy (cyclophosphamide 500 mg/m2 IV and cisplatin 50 mg/m2 IV Q 3 weeks x 3) prior to pelvic radiotherapy has been advocated by some institutions and will be carried out at KFSH&RC. 3.5 Follow-up Schedule • If no response to palliative systemic therapy (hormonal or chemotherapy) patient should be given symptomatic and supportive care and referred to appropriate services or local institutions. 4.0 UTERINE/GYNECOLOGIC SARCOMAS 4.1 Introduction/Background • Uncommon, therefore management more anecdotal. • Histology – homologous type (endometrial stromal sarcoma, leiomyosarcoma, supportive tissue sarcomas); heterologous (malignant mixed mullerian tumor or mixed mesodermal tumor – MMT, adenosarcoma, etc). • Extensive local growth a common clinical presentation. Distant spread common by a variety of mechanisms – nodal and peritoneal with MMT; hematogenous (eg. Lung, liver, bone) spread with most. Generally poor prognosis. 4.2 Staging • No official staging system. Usual to use the FIGO system of endometrial cancer. 4.3 Initial Work-up/Investigations • Chest X-ray and CT scan or ultrasound of abdomen and pelvis. • CA-125 may be elevated for MMT with peritoneal spread. 4.4 Treatment • Surgery important if possible (curative for small numbers versus palliative to control pain, bleeding, etc). • Radiotherapy – role unclear (as numbers small and distant failure is common). MMT or stromal sarcoma may have better local control with post-op adjuvant pelvic XRT. However, survival not influenced. • Chemotherapy – limited role. No role for adjuvant chemotherapy following initial surgery or radiotherapy. Leiomyosarcoma – doxorubicin likely as useful as drug 6

combinations (eg. Ifosfamide does not add substantially when combined with doxorubicin). Endometrial stromal sarcoma therapy is unclear. MMT may be treated with cisplatin or ifosfamide (the advantage of the combination is not clear – presently a GOG trial). However, there is no survival advantage. 4.5 Follow-up • Individualised. 5.0 CARCINOMA OF THE FALLOPIAN TUBE AND PERITONEAL CANCER • Uncommon as primary site. • Managed the same as epithelial ovarian cancer. • Frequently involved as secondary site from other gynecologic and gastro-intestinal tumors. 6.0 EPITHELIAL CARCINOMA OF THE OVARY 6.1 Introduction/Background • Epithelial cancers are the most common ovarian malignancies (commonest gyn cancer in Saudi Arabia, 7th in incidence among adult malignancies). They are usually asymptomatic until they present with a more advanced stage. • This group of tumors has the highest fatality to case ratio of all gynecologic malignancies. • Histology – Serous histologic type most common. Less common types are mucinous, endometrioid, clear cell carcinomas, etc. • An important group of tumors to distinguish is tumor of low malignant potential or borderline tumors. These lesions tend to remain confined to the ovary for long periods of time and generally are associated with a good prognosis. They tend to occur in younger women more often than invasive epithelial tumors. After appropriate surgical therapy systemic treatment is usually left until disease relapse, (ie adjuvant therapy not of significant benefit). If relapse occurs, repeat surgery needs to be considered. • Prognostic features: histology (clear cell carcinomas worst prognosis), tumor grade (high grade tumors have a worse prognosis), stage, dense adhesions and large growing ascites (for early stage tumors), residual disease left after surgery (greater than 1 - 2 cm a poorer prognosis), age, prior therapy (eg. Platinum resistant or not), and newer features (eg. Ploidy – diploid better; p53 gene expression). 7

6.2 Staging • FIGO staging most widely accepted (see Appendix). 6.3 Initial Work-up/Investigations • Clinical examination including assessment of the pelvis. • CA-125 (useful in assessing response to therapy as well as follow-up). • Chest X-ray. • CT scan or ultrasound of the abdomen. 6.4 Treatment • Appropriate surgery is extremely important. It is useful for making the diagnosis, carrying out appropriate exploration and staging, and in attempting to perform maximum debulking (as the extent of residual disease is an important prognostic factor). The role of second look surgery should be considered investigational. However in some situations interval debulking may have a useful role (eg young patient with good PS who could not be optimally debulked initially but who has a significant response after chemo – usually 3 cycles, its usefulness presently being examined through GOG and EORTC trials). • Radiotherapy. Many institutions utilize radiotherapy for early stage disease. If it is utilized it is important to use whole abdominal-pelvic radiotherapy. Because of the extent of the treatment field late toxicities include the GI tract as well as bone marrow. However, not generally utilized at KFSH&RC. • Chemotherapy. At present chemotherapy is advocated as adjuvant treatment for patients with stage 1 poorly differentiated disease up to advanced stage disease. Patients with maximum debulking are likely to accrue the most benefit (less than 1 cm maximum diameter residual disease). At present the most common front line or initial chemotherapy consists of the use of a platinum drug and taxol. It is now clear that a taxol and platinum combination is superior to a cychophosphamide and platinum combination. • The standard regimen at this institution consists of taxol 175 mg/m2 IV given over 3 hours and carboplatin 350 mg/m2 IV given every 4 weeks. In planned adjuvant treatment settings 6 cycles of chemotherapy are utilized. For elderly patients and some palliative situations single agent carboplatinum in the range of 300 – 350 mg/m2 every 4 weeks could be utilized. One reported study (Mogensen Gyn Onc 1992) has suggested that high CA-125 levels following the 3rd cycle of induction chemotherapy may be a good predictor of treatment failure. 8

• Disease relapse. If the patients don’t respond to initial platinum based therapy, or relapse within 6 months of ending a platinum based combination, they are likely platinum resistant. Those patients will be treated with single agent Liposomal Doxorubicin ( Caelyx). If patients relapse longer than 6- 12 months following their initial platinum based chemotherapy, they should be retreated with the initial program. • Alternative chemotherapy regimens for relapse. There is no clear consensus regarding the most appropriate salvage regimen particularly in the platinum resistant situation. These patients should be considered for investigative therapies if they are available. However other drugs that have shown some usefulness include oral etoposide (50-100 mg/m2 for 14 or 21 days every 4 weeks), and tamoxifen (20 mg bid). If patients are considered “platinum resistant” but have not received prior taxane therapy (eg previous therapy with cyclophosphamide and cis-platin) they should receive taxol (175 mg/m2 iv q 3 weeks). Other alternatives have included 5FU/leucovorin, hexamethylmelamine, topotecan, taxotere, gemcitabine (although the later 4 agents not presently available at KFSH&RC and should be used only in a protocol setting or if these agents can be supplied from another source). 7.0 NON-EPITHELIAL OVARIAN CANCER 7.1 Introduction/Background • Non-epithelial cancers are less common than their epithelial counterparts. • Germ cell tumors should be considered an important entity as they occur predominantly in younger women and are highly curable with appropriate therapy (surgery and chemotherapy). • Histologic typing of ovarian germ cell tumors – dysgerminoma, teratoma, endodermal sinus tumor, embryonal carcinoma, choriocarcinoma, and others. • In contrast to epithelial ovarian cancers, the germ cell malignancies tend to grow more rapidly and may become symptomatic at an earlier stage. Large tumors and high grade are adverse prognostic features. • Sex cord – stromal tumors are an uncommon group of ovarian tumors. The most common varieties are the granulosa cell tumors and the Sertoli Leydig tumors. These tumors often present at lower stages. The granulosa cell tumors often secrete estrogen. The Sertoli Leydig tumors may secrete androgens. Experience with chemotherapy in these lesions is much more limited (although platinum based combinations have been advocated; platinum alone or BEP). There is no benefit to adjuvant chemotherapy. 7.2 Staging • Staging systems should be similar to that of epithelial ovarian cancer. 9

7.3 Initial Work-up/Investigation • Work-up again should be similar to that of epithelial ovarian cancer with the exception of the markers involved. CA-125 does not have any significant usefulness in this group of tumors. For the germ cell tumors a serum BhCG and AFP should be determined and are useful markers for response and follow-up. 7.4 Treatment • Surgery should be considered first line treatment in these diseases. Conservative surgery (eg fertility sparing) is advocated for germ cell tumors of low stage although more extensive surgery is required for high-stage tumors to leave minimal residual disease. • All patients with germ cell tumors (with exception of Stage I well-differentiated dysgerminoma – resected; or Stage I mature teratoma – resected) should receive adjuvant chemotherapy. • Radiotherapy. At present there is no clearly defined role at KFSHRC. Dysgerminomas sensitive to both XRT and chemotherapy. • Chemotherapy. Chemotherapy regimens for germ cell tumors have been variable. Usually platinum based combinations including etoposide and bleomycin are the most common. VAC (vincristine, actinomycin D, cytoxan) regimens have also had extensive use in the past. At this institution the germ cell tumors are treated primarily by a modified BEP regimen (Bleomycin 30 u IV day 1, VP16 166 mg/m2 IV daily x 3 days, Cisplatin 33 mg/m2 daily x 3 days every 3 weeks). For adjuvant treatment (resected disease) 3 cycles of BEP or 4 cycles of EP are utilized. For patients with residual disease, 4 cycles of BEP are utilized. Recurrent or resistant disease is treated with VeIP (Vinblastine 0.11 mg/kg iv days 1 and 2, Ifosfamide 1.2 g/m2 iv days 1-5, Platinol 20 mg/m2 iv days 1-5, Mesna 400 mg/m2 iv pre and of 4 and 8 hr post ifosfamide x 5 days). Carboplatin should not be used to replace cisplatin. 8.0 TROPHOBLASTIC NEOPLASIA (GTN) 8.1 Introduction/Background • Gestational trophoblastic tumors are rare but highly curable tumors arising from the products of conception in the uterus. • The histologic subtypes range from a hydatidiform mole, to invasive mole (chorioadenoma destruens), to choriocarcinoma. • The probability of cure depends on the histologic type, the extent of spread of the disease, the level of the beta-HCG titer, the duration of disease from the initial pregnancy event to start of treatment, the specific sites of metastases, the nature of the 10

antecedent pregnancy, and the extent of prior treatment. See table Relating Prognostic Factors (Appendix). • The most common antecedent pregnancy is that of a hydatidiform mole. After evacuation patients with a plateau of the Beta-HCG over 3 weeks, an increasing level of Beta-HCG, or persistent elevation of Beta-HCG after 16 weeks of follow-up should be considered as having gestational trophoblastic neoplasia and should undergo the appropriate management. 8.2 Staging • Various staging systems have been developed, although most commonly an assessment of the various risk factors to divide patients into good prognosis to moderate and poor prognosis groupings are used for a decision of the actual treatment modality (see table in appendix). 8.3 Initial Workup/Investigation • Pelvic ultrasound is the preferred method of diagnosis in addition to an elevated Beta- HCG. • Initial diagnostic/therapeutic intervention should consist of a suction D and C. • Chest x-ray to rule out lung metastases. • Moderate to high risk patients should have a CT abdomen (eg liver) and CT brain. • After evacuation Beta-HCG should be determined weekly until 3 negative titers have been obtained. This should be followed by monthly tests for 6 months with effective contraception practiced during this duration. After evacuation of a molar pregnancy, Beta-HCG titers usually disappear within 8-10 weeks. Persistence or increasing titers need to be investigated for the potential of recurrent or metastatic disease. 8.4 Treatment • Treatment depends on the risk group of the disease. After appropriate evaluation low risk disease is usually treated with single agent methotrexate or actinomycin. In this regard various regimens of methotrexate have been reported with no clear comparison amongst the various regimens. At our institute methotrexate 1 mg/kg/IM/Q weekly has been utilized with the addition of Beta-HCG monitoring. This is continued until 3 normal marker values have been obtained. • Intermediate or high risk disease is usually managed with combination chemotherapy. Again, various regimens have been reported with the EMA-CO being the most commonly reported. At our institution a modified BEP chemotherapy regimen has been utilized (Bleomycin 30 units iv day 1, VP16 166 mg/m2 iv daily x 3 days, Cisplatin 33 mg/m2 iv daily x 3 days). 11

• Recurrent or resistant disease has been managed by a number of reported salvage regimens. At our institution a VeIP regimen every 3 weeks has been utilized (Vinblastin .11 mg/kg IV on days 1+2, ifosfamide 1.25 g/m2 daily x 5 days, Mesna 400 mg/m2 IV pre and q4 and 8 hrs post ifosfamide daily x 5 days, and cisplatin 20 mg/m2 IV daily x 5 days). • Patients with central nervous system metastases should be treated with whole brain radiotherapy and intrathecal methotrexate (2 x week x 6) along with the initiation of systemic chemotherapy. Approximately 50-60% of patients will achieve sustained remission using this treatment approach. Patients with CNS mets with hemorrhage should be assessed by neurosurgery. 8.5 Follow-up Schedule • The length of follow-up with adequate contraception is not entirely clear but should be for a minimum of 1 year. In general all recurrences likely to occur within 3 years with 85% before 18 months. 9.0 References (selected) Society of Gynecologic Oncologists Clinical Practice Guidelines. Oncology.12(1):119- 138,1998. National Cancer Institute PDQ – Treatment. Cervical Cancer, Endometrial Cancer, Uterine Sarcoma, Ovarian Epithelial Cancer, Ovarian Germ Cell Tumor, Gestational Trophoblastic Tumor. 1998. Cervical Cancer. NIH Consensus Statement. 14(1). April 1996. National Cancer Registry. The Kingdom of Saudi Arabia. 1994 Report. J S Berek and N F Hacker (Ed). Practical Gynecologic Oncology. 2nd Edition. Williams & Wilkins. 1994. COSA-NZ-UK Endometrial Cancer Study Groups. Adjuvant medroxyprogesterone acetate in high risk endometrial cancer. Int J Gyn Cancer.8(5):387-391,1998. VT De Vita, S Hellman, SA Rosenberg. Cancer: Principles and Practice of Oncology. 5th Edition. Lippincott-Raven.1997. DM Gershenson and WP McGuire (Ed). Ovarian Cancer. Churchill Livingstone. 1998. M Markman. Recurrence within 6 months of platinum therapy: An adequate definition of “platinum refractory” ovarian cancer? Gyn Onc.69:91-92, 1998. WP McGuire and RF Ozols. Chemotherapy of advanced ovarian cancer. Sem Onc 25(3):340-348, 1998. 12

O Mogensen. Prognostic value of CA 125 in advanced ovarian cancer. Gyn Onc 44:207- 212, 1992. C Trope and G Kristensen. Current status of chemotherapy in gynecologic cancer. Sem Onc. 24(5), Supp 15:515-22, 1997. PG Rose, LP Adler, M Rodriguez et al. PET for evaluating para-aortic nodal metastases in locally advanced cervical cancer before surgical staging: A surgicopathologic study. J Clin Oncol.17:41-45, 1999. 10.0 APPENDIX (STAGING) 11.0 SUMMARY OF COMMON GYNECOLOGIC CANCERS – SYSTEMIC TREATMENT 1. Ca Cervix: a. Locally advanced/primary treatment: XRT + cisplatin 40 mg/m2 iv q wk x 5 b. Palliative: Cisplatin 50 mg/m2 iv q 3 wk 2. Ca Endometrium (Adenocarcinoma): Systemic therapy palliative a. Hormonal: Medroxyprogesterone 400 mg po qd b. Chemotherapy: Adriamycin 50 mg/m2 and Cisplatin 50 mg/m2 iv q 3 wk 3. Epithelial Ca Ovary: a. Primary therapy after surgery: Taxol 175 mg/m2 iv and carboplatin 350 mg/m2 iv q 4 wk x 6 cycles b. Relapse >12 mo: Repeat Primary Therapy c. Relapse <12 mo or PD on Taxol/carboplatin = • Liposomal Doxorubicin 50 mg/m2 IV q 4 weeks Alternative therapies: • Etoposide 50-100 mg/m2/d po x 14-21 d q 28 days • Tamoxifen 20 mg po BID 4. Germ Cell Ca Ovary a. Primary Therapy (adjuvant) = BEP q 3 wk x 3 or EP q 3 wk x 4 b. Primary Therapy (disease residium): BEP q 3 wk x 4 c. Relapse: VeIP q 3 wk 13

5. Invasive Mole/Choriocarcinoma: a. Low-risk = MTX 1 mg/kg/IM q 1 wk (until 3 normal B-HCG) b. hi-risk = PEB q 3 wk x 4 c. Resistant = VeIP 14

MANAGEMENT GUIDELINES GYNECOLOGIC CANCER 1.0 Carcinoma of ...

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