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Ovarian Cancer

Ovarian cancer is the fifth leading cause of cancer death in women. 75% of cases present with stage III or IV disease due to vague symptoms. Risk factors include increasing age, family history, nulliparity, infertility and BRCA gene mutations. Diagnosis involves imaging such as ultrasound and CT scan along with serum marker CA-125. Staging follows the FIGO system and 5-year survival ranges from 80% for stage I to 10% for stage IV disease. Treatment involves surgical debulking followed by chemotherapy, with the goal of optimal cytoreduction to improve prognosis.

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OVARIAN CANCER Dr. Myat Su Aung
• Fifth leading cause of cancer death in women • leading cause of gynecologic cancer death.(WHO cancer statistics,2015) • Average lifetime risk is 1 in 70 • median age at diagnosis is 63 years. • 75% present with stage III or IV disease. • Early diagnosis is frequently difficult because of vague abdominal symptoms at presentation Epidemiology 6/23/2016 Ovarian cancer 2
Risk Factors for Ovarian Cancer Patient Characteristics • Increasing age • Personal history of breast cancer Genetic factor • Family history of ovarian cancer • BRCA 1 / 2 mutations • Hereditary nonpolyposis colorectal cancer Reproductive factors • Nulliparity • Early menarche • Late menopause • Infertility • Polycystic ovarian syndrome • Endometriosis • ovulation inducing drugs • Hormone replacement therapy Environmental factor • Obesity and high fat diet • Talc exposure • Cigarette smoking (for mucinous ovarian cancer) Ovarian cancer 3
A higher risk for developing epithelial ovarian cancer is for nulliparous women A lower risk for those • who have had children, • who have breastfed, • who have undergone tubal ligation, • or who have taken oral contraceptives. 6/23/2016 Ovarian cancer 4
• Strongest risk factor is a family history of ovarian cancer • only 5–10% of tumors result from a known genetic disposition. • Lifetime risk: - general population 1.8%, - one first-degree relative: 5%, - two first-degree relatives: 25–50%. 6/23/2016 Ovarian cancer 5
World Health Organization Classification of Ovarian Tumors 6/23/2016 Ovarian cancer 6
World Health Organization Classification of Ovarian Tumors 6/23/2016 Ovarian cancer 7
World Health Organization Classification of Ovarian Tumors 6/23/2016 Ovarian cancer 8
Classification of Ovarian tumors 6/23/2016 Ovarian cancer 9
EPITHELIAL OVARIAN CANCER 6/23/2016 Ovarian cancer 10
Histologic types • serous 50%, • endometrioid 20%, • undifferentiated 15%, • mucinous 10%, • clear cell <5% Boderline tumour Tumors of low malignant potential (LMP, borderline tumors) • have an excellent prognosis compared with invasive carcinomas • Lack stromal invasion • Occur in premenopausal women 6/23/2016 Ovarian cancer 11
• Histologic grade Grade Percentage of undifferentiated cells G1 0-25 G2 25-50 G3 >50 6/23/2016 Ovarian cancer 12
COMMON HISTOLOGIC TYPES OF EPITHELIAL OVARIAN CANCER Papillary serous • most common type of epithelial ovarian cancer. • May contain psammoma bodies • Is often associated with CA 125 elevation. Endometrioid • associated with endometriosis or an independent uterine cancer of similar histology. • May occur with early stage disease in younger patients, although advanced disease is also possible. Mucinous • rarely be associated with pseudomyxoma peritoneii. • CA 125 levels may not be markedly elevated. • Relatively chemoresistant. • Differential diagnosis of a mucinous ovarian tumor includes metastatic disease from an appendiceal primary. Clear cell • The most chemoresistant type of ovarian cancer. • Often contains "hobnail" cells with cleared out cytoplasm due to glycogen. • associated with endometriosis or humorally mediated hypercalcemia6/23/2016 Ovarian cancer 13
• Concentric rings of calcification called psammoma bodies- in the papillary serous epithelial ovarian cancer • May be seen in breast, lung, and papillary thyroid cancers 6/23/2016 Ovarian cancer 14 clear cell carcinoma shows prominent hobnail cells lining the glands. They have bulbous hyperchromatic nuclei that protrude into the gland lumen.
Pathogenesis and Patterns of Metastases Patterns of Spread • Local spread: intraperitoneally • Peritoneal carcinosis: intraperitoneal spread after rupture of the ovarian capsule • Lymphatic metastasis: para-aortic lymph nodes, in rare cases retrograde invasion of inguinal / femoral lymph nodes • Hematogenous metastasis - liver, lung, CNS, in rare cases bone involvement 6/23/2016 Ovarian cancer 15
Pathogenesis and Patterns of Metastases Molecular abnormalities identified in patients with epithelial ovarian cancer • Mutation in the p53 protooncogene • mutations in B-raf, K-ras, PTEN, or ,8-catenin • Amplification of the HER2/neu • Overexpression of pro-apoptotic genes such as BAX • Expression of angiogenic cytokines such as the vascular endothelial growth factor (VEGF) 6/23/2016 Ovarian cancer 16
Diagnosis • abdominal discomfort/pain, • increasing girth, • change in bowel habits, • early satiety, • dyspepsia, nausea, • ascites, • adnexal mass, • pleural effusion, • Sister Mary Joseph’s nodule, H&P with complete gynecologic exam No signs or symptoms until it spreads to the upper abdomen 6/23/2016 Ovarian cancer 17
H&P with complete gynecologic exam Other Associated Paraneoplastic syndrome • Neurological syndrome: peripheral neuropathy, cerebellar ataxia • Cushing syndrome • Hypercalcemia • Thrombophelebitis Diagnosis 6/23/2016 Ovarian cancer 18
Diagnosis Serum tumor marker CA 125 • Elevated in 80% of epithelial ovarian tumors • Also increased in endometrial, pancreatic & breast cancer and benign condition; endometriosis, inflammatory bowel disease, hepatitis • valuable as an early marker for disease recurrence, treatment response and early treatment failure • False positive possible, especially in premenopauseal women 6/23/2016 Ovarian cancer 19
Diagnosis Serum tumor marker CA 19-9 • Low sensitivity CEA – elevated in 58% with stage III disease AFP and βHCG - measure if <30 yrs old to help rule out germ cell tumor 6/23/2016 Ovarian cancer 20
Diagnosis Imaging Ultrasound abdomen Transvaginal Ultrasound (TVU) • TVU is an important diagnostic tool in the evaluation of patients with a pelvic mass. • The classic sonographic finding of malignancy is a "complex“ cyst, defined as containing both solid and cystic components, sometimes with septations and internal echogenicity • Simple cyst <3 cm can be followed by serial US. 6/23/2016 Ovarian cancer 21
Diagnosis Imaging CT/MRI abdomen/pelvis • especially helpful preoperatively if advanced disease. • Useful in assessment of retroperitoneal LN involvement Cystoscopy, sigmoidoscopy, barium enema, upper GI series, or endoscopy as clinically indicated. 6/23/2016 Ovarian cancer 22
Diagnosis Imaging Chest radiographs • to evaluate the presence of pleural effusions, which occur in 1 0 % of patients with epithelial ovarian cancer at diagnosis A definite histological diagnosis requires surgery It is best to avoid percutaneous biopsy during the initial evaluation, which can result in cyst rupture and spillage of malignant cells into the peritoneal cavity 6/23/2016 Ovarian cancer 23
STAGING 2014 FIGO ovarian cancer staging system Stage I – Tumor confirmed to ovaries IA Tumor limited to one ovary (capsule intact) no tumor on ovarian surface; no malignant cells in the ascites or peritoneal washings IB Tumor limited to both ovaries (capsules intact) no tumor on ovarian surface; no malignant cells in the ascites or peritoneal washings IC Tumor limited to one or both with any of the following IC 1 Surgical spill IC 2 Capsule ruptured before surgery or tumor on ovarian surface IC 3 Malignant cells in the ascites or peritoneal washing 6/23/2016 Ovarian cancer 24
STAGING Stage I 6/23/2016 Ovarian cancer 25
STAGING Stage II – Tumor involves one or both ovaries with pelvic extension (below pelvic brim) or primary peritoneal cancer IIA Extension and/or implants on uterus and/or fallopian tubes IIB Extension to other pelvic intraperitoneal tissues 6/23/2016 Ovarian cancer 26
STAGING Stage III. Tumor involves one or both ovaries with cytologically of histologically confirmed spread to the peritoneum outside the pelvis and /or metastasis to the retroperitoneal LN IIIA Positive retroperitoneal lymph nodes and /or microscopic metastasis beyond the pelvis) IIIA 1 Positive retroperitoneal lymph nodes only IIIA 1 (i) Metastasis up to 10mm in greatest dimension IIIA 1 (ii) Metastasis more than 10mm in greatest dimension IIIA 2 Microscopic, extrapelvic (above the brim) peritoneal involvement ± positive retroperitoneal lymph nodes IIIB Macroscopic, extrapelvic, peritoneal metastasis ≤ 2 cm ± positive retroperitoneal lymph nodes. Includes extension to capsule of liver/spleen IIIC Macroscopic, extrapelvic, peritoneal metastasis > 2 cm ± positive retroperitoneal lymph nodes. Includes extension to capsule of liver/spleen 6/23/2016 Ovarian cancer 27
STAGING Stage III 6/23/2016 Ovarian cancer 28
STAGING Stage IV – Distant metastasis excluding peritoneal metastasis Stage IVA Pleural effusion with positive cytology Stage IVB Parenchymal metastases and metastases to extra-abdominal organs (including inguinal lymph nodes and lymph nodes outside of the abdominal cavity 6/23/2016 Ovarian cancer 29
STAGING 5-year survival rate according to stage Stage 5-year survival rate (%) Stage I 80 Stage II 60 Stage III 30 IIIA 40 IIIB 25 IIIC 23 Stage IV 10 6/23/2016 Ovarian cancer 30
Prognostic Factors for Epithelial Ovarian Cancer Most important negative prognostic factors: • stage, • grade, • Residual volume of disease. Other negative factors: • age>65, • pre-op ascites, • CA125 elevated after 3c chemo or nadir >20 U/mL after first-line therapy. The extent to which the disease can be surgically debulked also affects prognosis. 6/23/2016 Ovarian cancer 31
Algorithm for management of ovarian cancer 6/23/2016
Management Stage IA and IB, grade1 (1) Premenopausal patients • After staging laparotomy , undergo unilateral oophretomy to preserve fertility • Follow up regular pelvic examination and monitor CA125 levels • The other ovary and uterus are removed when child bearing is completed (2) Postmenopausal patients • Should undergo TAH and BSO and staging 6/23/2016 Ovarian cancer 33
Stage IA and IB (grade2 and 3) • Treated with TAH/BSO and staging followed by chemotherapy Stage II, III, and IV • Surgery – cytoreductive surgery • chemotherapy Management 6/23/2016 Ovarian cancer 34
Full staging laparotomy • a total abdominal hysterectomy (TAH), • bilateral salpingo-oophorectomy (BSO), • omentectomy, • biopsies of suspicious areas, and • Peritoneal lavage or ascitic fluid sampling. • Blind peritoneal, paraaortic/ pelvic lymph node biopsies should be performed to exclude the possibility of microscopic Stage III disease, Surgery 6/23/2016 Ovarian cancer 35
Primary Cytoreductive surgery • removal of large, necrotic tumors with poor blood supply that might lead to impaired chemotherapy delivery • permit residual tumor to proliferate more rapidly and • thereby enhance sensitivity to postoperative chemotherapy 6/23/2016 Ovarian cancer 36
Primary cytoreduction • refers to performance of debulking surgery prior to administration of first-line chemotherapy and • is the standard approach for managing most patients with suspected epithelial ovarian cancer. 6/23/2016 Ovarian cancer 37
Interval Cytoreductive Surgery Interval cytoreduction is defined as a debulking procedure performed • after several cycles of chemotherapy have been administered, • typically in those patients who had a suboptimal cytoreduction at the time of initial surgery 6/23/2016 Ovarian cancer 38
Postoperative Chemotherapy • Platinum agents have proven to be a critical component of the treatment of epithelial ovarian cancer. • Carboplatin has less ototoxicity, neuropathy, renal impairment, and emetogenesis than cisplatin • However, carboplatin causes myelosuppression particularly if combined with other agents. • Carboplatin is now the standard platinum agent for treating ovarian carcinoma Chemotherapy 6/23/2016 Ovarian cancer 39
• The current standard first-line therapy for ovarian carcinoma is six cycles of carboplatin AUC 5-7 over one hour with paclitaxel (175 mg/m 2 ) as a three-hour infusion every 21 days. • Chemotherapy should begin within four to six weeks of surgery. • The platinum–paclitaxel combination is superior to single agent platinum • In patients who are poorly tolerated combination treatment, single agent carboplatin is a satisfactory alternative 6/23/2016 Ovarian cancer 40
Role of other agents • Liposomal doxorubicin, topotecan, gemcitabine, and epirubicin have been evaluated as first-line therapy in addition to the carboplatin and paclitaxel combination • The carboplatin–docetaxel combination was associated with less neurotoxicity and greater myelosuppression than carboplatin-paclitaxel 6/23/2016 Ovarian cancer 41
Intraperitoneal Chemotherapy • Epithelial ovarian cancer is largely confined to the peritoneal space during most of its natural history • Given this relatively localized distribution, instillation of chemotherapy directly into the peritoneal cavity is used • An option in patient with microscopic residual disease after cytoreductive surgery • cisplatin and paclitaxel have favorable peritoneal-to-plasma concentrations 6/23/2016 Ovarian cancer 42
Antiangiogenic Agents Bevacizumab • a monoclonal antibody • against Vascular Endothelial Growth Factor (VEGF-A), • the first targeted agent to show significant single agent activity in ovarian carcinoma. • Used during adjuvant carboplatin /paclitaxel and for maintenance therapy 6/23/2016 Ovarian cancer 43
• the value of radiation therapy as consolidation therapy following chemotherapy for patients with ovarian cancer is uncertain. Adjuvant Whole Abdominal Radiation Therapy (WART) Used in stage III ovarian cancer, • If not suitable for chemotherapy and • >2cm residual Complication of WART • Acute – diarrhea, nausea/vomiting, leukopenia, thrombocytopenia • Chronic - transient LFT elevation, chronic diarrhea, basal pneumonitis, serious bowel obstruction Radiotherapy 6/23/2016 Ovarian cancer 44
• Once epithelial ovarian cancer has recurred, treatment with curative intent is no longer feasible • However, the judicious use of palliative chemotherapy can improve both survival and quality of life for patients with recurrent disease Management of Recurrent Disease 6/23/2016 Ovarian cancer 45
Treatment is aimed • to relieve cancer-related symptoms, • optimize quality of life, • delay the time to symptomatic disease progression, and • prolong OS. Management of Recurrent Disease 6/23/2016 Ovarian cancer 46
Chemotherapy The management of recurrent EOC takes into account the duration of the platinum-free interval and the response to first-line platinum therapy. Management of Recurrent Disease Indication Treatment Platinum sensitive disease Platinum based combination therapy( with gemcitabine or taxane) Platinum resistant /refractory disease Single agent chemotherapy: Liposomal doxorubicin, topotecan, gemcitabine, and oral etoposide Maintinance in recurrence disease Bevacizumab, concurrent with carboplatin/gemcitabine for 10 cycles maximum, followed by bevacizumab alone 6/23/2016 Ovarian cancer 47
Management of Recurrent Disease Hormonal therapy • tamoxifen or an aromatase inhibitor – 10% to 20% efficacy Antiangiogenic Agents • Bevacizumab used alone or in combinaion with other cytotoxic drugs 6/23/2016 Ovarian cancer 48
Surgery • secondary cytoreductionisolated residual disease at relapse with no gross residual disease greater than 1 cm in diameter Palliative surgery • colostomy for relief of a large bowel bstruction, • lysis of adhesions, and • management of small bowel obstruction Management of Recurrent Disease 6/23/2016 Ovarian cancer 49
Radiotherapy • Symptoms from a growing pelvic mass can cause pain, bleeding, and rectal narrowing. • Palliative pelvic radiotherapy can provide rapid relief and, in some cases, may prevent or delay the need for diverting colostomy. • Doses of 8 to 10 Gy in a single fraction, 20 Gy in five fractions, 30 Gy in ten fractions were given • cerebral or bone metastases can be palliated with radiotherapy. Management of Recurrent Disease 6/23/2016 Ovarian cancer 50
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GERM CELL TUMORS OF THE OVARY 6/23/2016 Ovarian cancer 58
Germ cell tumor Natural History Serum marker Treatment 1.Dysgerminoma -secrete LDH -spread earlier through lymphatic LDH -primary surgery -adjuvant chemo for metastatic disease, BEP(Bleomycin,etoposide,cisplatin) -RT used in metastatic disease if fertility is not an issue 2.Immature teratoma Most common metastatic site is peritoneum - Normal AFP,β- HCG - Only ↑ in 30% -premenopauseunilateral later oophorectomy -postmenopauseTAH & BSO -stage IA, grade 2 or 3chemotherapy (BEP) 3. Endodermal sinus tumors(yolk sac carcinoma) -median age at diagnosis – 18 yrs -secrete AFP - AFP is useful - Surgical staging, unilateral oophorectomy - All patients are given adjuvant or therapeutic chemotherapy BEP – most effective 6/23/2016 Ovarian cancer 59
Germ cell tumor Natural History Serum marker Treatment 4. Embryonal carcinoma -median age at diagnosis – 14 yrs -secrete estrogen, AFP,β- HCG - AFP,β-HCG Unilateral or bilateral oophorotomy followed by chemotherapy BEP 5.Choriocarcinoma of ovary -rare - Most are younger than 20yrs -β-HCG Chemotherapy with combination of methotrexate,actinomycin D,cyclphosasphmide 6.Mixed germ cell tumor Commonly have dysgerminoma or endodermal sinus component β-HCG and AFP depend on component part Unilateral or bilateral oophorotomy followed by chemotherapy BEP 6/23/2016 Ovarian cancer 60
SEX CORD-STROMAL TUMORS 6/23/2016 Ovarian cancer 61
Granulosa cell tumors • Include granulosa cell tumors, thecomas and fibromas • Cells of granulosa cell tumors produce estrogenic or, less commonly, androgenic steroids • May secrete other factors such as inhibin and mullerian inhibitory substance, useful as tumor markers during follow up • Surgery alone is sufficient therapy 6/23/2016 Ovarian cancer 62
Sertoli-Leydig cell tumors • Most produce androgens • present with symptoms of virilization • Treatment – unilateral salpingo-oophorectomy with evaluation of contralateral ovary - TAH and BSO in older patients 6/23/2016 Ovarian cancer 63
OTHER TUMORS Lipoid cell tumors • Rare • Arise from adrenal cortical rests near ovary • Treatment – surgical Ovarian sarcoma • Extremely rare • Most occur in postmenopausal women • Aggressive and die within 2 years Lipoma of ovary • Usually bilateral, especially with Burkitt lymphoma • Treatment is as for lymphomas else in the body 6/23/2016 Ovarian cancer 64
Pregnancy with Ovarian Cancer • All pregnant patients have luteal cysts, which should be <5 to 6 cm in diameter • Masses that are larger or continue to enlarge over several weeks should be examined by laproscopy at 16 wks of gestation • Management is the same as for non-pregnant patients who desire childbearing 6/23/2016 Ovarian cancer 65
Screening and Early Detection • The potential benefit of screening is its ability to identify ovarian cancer at a more localized and curable stage, leading to reduced mortality from the disease • Risk reduction bilateral salpingo-oophorectomy (RRSO) is currently the most effective preventative strategy to reduce ovarian cancer risk in patients with B R CA mutations. 6/23/2016 Ovarian cancer 66
• Other risk-reducing strategies such as tubal ligation and hysterectomy have also been associated with a reduced incidence of ovarian cancer among high-risk women. • Women with a family history of breast/ovarian cancer should be offered genetic counseling 6/23/2016 Ovarian cancer 67
• Familial ovarian cancer syndrome patients and known BRCA1/2mut carriers who have not undergone (RRSO) may be offered screening consisting of  a pelvic examination,  TVU, and  a CA-125 blood test every 6 months beginning between the ages of 30 to 35 years, or 5 to 10 years earlier than the earliest age of first Epithelial ovarian cancer (EOC) diagnosis in the family. 6/23/2016 Ovarian cancer 68
The lifetime risk of ovarian cancer • BRCA 1 mutations - 20% to 40% • BRCA 2 mutations - 1 0 % to 20 The majority of BRCA 1-associated cancers • Serous adenocarcinomas, • with an average age at diagnosis of 48 years The mean age for BRCA 2-associated ovarian cancers is 60 years. 6/23/2016 Ovarian cancer 69
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Reference • DeVita, Hellman, and Rosenberg’s Cancer. Principle and Practice of Oncology. 2011. 9th edition. • Handbook of Evidence-Based Radiation Oncology. 2010. 2nd edition • Manual of Clinical Oncology. 2012. • Seventh EditionMahmood I. Shafi, Helena M. Earl and Li Tee Tan. Gynecological oncology. Cambridge University press.2009. • NCCN guidelines. Ovarian version 2.2015. • Textbook of Medical Oncology. 2009. 4th edition. 6/23/2016 Ovarian cancer 71

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Ovarian Cancer

  • 1.
  • 2.
    • Fifth leadingcause of cancer death in women • leading cause of gynecologic cancer death.(WHO cancer statistics,2015) • Average lifetime risk is 1 in 70 • median age at diagnosis is 63 years. • 75% present with stage III or IV disease. • Early diagnosis is frequently difficult because of vague abdominal symptoms at presentation Epidemiology 6/23/2016 Ovarian cancer 2
  • 3.
    Risk Factors forOvarian Cancer Patient Characteristics • Increasing age • Personal history of breast cancer Genetic factor • Family history of ovarian cancer • BRCA 1 / 2 mutations • Hereditary nonpolyposis colorectal cancer Reproductive factors • Nulliparity • Early menarche • Late menopause • Infertility • Polycystic ovarian syndrome • Endometriosis • ovulation inducing drugs • Hormone replacement therapy Environmental factor • Obesity and high fat diet • Talc exposure • Cigarette smoking (for mucinous ovarian cancer) Ovarian cancer 3
  • 4.
    A higher riskfor developing epithelial ovarian cancer is for nulliparous women A lower risk for those • who have had children, • who have breastfed, • who have undergone tubal ligation, • or who have taken oral contraceptives. 6/23/2016 Ovarian cancer 4
  • 5.
    • Strongest riskfactor is a family history of ovarian cancer • only 5–10% of tumors result from a known genetic disposition. • Lifetime risk: - general population 1.8%, - one first-degree relative: 5%, - two first-degree relatives: 25–50%. 6/23/2016 Ovarian cancer 5
  • 6.
    World Health OrganizationClassification of Ovarian Tumors 6/23/2016 Ovarian cancer 6
  • 7.
    World Health OrganizationClassification of Ovarian Tumors 6/23/2016 Ovarian cancer 7
  • 8.
    World Health OrganizationClassification of Ovarian Tumors 6/23/2016 Ovarian cancer 8
  • 9.
    Classification of Ovariantumors 6/23/2016 Ovarian cancer 9
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    Histologic types • serous50%, • endometrioid 20%, • undifferentiated 15%, • mucinous 10%, • clear cell <5% Boderline tumour Tumors of low malignant potential (LMP, borderline tumors) • have an excellent prognosis compared with invasive carcinomas • Lack stromal invasion • Occur in premenopausal women 6/23/2016 Ovarian cancer 11
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    • Histologic grade GradePercentage of undifferentiated cells G1 0-25 G2 25-50 G3 >50 6/23/2016 Ovarian cancer 12
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    COMMON HISTOLOGIC TYPESOF EPITHELIAL OVARIAN CANCER Papillary serous • most common type of epithelial ovarian cancer. • May contain psammoma bodies • Is often associated with CA 125 elevation. Endometrioid • associated with endometriosis or an independent uterine cancer of similar histology. • May occur with early stage disease in younger patients, although advanced disease is also possible. Mucinous • rarely be associated with pseudomyxoma peritoneii. • CA 125 levels may not be markedly elevated. • Relatively chemoresistant. • Differential diagnosis of a mucinous ovarian tumor includes metastatic disease from an appendiceal primary. Clear cell • The most chemoresistant type of ovarian cancer. • Often contains "hobnail" cells with cleared out cytoplasm due to glycogen. • associated with endometriosis or humorally mediated hypercalcemia6/23/2016 Ovarian cancer 13
  • 14.
    • Concentric ringsof calcification called psammoma bodies- in the papillary serous epithelial ovarian cancer • May be seen in breast, lung, and papillary thyroid cancers 6/23/2016 Ovarian cancer 14 clear cell carcinoma shows prominent hobnail cells lining the glands. They have bulbous hyperchromatic nuclei that protrude into the gland lumen.
  • 15.
    Pathogenesis and Patternsof Metastases Patterns of Spread • Local spread: intraperitoneally • Peritoneal carcinosis: intraperitoneal spread after rupture of the ovarian capsule • Lymphatic metastasis: para-aortic lymph nodes, in rare cases retrograde invasion of inguinal / femoral lymph nodes • Hematogenous metastasis - liver, lung, CNS, in rare cases bone involvement 6/23/2016 Ovarian cancer 15
  • 16.
    Pathogenesis and Patternsof Metastases Molecular abnormalities identified in patients with epithelial ovarian cancer • Mutation in the p53 protooncogene • mutations in B-raf, K-ras, PTEN, or ,8-catenin • Amplification of the HER2/neu • Overexpression of pro-apoptotic genes such as BAX • Expression of angiogenic cytokines such as the vascular endothelial growth factor (VEGF) 6/23/2016 Ovarian cancer 16
  • 17.
    Diagnosis • abdominal discomfort/pain, • increasinggirth, • change in bowel habits, • early satiety, • dyspepsia, nausea, • ascites, • adnexal mass, • pleural effusion, • Sister Mary Joseph’s nodule, H&P with complete gynecologic exam No signs or symptoms until it spreads to the upper abdomen 6/23/2016 Ovarian cancer 17
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    H&P with completegynecologic exam Other Associated Paraneoplastic syndrome • Neurological syndrome: peripheral neuropathy, cerebellar ataxia • Cushing syndrome • Hypercalcemia • Thrombophelebitis Diagnosis 6/23/2016 Ovarian cancer 18
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    Diagnosis Serum tumor marker CA125 • Elevated in 80% of epithelial ovarian tumors • Also increased in endometrial, pancreatic & breast cancer and benign condition; endometriosis, inflammatory bowel disease, hepatitis • valuable as an early marker for disease recurrence, treatment response and early treatment failure • False positive possible, especially in premenopauseal women 6/23/2016 Ovarian cancer 19
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    Diagnosis Serum tumor marker CA19-9 • Low sensitivity CEA – elevated in 58% with stage III disease AFP and βHCG - measure if <30 yrs old to help rule out germ cell tumor 6/23/2016 Ovarian cancer 20
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    Diagnosis Imaging Ultrasound abdomen Transvaginal Ultrasound(TVU) • TVU is an important diagnostic tool in the evaluation of patients with a pelvic mass. • The classic sonographic finding of malignancy is a "complex“ cyst, defined as containing both solid and cystic components, sometimes with septations and internal echogenicity • Simple cyst <3 cm can be followed by serial US. 6/23/2016 Ovarian cancer 21
  • 22.
    Diagnosis Imaging CT/MRI abdomen/pelvis • especiallyhelpful preoperatively if advanced disease. • Useful in assessment of retroperitoneal LN involvement Cystoscopy, sigmoidoscopy, barium enema, upper GI series, or endoscopy as clinically indicated. 6/23/2016 Ovarian cancer 22
  • 23.
    Diagnosis Imaging Chest radiographs • toevaluate the presence of pleural effusions, which occur in 1 0 % of patients with epithelial ovarian cancer at diagnosis A definite histological diagnosis requires surgery It is best to avoid percutaneous biopsy during the initial evaluation, which can result in cyst rupture and spillage of malignant cells into the peritoneal cavity 6/23/2016 Ovarian cancer 23
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    STAGING 2014 FIGO ovariancancer staging system Stage I – Tumor confirmed to ovaries IA Tumor limited to one ovary (capsule intact) no tumor on ovarian surface; no malignant cells in the ascites or peritoneal washings IB Tumor limited to both ovaries (capsules intact) no tumor on ovarian surface; no malignant cells in the ascites or peritoneal washings IC Tumor limited to one or both with any of the following IC 1 Surgical spill IC 2 Capsule ruptured before surgery or tumor on ovarian surface IC 3 Malignant cells in the ascites or peritoneal washing 6/23/2016 Ovarian cancer 24
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    STAGING Stage II –Tumor involves one or both ovaries with pelvic extension (below pelvic brim) or primary peritoneal cancer IIA Extension and/or implants on uterus and/or fallopian tubes IIB Extension to other pelvic intraperitoneal tissues 6/23/2016 Ovarian cancer 26
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    STAGING Stage III. Tumorinvolves one or both ovaries with cytologically of histologically confirmed spread to the peritoneum outside the pelvis and /or metastasis to the retroperitoneal LN IIIA Positive retroperitoneal lymph nodes and /or microscopic metastasis beyond the pelvis) IIIA 1 Positive retroperitoneal lymph nodes only IIIA 1 (i) Metastasis up to 10mm in greatest dimension IIIA 1 (ii) Metastasis more than 10mm in greatest dimension IIIA 2 Microscopic, extrapelvic (above the brim) peritoneal involvement ± positive retroperitoneal lymph nodes IIIB Macroscopic, extrapelvic, peritoneal metastasis ≤ 2 cm ± positive retroperitoneal lymph nodes. Includes extension to capsule of liver/spleen IIIC Macroscopic, extrapelvic, peritoneal metastasis > 2 cm ± positive retroperitoneal lymph nodes. Includes extension to capsule of liver/spleen 6/23/2016 Ovarian cancer 27
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    STAGING Stage IV –Distant metastasis excluding peritoneal metastasis Stage IVA Pleural effusion with positive cytology Stage IVB Parenchymal metastases and metastases to extra-abdominal organs (including inguinal lymph nodes and lymph nodes outside of the abdominal cavity 6/23/2016 Ovarian cancer 29
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    STAGING 5-year survival rateaccording to stage Stage 5-year survival rate (%) Stage I 80 Stage II 60 Stage III 30 IIIA 40 IIIB 25 IIIC 23 Stage IV 10 6/23/2016 Ovarian cancer 30
  • 31.
    Prognostic Factors forEpithelial Ovarian Cancer Most important negative prognostic factors: • stage, • grade, • Residual volume of disease. Other negative factors: • age>65, • pre-op ascites, • CA125 elevated after 3c chemo or nadir >20 U/mL after first-line therapy. The extent to which the disease can be surgically debulked also affects prognosis. 6/23/2016 Ovarian cancer 31
  • 32.
    Algorithm for managementof ovarian cancer 6/23/2016
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    Management Stage IA andIB, grade1 (1) Premenopausal patients • After staging laparotomy , undergo unilateral oophretomy to preserve fertility • Follow up regular pelvic examination and monitor CA125 levels • The other ovary and uterus are removed when child bearing is completed (2) Postmenopausal patients • Should undergo TAH and BSO and staging 6/23/2016 Ovarian cancer 33
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    Stage IA andIB (grade2 and 3) • Treated with TAH/BSO and staging followed by chemotherapy Stage II, III, and IV • Surgery – cytoreductive surgery • chemotherapy Management 6/23/2016 Ovarian cancer 34
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    Full staging laparotomy •a total abdominal hysterectomy (TAH), • bilateral salpingo-oophorectomy (BSO), • omentectomy, • biopsies of suspicious areas, and • Peritoneal lavage or ascitic fluid sampling. • Blind peritoneal, paraaortic/ pelvic lymph node biopsies should be performed to exclude the possibility of microscopic Stage III disease, Surgery 6/23/2016 Ovarian cancer 35
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    Primary Cytoreductive surgery •removal of large, necrotic tumors with poor blood supply that might lead to impaired chemotherapy delivery • permit residual tumor to proliferate more rapidly and • thereby enhance sensitivity to postoperative chemotherapy 6/23/2016 Ovarian cancer 36
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    Primary cytoreduction • refersto performance of debulking surgery prior to administration of first-line chemotherapy and • is the standard approach for managing most patients with suspected epithelial ovarian cancer. 6/23/2016 Ovarian cancer 37
  • 38.
    Interval Cytoreductive Surgery Intervalcytoreduction is defined as a debulking procedure performed • after several cycles of chemotherapy have been administered, • typically in those patients who had a suboptimal cytoreduction at the time of initial surgery 6/23/2016 Ovarian cancer 38
  • 39.
    Postoperative Chemotherapy • Platinumagents have proven to be a critical component of the treatment of epithelial ovarian cancer. • Carboplatin has less ototoxicity, neuropathy, renal impairment, and emetogenesis than cisplatin • However, carboplatin causes myelosuppression particularly if combined with other agents. • Carboplatin is now the standard platinum agent for treating ovarian carcinoma Chemotherapy 6/23/2016 Ovarian cancer 39
  • 40.
    • The currentstandard first-line therapy for ovarian carcinoma is six cycles of carboplatin AUC 5-7 over one hour with paclitaxel (175 mg/m 2 ) as a three-hour infusion every 21 days. • Chemotherapy should begin within four to six weeks of surgery. • The platinum–paclitaxel combination is superior to single agent platinum • In patients who are poorly tolerated combination treatment, single agent carboplatin is a satisfactory alternative 6/23/2016 Ovarian cancer 40
  • 41.
    Role of otheragents • Liposomal doxorubicin, topotecan, gemcitabine, and epirubicin have been evaluated as first-line therapy in addition to the carboplatin and paclitaxel combination • The carboplatin–docetaxel combination was associated with less neurotoxicity and greater myelosuppression than carboplatin-paclitaxel 6/23/2016 Ovarian cancer 41
  • 42.
    Intraperitoneal Chemotherapy • Epithelialovarian cancer is largely confined to the peritoneal space during most of its natural history • Given this relatively localized distribution, instillation of chemotherapy directly into the peritoneal cavity is used • An option in patient with microscopic residual disease after cytoreductive surgery • cisplatin and paclitaxel have favorable peritoneal-to-plasma concentrations 6/23/2016 Ovarian cancer 42
  • 43.
    Antiangiogenic Agents Bevacizumab • amonoclonal antibody • against Vascular Endothelial Growth Factor (VEGF-A), • the first targeted agent to show significant single agent activity in ovarian carcinoma. • Used during adjuvant carboplatin /paclitaxel and for maintenance therapy 6/23/2016 Ovarian cancer 43
  • 44.
    • the valueof radiation therapy as consolidation therapy following chemotherapy for patients with ovarian cancer is uncertain. Adjuvant Whole Abdominal Radiation Therapy (WART) Used in stage III ovarian cancer, • If not suitable for chemotherapy and • >2cm residual Complication of WART • Acute – diarrhea, nausea/vomiting, leukopenia, thrombocytopenia • Chronic - transient LFT elevation, chronic diarrhea, basal pneumonitis, serious bowel obstruction Radiotherapy 6/23/2016 Ovarian cancer 44
  • 45.
    • Once epithelialovarian cancer has recurred, treatment with curative intent is no longer feasible • However, the judicious use of palliative chemotherapy can improve both survival and quality of life for patients with recurrent disease Management of Recurrent Disease 6/23/2016 Ovarian cancer 45
  • 46.
    Treatment is aimed •to relieve cancer-related symptoms, • optimize quality of life, • delay the time to symptomatic disease progression, and • prolong OS. Management of Recurrent Disease 6/23/2016 Ovarian cancer 46
  • 47.
    Chemotherapy The management ofrecurrent EOC takes into account the duration of the platinum-free interval and the response to first-line platinum therapy. Management of Recurrent Disease Indication Treatment Platinum sensitive disease Platinum based combination therapy( with gemcitabine or taxane) Platinum resistant /refractory disease Single agent chemotherapy: Liposomal doxorubicin, topotecan, gemcitabine, and oral etoposide Maintinance in recurrence disease Bevacizumab, concurrent with carboplatin/gemcitabine for 10 cycles maximum, followed by bevacizumab alone 6/23/2016 Ovarian cancer 47
  • 48.
    Management of RecurrentDisease Hormonal therapy • tamoxifen or an aromatase inhibitor – 10% to 20% efficacy Antiangiogenic Agents • Bevacizumab used alone or in combinaion with other cytotoxic drugs 6/23/2016 Ovarian cancer 48
  • 49.
    Surgery • secondary cytoreductionisolatedresidual disease at relapse with no gross residual disease greater than 1 cm in diameter Palliative surgery • colostomy for relief of a large bowel bstruction, • lysis of adhesions, and • management of small bowel obstruction Management of Recurrent Disease 6/23/2016 Ovarian cancer 49
  • 50.
    Radiotherapy • Symptoms froma growing pelvic mass can cause pain, bleeding, and rectal narrowing. • Palliative pelvic radiotherapy can provide rapid relief and, in some cases, may prevent or delay the need for diverting colostomy. • Doses of 8 to 10 Gy in a single fraction, 20 Gy in five fractions, 30 Gy in ten fractions were given • cerebral or bone metastases can be palliated with radiotherapy. Management of Recurrent Disease 6/23/2016 Ovarian cancer 50
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    GERM CELL TUMORSOF THE OVARY 6/23/2016 Ovarian cancer 58
  • 59.
    Germ cell tumorNatural History Serum marker Treatment 1.Dysgerminoma -secrete LDH -spread earlier through lymphatic LDH -primary surgery -adjuvant chemo for metastatic disease, BEP(Bleomycin,etoposide,cisplatin) -RT used in metastatic disease if fertility is not an issue 2.Immature teratoma Most common metastatic site is peritoneum - Normal AFP,β- HCG - Only ↑ in 30% -premenopauseunilateral later oophorectomy -postmenopauseTAH & BSO -stage IA, grade 2 or 3chemotherapy (BEP) 3. Endodermal sinus tumors(yolk sac carcinoma) -median age at diagnosis – 18 yrs -secrete AFP - AFP is useful - Surgical staging, unilateral oophorectomy - All patients are given adjuvant or therapeutic chemotherapy BEP – most effective 6/23/2016 Ovarian cancer 59
  • 60.
    Germ cell tumorNatural History Serum marker Treatment 4. Embryonal carcinoma -median age at diagnosis – 14 yrs -secrete estrogen, AFP,β- HCG - AFP,β-HCG Unilateral or bilateral oophorotomy followed by chemotherapy BEP 5.Choriocarcinoma of ovary -rare - Most are younger than 20yrs -β-HCG Chemotherapy with combination of methotrexate,actinomycin D,cyclphosasphmide 6.Mixed germ cell tumor Commonly have dysgerminoma or endodermal sinus component β-HCG and AFP depend on component part Unilateral or bilateral oophorotomy followed by chemotherapy BEP 6/23/2016 Ovarian cancer 60
  • 61.
  • 62.
    Granulosa cell tumors •Include granulosa cell tumors, thecomas and fibromas • Cells of granulosa cell tumors produce estrogenic or, less commonly, androgenic steroids • May secrete other factors such as inhibin and mullerian inhibitory substance, useful as tumor markers during follow up • Surgery alone is sufficient therapy 6/23/2016 Ovarian cancer 62
  • 63.
    Sertoli-Leydig cell tumors •Most produce androgens • present with symptoms of virilization • Treatment – unilateral salpingo-oophorectomy with evaluation of contralateral ovary - TAH and BSO in older patients 6/23/2016 Ovarian cancer 63
  • 64.
    OTHER TUMORS Lipoid celltumors • Rare • Arise from adrenal cortical rests near ovary • Treatment – surgical Ovarian sarcoma • Extremely rare • Most occur in postmenopausal women • Aggressive and die within 2 years Lipoma of ovary • Usually bilateral, especially with Burkitt lymphoma • Treatment is as for lymphomas else in the body 6/23/2016 Ovarian cancer 64
  • 65.
    Pregnancy with OvarianCancer • All pregnant patients have luteal cysts, which should be <5 to 6 cm in diameter • Masses that are larger or continue to enlarge over several weeks should be examined by laproscopy at 16 wks of gestation • Management is the same as for non-pregnant patients who desire childbearing 6/23/2016 Ovarian cancer 65
  • 66.
    Screening and EarlyDetection • The potential benefit of screening is its ability to identify ovarian cancer at a more localized and curable stage, leading to reduced mortality from the disease • Risk reduction bilateral salpingo-oophorectomy (RRSO) is currently the most effective preventative strategy to reduce ovarian cancer risk in patients with B R CA mutations. 6/23/2016 Ovarian cancer 66
  • 67.
    • Other risk-reducingstrategies such as tubal ligation and hysterectomy have also been associated with a reduced incidence of ovarian cancer among high-risk women. • Women with a family history of breast/ovarian cancer should be offered genetic counseling 6/23/2016 Ovarian cancer 67
  • 68.
    • Familial ovariancancer syndrome patients and known BRCA1/2mut carriers who have not undergone (RRSO) may be offered screening consisting of  a pelvic examination,  TVU, and  a CA-125 blood test every 6 months beginning between the ages of 30 to 35 years, or 5 to 10 years earlier than the earliest age of first Epithelial ovarian cancer (EOC) diagnosis in the family. 6/23/2016 Ovarian cancer 68
  • 69.
    The lifetime riskof ovarian cancer • BRCA 1 mutations - 20% to 40% • BRCA 2 mutations - 1 0 % to 20 The majority of BRCA 1-associated cancers • Serous adenocarcinomas, • with an average age at diagnosis of 48 years The mean age for BRCA 2-associated ovarian cancers is 60 years. 6/23/2016 Ovarian cancer 69
  • 70.
  • 71.
    Reference • DeVita, Hellman,and Rosenberg’s Cancer. Principle and Practice of Oncology. 2011. 9th edition. • Handbook of Evidence-Based Radiation Oncology. 2010. 2nd edition • Manual of Clinical Oncology. 2012. • Seventh EditionMahmood I. Shafi, Helena M. Earl and Li Tee Tan. Gynecological oncology. Cambridge University press.2009. • NCCN guidelines. Ovarian version 2.2015. • Textbook of Medical Oncology. 2009. 4th edition. 6/23/2016 Ovarian cancer 71

Editor's Notes

  • #4 s
  • #14 Identical histology is observed for primary peritoneal serous cancer (PPSC)
  • #15 Staining for cytokeratin CK7 is positive and CK20 is negative in most cases of primary serous ovarian cancer
  • #17 Mutation in the p53 protooncogene occurs in over 5 0 % of cases, predominantly involving tumors in patients with advanced stage and high-grade serous istology mutations in B-raf, K-ras, PTEN, or ,8-catenin may be seen in endometrioid, mucinous, or low-grade histologies. Amplification of the HER2/neu gene is observed in only approximately 8 % of patients and confers a poorer prognosis. Overexpression of pro-apoptotic genes such as BAX is associated with chemoresponsiveness and a more favorable prognosis Expression of angiogenic cytokines such as the vascular endothelial growth factor (VEGF) is frequently observed in epithelial ovarian cancer, with high serum levels conferring a worse prognosis
  • #21 CA 19-9- elevated in some mucinous ovarian carcinomas
  • #22 TVU more sensitive at detecting ovarian tumors compared to other tests such as computed tomography ( CT) Provide qualitative information about the mass that might suggest malignancy. Complex ovarian cyst or postmenopausal women with simple cyst and CA-125 >65 U/mL suggestive of cancer → surgery indicated.
  • #48 Patients with a progression-free interval of ≥6 months have platinum-sensitive disease. Second-line platinum-based therapy, single agent or combination, improves survival in women with platinumsensitive disease (Table 17.3). ■ Recurrence within 6 months of initial platinum-based chemotherapy is defined as platinum-resistant disease. Progression while on initial chemotherapy is platinum-refractory disease
  • #49 The response to hormonal agents is typically slow and may require approximately 2 to 3 months before a reduction in the CA 125 level is evident.
  • #50 Secondary cytoreductive surgery refers to an attempt at surgical debulking of disease at the time of relapse and is performed in selected patients prior to the administration of second-line chemotherapy.
  • #63  5% of all ovarian cancers Often present with stage I, excellent prognosis Long-term follow-up for late relapse, sometimes occurring more than 10 years after diagnosis
  • #64 Cells of granulosa cell tumors are characterized by a longitudinal cleft that resembles a coffee bean and they may be organized into fluid-filled spherical structures known as Call-Exner bodies Estradiol is due to production of androstenedione by normal theca cells within the ovarian stroma, which is then converted to estradiol under the influence of aromatase present in the granulosa cell tumor
  • #69 The CA 125 serum level is not a useful screening test when used alone for enhancing the accuracy of CA 125 levels, such as HE4 (human epididymis 4), osteopontin, mesothelin, and osteoblast-stimulating factor-2