- •Contents
- •Contributors
- •1 Introduction
- •2.1 Posterior Compartment
- •2.2 Anterior Compartment
- •2.3 Middle Compartment
- •2.4 Perineal Body
- •3 Compartments
- •3.1 Posterior Compartment
- •3.1.1 Connective Tissue Structures
- •3.1.2 Muscles
- •3.1.3 Reinterpreted Anatomy and Clinical Relevance
- •3.2 Anterior Compartment
- •3.2.1 Connective Tissue Structures
- •3.2.2 Muscles
- •3.2.3 Reinterpreted Anatomy and Clinical Relevance
- •3.2.4 Important Vessels, Nerves, and Lymphatics of the Anterior Compartment
- •3.3 Middle Compartment
- •3.3.1 Connective Tissue Structures
- •3.3.2 Muscles
- •3.3.3 Reinterpreted Anatomy and Clinical Relevance
- •3.3.4 Important Vessels, Nerves, and Lymphatics of the Middle Compartment
- •4 Perineal Body
- •References
- •MR and CT Techniques
- •1 Introduction
- •2.1 Introduction
- •2.2.1 Spasmolytic Medication
- •2.3.2 Diffusion-Weighted Imaging
- •2.3.3 Dynamic Contrast Enhancement
- •3 CT Technique
- •3.1 Introduction
- •3.2 Technical Disadvantages
- •3.4 Oral and Rectal Contrast
- •References
- •Uterus: Normal Findings
- •1 Introduction
- •References
- •1 Clinical Background
- •1.1 Epidemiology
- •1.2 Clinical Presentation
- •1.3 Embryology
- •1.4 Pathology
- •2 Imaging
- •2.1 Technique
- •2.2.1 Class I Anomalies: Dysgenesis
- •2.2.2 Class II Anomalies: Unicornuate Uterus
- •2.2.3 Class III Anomalies: Uterus Didelphys
- •2.2.4 Class IV Anomalies: Bicornuate Uterus
- •2.2.5 Class V Anomalies: Septate Uterus
- •2.2.6 Class VI Anomalies: Arcuate Uterus
- •2.2.7 Class VII Anomalies
- •References
- •Benign Uterine Lesions
- •1 Background
- •1.1 Uterine Leiomyomas
- •1.1.1 Epidemiology
- •1.1.2 Pathogenesis
- •1.1.3 Histopathology
- •1.1.4 Clinical Presentation
- •1.1.5 Therapy
- •1.1.5.1 Indications
- •1.1.5.2 Medical Therapy and Ablation
- •1.1.5.3 Surgical Therapy
- •1.1.5.4 Uterine Artery Embolization (UAE)
- •1.1.5.5 Magnetic Resonance-Guided Focused Ultrasound
- •2 Adenomyosis of the Uterus
- •2.1 Epidemiology
- •2.2 Pathogenesis
- •2.3 Histopathology
- •2.4 Clinical Presentation
- •2.5 Therapy
- •3 Imaging
- •3.2 Magnetic Resonance Imaging
- •3.2.1 Magnetic Resonance Imaging: Technique
- •3.2.2 MR Appearance of Uterine Leiomyomas
- •3.2.3 Locations, Growth Patterns, and Imaging Characteristics
- •3.2.4 Histologic Subtypes and Forms of Degeneration
- •3.2.5 Differential Diagnosis
- •3.2.6 MR Appearance of Uterine Adenomyosis
- •3.2.7 Locations, Growth Patterns, and Imaging Characteristics
- •3.2.8 Differential Diagnosis
- •3.3 Computed Tomography
- •3.3.1 CT Technique
- •3.3.2 CT Appearance of Uterine Leiomyoma and Adenomyosis
- •3.3.3 Atypical Appearances on CT and Differential Diagnosis
- •4.1 Indications
- •4.2 Technique
- •Bibliography
- •Cervical Cancer
- •1 Background
- •1.1 Epidemiology
- •1.2 Pathogenesis
- •1.3 Screening
- •1.4 HPV Vaccination
- •1.5 Clinical Presentation
- •1.6 Histopathology
- •1.7 Staging
- •1.8 Growth Patterns
- •1.9 Treatment
- •1.9.1 Treatment of Microinvasive Cervical Cancer
- •1.9.2 Treatment of Grossly Invasive Cervical Carcinoma (FIGO IB-IVA)
- •1.9.3 Treatment of Recurrent Disease
- •1.9.4 Treatment of Cervical Cancer During Pregnancy
- •1.10 Prognosis
- •2 Imaging
- •2.1 Indications
- •2.1.1 Role of CT and MRI
- •2.2 Imaging Technique
- •2.2.2 Dynamic MRI
- •2.2.3 Coil Technique
- •2.2.4 Vaginal Opacification
- •2.3 Staging
- •2.3.1 General MR Appearance
- •2.3.2 Rare Histologic Types
- •2.3.3 Tumor Size
- •2.3.4 Local Staging
- •2.3.4.1 Stage IA
- •2.3.4.2 Stage IB
- •2.3.4.3 Stage IIA
- •2.3.4.4 Stage IIB
- •2.3.4.5 Stage IIIA
- •2.3.4.6 Stage IIIB
- •2.3.4.7 Stage IVA
- •2.3.4.8 Stage IVB
- •2.3.5 Lymph Node Staging
- •2.3.6 Distant Metastases
- •2.4 Specific Diagnostic Queries
- •2.4.1 Preoperative Imaging
- •2.4.2 Imaging Before Radiotherapy
- •2.5 Follow-Up
- •2.5.1 Findings After Surgery
- •2.5.2 Findings After Chemotherapy
- •2.5.3 Findings After Radiotherapy
- •2.5.4 Recurrent Cervical Cancer
- •2.6.1 Ultrasound
- •2.7.1 Metastasis
- •2.7.2 Malignant Melanoma
- •2.7.3 Lymphoma
- •2.8 Benign Lesions of the Cervix
- •2.8.1 Nabothian Cyst
- •2.8.2 Leiomyoma
- •2.8.3 Polyps
- •2.8.4 Rare Benign Tumors
- •2.8.5 Cervicitis
- •2.8.6 Endometriosis
- •2.8.7 Ectopic Cervical Pregnancy
- •References
- •Endometrial Cancer
- •1.1 Epidemiology
- •1.2 Pathology and Risk Factors
- •1.3 Symptoms and Diagnosis
- •2 Endometrial Cancer Staging
- •2.1 MR Protocol for Staging Endometrial Carcinoma
- •2.2.1 Stage I Disease
- •2.2.2 Stage II Disease
- •2.2.3 Stage III Disease
- •2.2.4 Stage IV Disease
- •4 Therapeutic Approaches
- •4.1 Surgery
- •4.2 Adjuvant Treatment
- •4.3 Fertility-Sparing Treatment
- •5.1 Treatment of Recurrence
- •6 Prognosis
- •References
- •Uterine Sarcomas
- •1 Epidemiology
- •2 Pathology
- •2.1 Smooth Muscle Tumours
- •2.2 Endometrial Stromal Tumours
- •3 Clinical Background
- •4 Staging
- •5 Imaging
- •5.1 Leiomyosarcoma
- •5.2.3 Undifferentiated Uterine Sarcoma
- •5.3 Adenosarcoma
- •6 Prognosis and Treatment
- •References
- •1.1 Anatomical Relationships
- •1.4 Pelvic Fluid
- •2 Developmental Anomalies
- •2.1 Congenital Abnormalities
- •2.2 Ovarian Maldescent
- •3 Ovarian Transposition
- •References
- •1 Introduction
- •4 Benign Adnexal Lesions
- •4.1.1 Physiological Ovarian Cysts: Follicular and Corpus Luteum Cysts
- •4.1.1.1 Imaging Findings in Physiological Ovarian Cysts
- •4.1.1.2 Differential Diagnosis
- •4.1.2 Paraovarian Cysts
- •4.1.2.1 Imaging Findings
- •4.1.2.2 Differential Diagnosis
- •4.1.3 Peritoneal Inclusion Cysts
- •4.1.3.1 Imaging Findings
- •4.1.3.2 Differential Diagnosis
- •4.1.4 Theca Lutein Cysts
- •4.1.4.1 Imaging Findings
- •4.1.4.2 Differential Diagnosis
- •4.1.5 Polycystic Ovary Syndrome
- •4.1.5.1 Imaging Findings
- •4.1.5.2 Differential Diagnosis
- •4.2.1 Cystadenoma
- •4.2.1.1 Imaging Findings
- •4.2.1.2 Differential Diagnosis
- •4.2.2 Cystadenofibroma
- •4.2.2.1 Imaging Features
- •4.2.3 Mature Teratoma
- •4.2.3.1 Mature Cystic Teratoma
- •Imaging Findings
- •Differential Diagnosis
- •4.2.3.2 Monodermal Teratoma
- •Imaging Findings
- •4.2.4 Benign Sex Cord-Stromal Tumors
- •4.2.4.1 Fibroma and Thecoma
- •Imaging Findings
- •4.2.4.2 Sclerosing Stromal Tumor
- •Imaging Findings
- •4.2.5 Brenner Tumors
- •4.2.5.1 Imaging Findings
- •4.2.5.2 Differential Diagnosis
- •5 Functioning Ovarian Tumors
- •References
- •1 Introduction
- •2.1 Context
- •2.2.2 Indications According to Simple Rules
- •References
- •CT and MRI in Ovarian Carcinoma
- •1 Introduction
- •2.1 Familial or Hereditary Ovarian Cancers
- •3 Screening for Ovarian Cancer
- •5 Tumor Markers
- •6 Clinical Presentation
- •7 Imaging of Ovarian Cancer
- •7.1.2 Peritoneal Carcinomatosis
- •7.1.3 Ascites
- •7.3 Staging of Ovarian Cancer
- •7.3.1 Staging by CT and MRI
- •Imaging Findings According to Tumor Stages
- •Value of Imaging
- •7.3.2 Prediction of Resectability
- •7.4 Tumor Types
- •7.4.1 Epithelial Ovarian Cancer
- •High-Grade Serous Ovarian Cancer
- •Low-Grade Serous Ovarian Cancer
- •Mucinous Epithelial Ovarian Cancer
- •Endometrioid Ovarian Carcinomas
- •Clear Cell Carcinomas
- •Imaging Findings of Epithelial Ovarian Cancers
- •Differential Diagnosis
- •Borderline Tumors
- •Imaging Findings
- •Differential Diagnosis
- •Recurrent Ovarian Cancer
- •Imaging Findings
- •Differential Diagnosis
- •Value of Imaging
- •Malignant Germ Cell Tumors
- •Dysgerminomas
- •Imaging Findings
- •Differential Diagnosis
- •Immature Teratomas
- •Imaging Findings
- •Malignant Transformation in Benign Teratoma
- •Imaging Findings
- •Differential Diagnosis
- •Sex-Cord Stromal Tumors
- •Granulosa Cell Tumors
- •Imaging Findings
- •Sertoli-Leydig Cell Tumor
- •Imaging Findings
- •Ovarian Lymphoma
- •Imaging Findings
- •Differential Diagnosis
- •7.4.3 Ovarian Metastases
- •Imaging Findings
- •Differential Diagnosis
- •7.5 Fallopian Tube Cancer
- •7.5.1 Imaging Findings
- •Differential Diagnosis
- •References
- •Endometriosis
- •1 Introduction
- •2.1 Sonography
- •3 MR Imaging Findings
- •References
- •Vagina and Vulva
- •1 Introduction
- •3.1 CT Appearance
- •3.2 MRI Protocol
- •3.3 MRI Appearance
- •4.1 Imperforate Hymen
- •4.2 Congenital Vaginal Septa
- •4.3 Vaginal Agenesis
- •5.1 Vaginal Cysts
- •5.1.1 Gardner Duct Cyst (Mesonephric Cyst)
- •5.1.2 Bartholin Gland Cyst
- •5.2.1 Vaginal Infections
- •5.2.1.1 Vulvar Infections
- •5.2.1.2 Vulvar Thrombophlebitis
- •5.3 Vulvar Trauma
- •5.4 Vaginal Fistula
- •5.5 Post-Radiation Changes
- •5.6 Benign Tumors
- •6.1 Vaginal Malignancies
- •6.1.1 Primary Vaginal Carcinoma
- •6.1.1.1 MRI Findings
- •6.1.1.2 Lymph Node Drainage
- •6.1.1.3 Recurrence and Complications
- •6.1.2 Non-squamous Cell Carcinomas of the Vagina
- •6.1.2.1 Adenocarcinoma
- •6.1.2.2 Melanoma
- •6.1.2.3 Sarcomas
- •6.1.2.4 Lymphoma
- •6.2 Vulvar Malignancies
- •6.2.1 Vulvar Carcinoma
- •6.2.2 Melanoma
- •6.2.3 Lymphoma
- •6.2.4 Aggressive Angiomyxoma of the Vulva
- •7 Vaginal Cuff Disease
- •7.1 MRI Findings
- •8 Foreign Bodies
- •References
- •Imaging of Lymph Nodes
- •1 Background
- •3 Technique
- •3.1.1 Intravenous Unspecific Contrast Agents
- •3.1.2 Intravenous Tissue-Specific Contrast Agents
- •References
- •1 Introduction
- •2.1.1 Imaging Findings
- •2.1.2 Differential Diagnosis
- •2.1.3 Value of Imaging
- •2.2 Pelvic Inflammatory
- •2.2.1 Imaging Findings
- •2.3 Hydropyosalpinx
- •2.3.1 Imaging Findings
- •2.3.2 Differential Diagnosis
- •2.4 Tubo-ovarian Abscess
- •2.4.1 Imaging Findings
- •2.4.2 Differential Diagnosis
- •2.4.3 Value of Imaging
- •2.5 Ovarian Torsion
- •2.5.1 Imaging Findings
- •2.5.2 Differential Diagnosis
- •2.5.3 Diagnostic Value
- •2.6 Ectopic Pregnancy
- •2.6.1 Imaging Findings
- •2.6.2 Differential Diagnosis
- •2.6.3 Value of Imaging
- •3.1 Pelvic Congestion Syndrome
- •3.1.1 Imaging Findings
- •3.1.2 Differential Diagnosis
- •3.1.3 Value of Imaging
- •3.2 Ovarian Vein Thrombosis
- •3.2.1 Imaging Findings
- •3.2.2 Differential Diagnosis
- •3.2.3 Value of Imaging
- •3.3 Appendicitis
- •3.3.1 Imaging Findings
- •3.3.2 Value of Imaging
- •3.4 Diverticulitis
- •3.4.1 Imaging Findings
- •3.4.2 Differential Diagnosis
- •3.4.3 Value of Imaging
- •3.5 Epiploic Appendagitis
- •3.5.1 Imaging Findings
- •3.5.2 Differential Diagnosis
- •3.5.3 Value of Imaging
- •3.6 Crohn’s Disease
- •3.6.1 Imaging Findings
- •3.6.2 Differential Diagnosis
- •3.6.3 Value of Imaging
- •3.7 Rectus Sheath Hematoma
- •3.7.1 Imaging Findings
- •3.7.2 Differential Diagnosis
- •3.7.3 Value of Imaging
- •References
- •MRI of the Pelvic Floor
- •1 Introduction
- •2 Imaging Techniques
- •3.1 Indications
- •3.2 Patient Preparation
- •3.3 Patient Instruction
- •3.4 Patient Positioning
- •3.5 Organ Opacification
- •3.6 Sequence Protocols
- •4 MR Image Analysis
- •4.1 Bony Pelvis
- •5 Typical Findings
- •5.1 Anterior Compartment
- •5.2 Middle Compartment
- •5.3 Posterior Compartment
- •5.4 Levator Ani Muscle
- •References
- •Evaluation of Infertility
- •1 Introduction
- •2 Imaging Techniques
- •2.1 Hysterosalpingography
- •2.1.1 Cycle Considerations
- •2.1.2 Technical Considerations
- •2.1.3 Side Effects and Complications
- •2.1.5 Pathological Findings
- •2.1.6 Limitations of HSG
- •2.2.1 Cycle Considerations
- •2.2.2 Technical Considerations
- •2.2.2.1 Normal and Abnormal Anatomy
- •2.2.3 Accuracy
- •2.2.4 Side Effects and Complications
- •2.2.5 Limitations of Sono-HSG
- •2.3 Magnetic Resonance Imaging
- •2.3.1 Indications
- •2.3.2 Technical Considerations
- •2.3.3 Limitations
- •3 Ovulatory Dysfunction
- •4 Pituitary Adenoma
- •5 Polycystic Ovarian Syndrome
- •7 Uterine Disorders
- •7.1 Müllerian Duct Anomalies
- •7.1.1 Class I: Hypoplasia or Agenesis
- •7.1.2 Class II: Unicornuate
- •7.1.3 Class III: Didelphys
- •7.1.4 Class IV: Bicornuate
- •7.1.5 Class V: Septate
- •7.1.6 Class VI: Arcuate
- •7.1.7 Class VII: Diethylstilbestrol Related
- •7.2 Adenomyosis
- •7.3 Leiomyoma
- •7.4 Endometriosis
- •References
- •MR Pelvimetry
- •1 Clinical Background
- •1.3.1 Diagnosis
- •1.3.2.1 Cephalopelvic Disproportion
- •1.3.4 Inadequate Progression of Labor due to Inefficient Contraction (“the Powers”)
- •2.2 Palpation of the Pelvis
- •3 MR Pelvimetry
- •3.2 MR Imaging Protocol
- •3.3 Image Analysis
- •3.4 Reference Values for MR Pelvimetry
- •5 Indications for Pelvimetry
- •References
- •MR Imaging of the Placenta
- •2 Imaging of the Placenta
- •3 MRI Protocol
- •4 Normal Appearance
- •4.1 Placenta Variants
- •5 Placenta Adhesive Disorders
- •6 Placenta Abruption
- •7 Solid Placental Masses
- •9 Future Directions
- •References
- •Erratum to: Endometrial Cancer
CT and MRI in Ovarian Carcinoma
Rosemarie Forstner
Contents
1 |
Introduction\ |
|
288 |
2 Epidemiology and Risk Factors\ |
|
288 |
|
2.1 Familial or Hereditary Ovarian Cancers\ |
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288 |
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3 Screening for Ovarian Cancer\ |
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289 |
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4 Tumorigenesis of Ovarian Cancer\ |
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289 |
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5 |
Tumor Markers\ |
|
290 |
6 |
Clinical Presentation\ |
|
290 |
7 Imaging of Ovarian Cancer\ |
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290 |
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7.1 Imaging Findings in Ovarian Cancer\ |
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290 |
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7.2 Pathways of Spread in Ovarian Cancer\ |
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297 |
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7.3 Staging of Ovarian Cancer\ |
|
298 |
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7.4 |
Tumor Types\ |
|
302 |
7.5 |
Fallopian Tube Cancer\ |
|
318 |
References\ |
|
319 |
|
Abstract
Primary ovarian cancer is categorized as surface epithelial cancer, germ cell tumors, and sex cord stromal tumors. Epithelial ovarian cancer is now understood as a spectrum of different cancer entities that vary considerably on a clinicopathological and molecular level. Disseminated peritoneal spread and ascites is typical of the most common cancer type, high grade serous ovarian cancer. Other cancer subtypes may show distinct features in imaging. CT and MRI are usually complementary techniques to ultrasonography to further assess indeterminate or frankly malignant ovarian lesions. In the latter CT is the imaging modality of choice for triaging patients with ovarian cancer. MRI is emerging as a new technique to assess peritoneal spread and is superior to CT in lesion characterization. This chapter will make familiar with recent concepts in ovarian cancer. Typical imaging findings and differential diagnostic aspects of various types of ovarian malignancies as well as the update of the FIGO staging classification and respectability criteria will be covered.
The original version of this chapter was revised. The |
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Abbreviations |
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erratum to this chapter is available online at DOI |
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10.1007/174_2018_189. |
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R. Forstner (*) |
ADC\ |
Apparent diffusion coefficient |
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Salzburger Landeskliniken, Paracelsus Medical |
BT\ |
Borderline tumor |
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University, Müllner Hauptstr. 48, Salzburg, 5020, |
CT\ |
Computed tomography |
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Austria |
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DCE\ |
Dynamic contrast enhanced |
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e-mail: R.Forstner@salk.at |
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Med Radiol Diagn Imaging (2017) |
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287 |
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DOI 10.1007/174_2017_17, © Springer International Publishing AG |
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Published Online: 17 March 2017 |
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288 |
R. Forstner |
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DWI\ |
Diffusion-weighted imaging |
IV\ |
Intravenous |
MRI\ |
Magnetic resonance imaging |
SI\ |
Signal intensity |
1\ Introduction
The vast majority of ovarian carcinomas are epithelial in origin, accounting for more than 90% of the estimated 22,280 new cases of ovarian cancer diagnosed in 2016 in the United States (Cancer Fact and Figures 2016). Most fallopian tube carcinomas and peritoneal carcinomas are now considered a clinical entity with high-grade serous ovarian cancer. While early-stage cancer is often curable, advanced-stage ovarian cancer is one of the most lethal cancers in women, with a 5-year survival of approximately 28% when a patient is diagnosed with tumor spread outside the pelvis (Clarke-Pearson 2009). Nowadays ovarian cancer is understood as a spectrum of different cancer entities that vary considerably on a clinicopathological and molecular level. Genomic profiling may open new approaches of personalized medicine in treatment of ovarian cancer (Jayson et al. 2014).
2\ Epidemiology and Risk
Factors
In developed countries, ovarian cancer accounts for only 3% of cancer in females, but ranks fifth in cancer mortality, and is the leading cause of death among the gynecological cancers (Cancer Fact and Figures 2016). It is estimated that one woman in 75 will develop ovarian cancer, and one woman in 100 will die of the disease. Ovarian cancer is often clinically silent and about 75% of women present with advanced stages.
The incidence rate of ovarian cancer is higher in White women than in Black or Asian women and differs across the world (Cancer Fact and Figures 2016). The strongest patient-related risk factors for ovarian cancer are family history and increasing age. The vast majority of epithelial ovarian carcinomas are diagnosed in the postmenopausal period, with more than half of the
cases diagnosed in the UK are females aged 65 years or older (Ovarian Cancer Statistics).
In patients with genetic predisposition, ovarian cancers occur approximately 10 years earlier (Jayson et al. 2014). In females younger than 20 years of age, germ cell tumors account for more than two-thirds of malignant ovarian tumors. Prolonged times of uninterrupted ovulations seem to play a role in the development of ovarian cancer. Infertility, nulliparity, late menopause, early menarche, polycystic ovary syndrome, endometriosis, and cigarette smoking harbor an increased risk of ovarian cancer (Carlson 2016).
2.1\ Familial or Hereditary Ovarian Cancers
Genetic, reproductive, and environmental factors have been identified to play a role in the development of ovarian cancer. Approximately 5–15% of ovarian cancers are considered hereditary cancers. Families with three or more first-degree relatives with ovarian and/or ovarian and breast cancer carry a substantially (16–60%) increased risk for developing ovarian cancer (Pennington and Wsisher 2012).
Hereditary breast-ovarian cancer syndrome (HBOC) accounts for the vast majority (85–90%) of all hereditary ovarian cancers (Jayson et al. 2014; Ozols et al. 2001). In hereditary nonpolyposis colorectal cancer (HNPCC) syndrome, the Lynch syndrome, patients present with colon, endometrial, breast, ovarian, and other cancers (Pennington and Wsisher 2012). Their estimated ovarian cancer risk is 8–10% (Pennington and Wsisher 2012). BRCA mutation carriers have a substantially higher lifetime risk of 10–40% to develop ovarian cancer. It is higher in BRCA1 (35–60%) than in BRCA2 (12–25%) mutation carriers (Pennington and Wsisher 2012). Hereditary ovarian cancer has been attributed mainly to mutations in BRCA1 and BRCA2 genes, but numerous new high-risk genes including PTEN, TP53, CDH1, and STK11 and other germ line mutations have been identified with advances in genomic testing (Runnebaum and Arnold 2013). BRCA mutations are associated mostly with high-grade serous cancers that present