| What are follicle and luteal cysts? | ➢ Follicle and luteal cysts in the ovaries are so commonplace that they may be considered variants of normal physiology.
➢ These innocuous lesions originate from unruptured graafian follicles
or from follicles that rupture and then immediately seal.
➢ Such cysts often are multiple and develop subjacent to the serosa of the ovary.
➢ They typically are small (1–1.5 cm in diameter) and are filled with clear serous fluid.
Occasionally, they become sufficiently large (4–5 cm) to produce palpable masses and pelvic pain.
➢ When small, they are lined by granulosa lining cells or luteal cells, but as fluid accumulates, pressure may cause atrophy of these cells.
➢ Sometimes these cysts rupture, producing intraperitoneal bleeding and peritoneal symptoms (acute abdomen). |
| What are ovarian tumors? | ➢ Tumors of the ovary are remarkably varied as they may arise from any of the three cell types in the normal ovary: the
multipotent surface (coelomic) epithelium, the totipotent germ cells, and the sex cord–stromal cells.
➢ Neoplasms of epithelial origin account for the great majority of ovarian tumors and, in their malignant forms, account for almost 90% of ovarian cancers
➢ Germ cell and sex cord–stromal cell tumors are much less frequent; although they constitute 20% to 30% of ovarian tumors, they are collectively responsible for less than 10% of malignant tumors of the ovary. |
| What are surface epithelial tumors? | ➢ Most frequent
➢ Benign lesions usually are cystic (cystadenoma) and may have an accompanying stromal component (cystadenofibroma).
➢ Malignant tumors also may be cystic (cystadenocarcinoma) or solid (carcinoma).
➢ Some ovarian epithelial tumors fall into an intermediate category currently referred to as borderline tumors.
➢ Although the majority of borderline tumors behave in a benign manner they can recur and some can progress to carcinoma. |
| How is incidence of surface epithelial tumors? | ➢ Important risk factors for ovarian cancer include nulliparity, family history, and germline mutations in certain tumor suppressor genes.
➢ There is a higher incidence of carcinoma in unmarried women and married women with low parity.
➢ Of interest, prolonged use of oral contraceptives reduces the risk.
➢ Around 5% to 10% of ovarian cancers are familial (most associated with mutations in the BRCA1 or BRCA2 tumor suppressor genes).
➢ The average lifetime risk for ovarian cancer is approximately 30% in BRCA1 carriers; the risk in BRCA2 carriers is somewhat lower.
➢ BRCA1 and BRCA2 mutations are found in only 8% to 10% of sporadic ovarian cancers. |
| What are serous ovarian tumors? | ➢ Serous tumors are the most common of the ovarian epithelial tumors overall
➢ Greatest fraction of malignant ovarian tumors.
➢ About 60% are benign, 15% are borderline, and 25% are malignant.
➢ Benign lesions are usually encountered in patients between 30 and 40 years of age, and malignant serous tumors are more commonly seen between 45 and 65 years of age.
➢ There are two types of serous carcinomas, low-grade and highgrade. |
| How is incidence of serous ovarian tumors? | ➢ The low grade serous carcinoma arise from benign or
borderline lesions and progress slowly in a stepwise manner to become invasive carcinoma.
➢ These low-grade tumors are associated with mutations in genes encoding signaling proteins, such as KRAS, a member of the RAS gene family.
➢ The high-grade serous tumors develop rapidly.
➢ TP53 mutations are virtually ubiquitous in high-grade serous cancers, being present in over 95% of cases.
➢ Other frequently mutated genes include the tumor suppressors NF1 and RB, as well as BRCA1 and BRCA2 in familial ovarian cancers. |
| How is presentation of serous ovarian tumors? | ➢ Most serous tumors are large, spherical to ovoid, cystic
structures up to 30 to 40 cm in diameter.
➢ About 25% of the benign tumors are bilateral.
➢ In the benign tumors, the serosal covering is smooth and
glistening.
➢ By contrast, the surface of adenocarcinomas often has nodular irregularities representing areas in which the tumor has invaded the serosa.
➢ On cut section, small cystic tumors may have a single cavity, but larger ones frequently are divided by multiple septa into multiloculated masses. |
| How is microscopy of serous ovarian tumors? | ➢ The cystic spaces usually are filled with a clear serous fluid. Protruding into the cystic cavities are papillary projections, which are more prominent in malignant tumors
➢ On histologic examination, benign tumors contain a single layer of columnar epithelial cells that line the cyst or cysts.
➢ The cells often are ciliated.
➢ Psammoma bodies are common in the tips of papillae.
➢ In high-grade carcinoma the cells are markedly atypical, the papillary formations are usually complex and multilayered, and by definition nests or sheets of malignant cells invade the ovarian stroma. |
| How is classification of serous ovarian tumors? | ➢ Between clearly benign and obviously malignant forms lie borderline tumors, which exhibit less cytologic atypia and typically no stromal invasion
➢ Borderline tumors may seed the peritoneum, but fortunately the tumor implants usually are “noninvasive.”
➢ In general, malignant serous tumors spread throughout the peritoneal cavity and to regional lymph nodes
➢ Distant lymphatic and hematogenous metastases are infrequent.
➢ The prognosis for patients with high-grade serous carcinoma is poor, even after surgery and chemotherapy, and depends heavily
on the stage of the disease at diagnosis.
➢ borderline tumors are associated with nearly 100% survival.
➢ women with BRCA1/2 somatic mutations tend to have a better prognosis. |
| What are mucinous ovarian tumors? | ➢ Mucinous tumors differ from serous tumors in two respects:
The neoplastic epithelium consists of mucin-secreting cells;
Mucinous tumors are considerably less likely to be malignant.
➢ Overall, only 10% of mucinous tumors are malignant; another 10% are borderline, and 80% are benign.
➢ The prognosis of mucinous cystadenocarcinoma is somewhat better than that of its serous counterpart
➢ Although stage rather than histologic type (serous versus
mucinous) is the major determinant of outcome.
➢ Mutations in KRAS are detected in approximately 50% of ovarian mucinous carcinomas, |
| What are endometriod tumors? | ➢ These tumors may be solid or cystic;
➢ They sometimes develop in association with endometriosis.
➢ On microscopic examination, they are distinguished by the formation of tubular glands, similar to those of the endometrium,within the lining of cystic spaces.
➢ Although benign andborderline forms exist, endometrioid tumors
usually are malignant.
➢ They are bilateral in about 30% of cases, and 15% to 30% of women with these ovarian tumors have a concomitant endometrial carcinoma.
➢ Similar to endometrioid-type carcinoma of the endometrium, endometrioid carcinomas of the ovary frequently have mutations in the PTEN tumor suppressor gene as well as mutations in other genes |
| What is Brenner tumor? | ➢ The Brenner tumor is an uncommon, solid, usually unilateral ovarian tumor consisting of abundant stroma containing nests of transitional-type epithelium resembling that of the urinary tract.
➢ Occasionally, the nests are cystic and are lined by columnar mucus-secreting cells.
➢ Brenner tumors generally are smoothly encapsulated and graywhite on cut section, ranging from a few centimeters to 20 cm in diameter.
➢ Although most are benign, both malignant and borderline tumors have been described. |
| What are teratomas? | ➢ Teratomas constitute 15% to 20% of ovarian tumors.
➢ Predilection to arise in the first 2 decades of life;
➢ The younger the person, the greater the likelihood of malignancy.
➢ More than 90% of these germ cell neoplasms, however, are benign mature cystic teratomas;
➢ The immature, malignant variant is rare. |
| What are benign cystic teratomas? | ➢ Marked by the presence of mature tissues derived from all three germ cell layers: ectoderm, endoderm, and mesoderm.
➢ Usually these tumors contain cysts lined by epidermis replete with adnexal appendages—hence the common designation dermoid cysts.
➢ Most are discovered in young women as ovarian masses or are found incidentally on abdominal radiographs or scans because they contain foci of calcification produced by toothlike structures contained within the tumor |
| How is presentation of benign cystic teratomas? | ➢ About 90% are unilateral, with the right side more commonly affected. Rarely do these cystic masses exceed 10 cm in diameter.
➢ On cut section, they often are filled with sebaceous secretion and matted hair that, when removed, reveal a hair-bearing epidermal lining (
➢ Sometimes there is a nodular projection from which teeth protrude.
➢ Occasionally, foci of bone and cartilage, nests of bronchial or gastrointestinal epithelium, or other tissues are present.
➢ These neoplasms sometimes produce infertility and are prone to undergo torsion (in 10%–15% of cases.
➢ Limbic encephalitis, may develop in women with teratomas containing mature neural tissue and often remits with tumor resection (Paraneoplastic complication.).
➢ Malignant transformation, usually to a squamous cell carcinoma, is seen in about 1% of cases. |
| What are immature malignant teratomas? | ➢ Found early in life, the mean age at clinical detection being 18 years.
➢ They typically are bulky and appear solid on cut section, and they often contain areas of necrosis;
➢ Uncommonly, cystic foci are present that contain sebaceous secretion, hair, and other features similar to those of mature teratomas.
➢ On microscopic examination, the distinguishing feature is the presence of immature elements or minimally differentiated cartilage, bone, muscle, nerve, or other tissues.
➢ As with other tumors, the prognosis depends on grade and stage. |
| What are specialized teratomas? | ➢ A rare subtype of teratoma is composed entirely of specialized tissue.
➢ The most common example is struma ovarii, which is
composed entirely of mature thyroid tissue that may actually
produce hyperthyroidism.
➢ These tumors appear as small, solid, unilateral brown ovarian masses.
➢ Other specialized teratomas include ovarian carcinoid, which in rare instances produces carcinoid syndrome |
| What is dysgerminoma? | ➢ Young patients, aged 30 years
➢ 5% of abnormal gonades (dysgenesis)
➢ Macros: Large size, encapsulated, surface boxed. Tranche de section: solid, gray
➢ History:
Nids of cells in strongly nucleid noxious cells Tractus fibers infiltrated by lymphocytes/ |
| What is yolk sac tumor? | ➢ 19 years old
➢ High AFP
➢ Macro:
Large size, smooth shiny external surface. Section: partially cystic, foci of hemorrhage and necrosis
➢ History:
Variable: reticulate/microcystic/solid/pseudopapillae architecture (body of Schiller Duval) |
| What is embryonal carcinoma? | ➢ 15 years
➢ High chorionic gonadotropin, AFP+-
➢ Macro:
Large size, smooth external surface, Section slice: solid, hemorrhagic areas
➢ History: Sheets of poorly differentiated primitive cells |
| What is choriocarcinoma? | ➢ Most often: uterine tumor metastases
➢ History:
Association of syncytial and cytotrophoblastic elements, background necrotic and hemorrhagic |
| What is granulosa cell tumor? | ➢ Divided into Adult Type and Juvenile Type
– Adult type:
• Increased estrogen secretion
• Macro:
smooth lobulated external surface, solid section edge
• History:
variable: microfollicular, macrofollicular, trabecular, insular,
diffuse. Cells with incised nuclei in coffee beans
➢ Juvenile type:
– First 2 decades
– At the same stage, more aggressive than the adult granulosa (meta +++)
– History:
Diffuse, macrofollicular,
No nuclear incisions |
| What are disorders of early pregnancy? | spotaneous abortions, ectopic pregnancy |
| What is spontaneous abortion? | ➢ Spontaneous abortion, or “miscarriage,” is defined as pregnancy loss before 20 weeks of gestation.
➢ Most of these occur before 12 weeks.
➢ 10 to 15% of clinically recognized pregnancies terminate in spontaneous abortion. ➢ Multiple fetal and maternal causes of spontaneous abortion have been identified:
• Fetal chromosomal anomalies: aneuploidy,polyploidy, and translocations, are present in approximately 50% of early abortuses.
• Maternal endocrine factors: luteal-phase defect, poorly controlled diabetes, and other uncorrected endocrine disorders
• Physical defects of the uterus: submucosal leiomyomas, uterine polyps, or uterine malformations, may prevent or disrupt implantation
• Systemic disorders affecting the maternal vasculature: antiphospholipid antibody syndrome, coagulopathies, and hypertension
• Infections with protozoa (Toxoplasma), bacteria (Mycoplasma, Listeria), or a number of viruses
Ascending infection is particularly common in second trimester losses |
| What is ectopic pregnancy? | ➢ Ectopic pregnancy is defined as implantation of a fertilized ovum in any site other than the uterus.
➢ May occur in as many as 1% of pregnancies.
➢ Fallopian tube: more than 90% of these cases, (tubal pregnancy);
➢ Ovaries: probably result from rare instances in which the ovum is fertilized just as the follicle ruptures.
➢ Abdominal cavity: occurs when the fertilized egg drops out of the fimbriated end of the fallopian tube and implants on the peritoneum.
➢ Any factor that retards passage of the ovum through the fallopian tube predisposes to ectopic pregnancy.
➢ In about half of the cases, slowed passage results from chronic inflammation and scarring in the oviduct; intrauterine tumors and endometriosis may also hamper passage of the ovum.
➢ In the other 50% of tubal pregnancies, no anatomic cause is evident. |
| How is presentation of ectopic pregnancy? | ➢ Until rupture occurs, an ectopic pregnancy may be
indistinguishable from a normal pregnancy, with cessation of menstruation and elevation of serum and urinary placental hormones.
➢ Under the influence of these hormones, the endometrium (in approximately 50% of cases) undergoes the characteristic hypersecretory and decidual changes of pregnancy.
➢ The absence of elevated gonadotropin levels does not exclude the diagnosis because poor attachment and necrosis of the ectopic placenta are common.
➢ Rupture of an ectopic pregnancy is a medical emergency that, if left untreated, may result in exsanguination and death. |
| How is morphology of ectopic pregnancy? | ➢ In all sites, early development of ectopic pregnancies proceeds normally, with formation of placental tissue, the amniotic sac, and decidual changes.
➢ With tubal pregnancies, the invading placenta eventually
burrows through the wall of the fallopian tube, causing
intratubal hematoma (hematosalpinx), intraperitoneal
hemorrhage, or both.
➢ The tube is usually distended by freshly clotted blood
containing bits of gray placental tissue and fetal parts.
➢ The histologic diagnosis depends on visualization of
placental villi or, rarely, of the embryo |
| What are disorders of late pregnancy? | Twin Placentas
Abnormalities of Placental Implantation
Placental Infections
Preeclampsia and Eclampsia |
| What are abnormalities of placental implantation? | ➢ Placenta previa is a condition in which the placenta implants in the lower uterine segment or cervix, often leading to serious thirdtrimester bleeding.
– A complete placenta previa covers the internal cervical os
→requires delivery via cesarean section to avert placental rupture and fatal maternal hemorrhage during vaginal delivery.
➢ Placenta accreta: is caused by partial or complete absence of the decidua, → the placental villous tissue adheres directly to the myometrium
→ failure of placental separation at birth.
– Important cause of severe, potentially lifethreatening postpartum bleeding.
– Common predisposing factors : placenta previa (in up to 60% of cases) and history of previous cesarean section |
| What is twin placentas? | ➢ Twin pregnancies arise from fertilization of two ova (dizygotic) or from division of one fertilized ovum (monozygotic).
➢ There are three basic types of twin placentas:
– diamnionic dichorionic (which may be fused),
– diamnionic monochorionic, and
– monoamnionic monochorionic.
➢ Monochorionic placentas imply monozygotic (identical) twins, and the time at which splitting of the developing embryo occurs determines whether one or two amnions are present.
➢ Dichorionic placentation may occur with either monozygotic or dizygotic twins and is not specific |
| What are placental inflammations and infections? | Infections may reach the placenta by either of two paths:
(1) ascension through the birth canal or
(2) hematogenous (transplacental) spread.
Ascending infections are by far the more common;
➢ in most instances they are bacterial and are associated with premature rupture of the fetal membranes.
➢ On microscopic examination, the chorioamnion shows neutrophilic infiltration associated with edema and congestion (acute chorioamnionitis).
➢ With extension beyond the membranes, the infection may involve the umbilical cord and placental villi, resulting in acute vasculitis of the cord (funisitis).
➢ Ascending infections are caused by Mycoplasma, Candida, and bacteria of the vaginal flora |
| How is hematogenous spread of placental infections? | Uncommonly, placental infections may arise by hematogenous spread of bacteria and other organisms;
➢ on histologic examination, placental villi are the most
frequently affected structures (villitis)
➢ Syphilis, tuberculosis, listeriosis, toxoplasmosis, and various viruses (rubella, cytomegalovirus, herpes simplex virus) all can cause placental villitis.
➢ Transplacental infections can affect the fetus and give rise to the so-called “TORCH” complex (toxoplasmosis, other
infections, rubella, cytomegalovirus infection, herpes). |
| What is preeclampsia/ecclampsia? | ➢ The development of hypertension, accompanied by
proteinuria and edema in the third trimester of pregnancy,
is referred to as preeclampsia.
➢ This syndrome occurs in 5% to 10% of pregnancies,
particularly with first pregnancies in women older than 35
years.
➢ In those severely affected, seizures may occur, and the
symptom complex is then termed eclampsia.
➢ Prompt therapy early in the course aborts the associated organ changes, with all abnormalities resolving promptly after delivery or after cesarean section.
➢ Recognition and early treatment of preeclampsia have now made eclampsia, particularly fatal eclampsia, rare. |
| What are causes leading to preeclampsia? | ➢ While exact triggering events initiating these syndromes are unknown, a common feature underlying all cases is insufficient maternal blood flow to the placenta secondary to inadequate remodeling of the spiral arteries of the uteroplacental vascular bed.
➢ Although the exact basis of preeclampsia remains to be further defined, several serious consequences have been associated with this condition:
➢ Placental infarction, stemming from chronic hypoperfusion
• Hypertension, resulting from reduced endothelial production of the vasodilators prostacyclin and prostaglandin E2 and from increased production of the vasoconstrictor thromboxane A2
• Hypercoagulability, due to endothelial dysfunction and release of tissue factor from the placenta
• End-organ failure, most notably of the kidney and the liver, which occurs in patients with full-blown eclampsia |
| What is HELLP syndrome? | Approximately 10% of the patients with severe preeclampsia develop the so-called “HELLP syndrome”:
→elevated liver enzymes,
→microangiopathic hemolytic anemia,
→thrombocytopenia due to platelet consumption,
→sometimes fullblown disseminated intravascular coagulation (DIC). |
| What are placental abnormalities of ecclampsia? | The morphologic changes of preeclampsia and eclampsia are variable and correlate to some degree with the severity of the disorder. Placental abnormalities include
• Infarcts, which can be a feature of normal pregnancy, but are much more numerous with severe preeclampsia or eclampsia
• Retroplacental hemorrhages
• Premature maturation of placental villi associated with
villous edema, hypovascularity, and increased production of syncytial epithelial knots
• Fibrinoid necrosis and focal accumulation of lipid-containing macrophages (acute atherosis) of decidual vessels |
| What is gestational trophoblastic disease? | ➢ Gestational trophoblastic disease refers to an abnormal
proliferation of fetal trophoblast cells.
➢ The WHO divides these diseases into two categories: molar lesions and nonmolar lesions.
➢ The molar lesions are further divided into partial, complete, and invasive hydatidiform moles.
➢ The nonmolar category consists of choriocarcinoma and other more uncommon types of trophoblast-derived malignancies.
➢ All elaborate human chorionic gonadotropins (hCG), which is detected in the blood and urine at levels considerably higher than those found during normal pregnancy.
➢ In addition to aiding diagnosis, hCG levels in the blood or urine can be used to monitor treatment efficacy |
| What is hydatidiform mole (complete and partial)? | ➢ The typical hydatidiform mole is a voluminous mass of swollen, sometimes cystically dilated, chorionic villi, appearing grossly as grapelike structures.
➢ Varying amounts of normal to highly atypical chorionic epithelium cover the swollen villi.
➢ There are two distinctive subtypes of hydatidiform moles: complete and partial.
➢ Complete hydatidiform moles are not compatible with
embryogenesis and rarely contain fetal parts. All of the chorionic villi are abnormal, and the chorionic epithelial cells are diploid (46,XX or, uncommonly, 46,XY).
➢ The partial hydatidiform mole is compatible with early embryo formation and therefore may contain fetal parts, has some normal chorionic villi, and is almost always triploid (e.g., 69,XXY)
➢ Both types result from abnormal fertilization with an excess of paternal genetic material.
➢ In a complete mole the entire genetic content is supplied by two spermatozoa (or a diploid sperm), yielding diploid cells containing only paternal chromosomes.
➢ Whereas in a partial mole a normal egg is fertilized by two spermatozoa (or a diploid sperm), resulting in a triploid karyotype with a preponderance of paternal genes. |
| How is incidence of hydatidiform mole? | ➢ The incidence of complete hydatidiform mole is about 1 to 1.5 per 2000 pregnancies in the United States and other Western countries.
➢ For unknown reasons, the incidence is much higher in Asian countries.
➢ Moles are most common before the age of 20 and after the age of 40 years, and a history of the condition increases the risk for molar disease in subsequent pregnancies.
➢ Although molar disease formerly was discovered at 12 to 14 weeks of pregnancy during investigation for a gestation that was “too large for dates,” early monitoring of pregnancies by ultrasound has lowered the gestational age at detection.
➢ In both complete and partial moles, elevation of hCG in the maternal blood and absence of fetal heart sounds are typical. |
| How is morphology of hydatidiform mole? | ➢ In advanced cases the uterine cavity is expanded by a delicate, friable mass of thin-walled, translucent cystic structures.
➢ Fetal parts are rarely seen in complete moles but are common in partial moles.
➢ On microscopic examination, the complete mole shows hydropic swelling of poorly vascularized chorionic villi with a loose, myxomatous, edematous stroma.
➢ The chorionic epithelium typically shows a proliferation of both cytotrophoblasts and syncytiotrophoblasts .
➢ Histologic grading to predict the clinical outcome of moles has been supplanted by monitoring of hCG levels
➢ In partial moles, villous edema involves only a subset of the villi, and the trophoblastic proliferation is focal and slight.
➢ In most cases of partial mole, some fetal cells are present, ranging from fetal red cells in placental villi to, in rare cases, a fully formed fetus.
➢ Overall, 80% to 90% of moles do not recur after thorough curettage, but 10% of complete moles are invasive.
➢ No more than 2% to 3% give rise to choriocarcinoma. |
| what is invasive mole? | ➢ Invasive moles are complete moles that are locally invasive but lack the metastatic potential of choriocarcinoma.
➢ An invasive mole retains hydropic villi, which penetrate the uterine wall deeply, possibly causing rupture and sometimes life-threatening hemorrhage.
➢ On microscopic examination, the epithelium of the villi shows atypical changes, with proliferation of both trophoblastic and syncytiotrophoblast components.
➢ Although the marked invasiveness of this lesion makes
removal technically difficult, metastases do not occur.
➢ Hydropic villi may embolize to distant organs, such as lungs or brain, but these emboli do not behave like true metastases and may regress spontaneously.
➢ Because of deeper invasion into the myometrium, an invasive mole is difficult to remove completely by curettage, so if serum β-hCG remains elevated, further treatment is required.
➢ Fortunately, in most cases cure is possible with chemotherapy. |
| What is gestational choriocarcinoma? | ➢ Choriocarcinoma, a very aggressive malignant tumor, arises from gestational chorionic epithelium or, less frequently, from totipotential cells within the gonads (as a germ cell tumor).
➢ They are rare tumors.
➢ Approximately 50% of choriocarcinomas arise from complete hydatidiform moles.
➢ About 25% arise after an abortion.
➢ The remainder manifest following an apparently normal pregnancy.
➢ In most cases, choriocarcinoma presents as a bloody, brownish discharge accompanied by a rising titer of β-hCG in blood and urine, in the absence of marked uterine enlargement, such as would be seen with a mole.
➢ In general, the β-hCG titers are much higher than those associated with a mole |
| How is morphology of gestational choriocarcinoma? | ➢ Choriocarcinomas usually appear as hemorrhagic, necrotic uterine masses.
➢ Sometimes the necrosis is so extensive that little viable tumor remains.
➢ The primary lesion may “selfdestruct,” and only the metastases tell the story.
➢ Very early, the tumor insinuates itself into the myometrium and into vessels.
➢ In contrast with hydatidiform moles and invasive moles, chorionic villi are not formed; instead, the tumor is composed of anaplastic cuboidal cytotrophoblasts and syncytiotrophoblasts.
➢ By the time a choriocarcinoma is discovered, widespread vascular spread usually has occurred to the lungs (50%), vagina (30%–40%), brain, liver, or kidneys.
➢ Lymphatic invasion is uncommon. |
| What are clinical features of gestational choriocarcinoma? | ➢ Despite the extremely aggressive nature of placental
choriocarcinoma, these tumors are remarkably sensitive to
chemotherapy.
➢ Nearly 100% of affected patients are cured, even those with metastases at distant sites such as the lungs.
➢ By contrast, response to chemotherapy with choriocarcinomas that arise in the gonads (ovary or testis) is relatively poor. |
| What are placental site trophoblastic tumor? | ➢ Placental site trophoblastic tumors are derived from the placental site or intermediate trophoblast, a cell that has morphologic and functional features that overlap with those of trophoblasts and syncytiotrophoblasts.
➢ These uncommon diploid tumors, often XX in karyotype, typically arise a few months after pregnancy.
➢ Because intermediate trophoblasts do not produce hCG in large amounts, hCG concentrations are only slightly elevated.
➢ These tumors produce human placental lactogen.
➢ An indolent clinical course is typical, with a generally favorable outcome if the tumor is confined to the endomyometrium.
➢ Not as sensitive to chemotherapy as are other trophoblastic tumors, and the prognosis is poor when spread occurs beyond the uterus |
