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Trophoblastic neoplasia
Trophoblast Research 8:423-424,1994
TROPHOBLASTIC
NEOPLASIA
- A Workshop Report -
Donald Goldstein ~ and Hiroaki Soma 2
1Department of Obstetrics and Gynecology Harvard Medical School 25 Sunset Street Boston, Massachusetts 02120 USA 2Department of Obstetrics and Gynecology Tokyo Medical College Hospital Tokyo 160, Japan The workshop on trophoblastic neoplasia was conducted by Dr. Goldstein (Boston, MA) who addressed a keynote about historical progress in diagnosis and chemotherapy for trophoblastic disease. Although gestational trophoblastic disease has been presently classified into hydatidiform moles (complete and partial), invasive mole and choriocarcinoma, in addition to persistent trophoblastic disease, the whole aspect of these diseases have been gradually brought to light by recent morphological, epidemiological, immunohistochemical, endocrinological, ultrasonar, radiological, as well as cytogenetic studies, while there still exists ambiguous identities which do not show clear-cut definition among these diseases. Most epidemiological studies concerning hydatidiform mole have not separated complete and partial moles. It is now accepted that complete and partial moles are not only cytogenetically different in origin, but also both moles are different in clinical sequelae following evacuation of the moles. According to the statistical report registered by the Japanese Trophoblastic Disease Committee, the frequency of complete and partial moles ranged from 2.35 and 0.57 in 1000 births in 1981 to 1.98 and 0.88 in 1000 births in 1983, respectively. The ratio of both moles is now approaching. Dr. Hiroaki Soma (Tokyo, Japan) proposed some questionable points about partial mole as follows: 1) histogenesis and clinical criteria of partial mole, 2) genetic and histochemical differentiation of partial mole from complete mole and spontaneous hydropic abortion, and 3) malignant progression of partial mole. Progress in techniques for first trimester prenatal diagnosis and improved surveillance through prenatal chromosomal analysis, ultrasound scan, maternal serum hCG, and serum AFP screening has created a complex situation, allowing confirmation of hydatidiform mole with a coexisting fetus.
424
Goldstein and S o m a
Since hCG and LH have identical alpha chains, most tests do not differentiate between the two gonadotropins. However, beta chains of hCG and LH are not the same. A specific beta subunit assay for hCG that allows precise hCG determination to a level approaching zero is available. Because the titers drop to a very low level, a nonspecific pregnancy test cannot be utilized because of cros s reactivity with LH. Recently the hCG-CTP test (EIA) has been developed. The polyclonal antibody being recognizable hCB-[3 subunit carboxyl terminal peptide is used, thereby the sensitivity of hCG-CTP test to detect hCG in serum and urine is less than 0.2 mIU/ml, and the crossreactivity for LH is extremely low and nearly negligible. Ascertainment of a partial mole has been a problem. Series of partial mole with follow up information have either emphasized triploidy of were based on morphologic classification without cytogenetics. DNA flow cytometry has been shown to be a rapid and inexpensive technique for determining nuclear ploidy. It can be applicable as an alternative to cytogenetics. If morphologic features are the basis of partial mole diagnosis, DNA ploidy can serve to separate mole subsets without bias. A combination of chromosomal or DNA and morphologic evaluation is required for accurate assessment of biological potential in molar disease. DNA fingerprint method is available for distinguishing partial mole from complete mole. Dr. Toshio Hata (Saitama, Japan) presented a case of choriocarcinoma with coexistent normal pregnancy. The patient was delivered of a premature female infant by cesarean section at 29 weeks because of extensive pulmonary metastases, thereby choriocarcinoma lesions were found in enlarged cystic ovaries. The placenta was grossly normal, but on microscopic examination, choriocarcinoma foci mixed with normal chorionic villi were also detected. To determine the genetic origin of choriocarcinoma occurring during pregnancy, DNA fingerprint method was performed. As a result, it was presumed that intraplacental choriocarcinoma might be derived form ovarian choriocarcinoma.
TROPHOBLASTIC
NEOPLASIA
- A Workshop Report -
Donald Goldstein ~ and Hiroaki Soma 2
1Department of Obstetrics and Gynecology Harvard Medical School 25 Sunset Street Boston, Massachusetts 02120 USA 2Department of Obstetrics and Gynecology Tokyo Medical College Hospital Tokyo 160, Japan The workshop on trophoblastic neoplasia was conducted by Dr. Goldstein (Boston, MA) who addressed a keynote about historical progress in diagnosis and chemotherapy for trophoblastic disease. Although gestational trophoblastic disease has been presently classified into hydatidiform moles (complete and partial), invasive mole and choriocarcinoma, in addition to persistent trophoblastic disease, the whole aspect of these diseases have been gradually brought to light by recent morphological, epidemiological, immunohistochemical, endocrinological, ultrasonar, radiological, as well as cytogenetic studies, while there still exists ambiguous identities which do not show clear-cut definition among these diseases. Most epidemiological studies concerning hydatidiform mole have not separated complete and partial moles. It is now accepted that complete and partial moles are not only cytogenetically different in origin, but also both moles are different in clinical sequelae following evacuation of the moles. According to the statistical report registered by the Japanese Trophoblastic Disease Committee, the frequency of complete and partial moles ranged from 2.35 and 0.57 in 1000 births in 1981 to 1.98 and 0.88 in 1000 births in 1983, respectively. The ratio of both moles is now approaching. Dr. Hiroaki Soma (Tokyo, Japan) proposed some questionable points about partial mole as follows: 1) histogenesis and clinical criteria of partial mole, 2) genetic and histochemical differentiation of partial mole from complete mole and spontaneous hydropic abortion, and 3) malignant progression of partial mole. Progress in techniques for first trimester prenatal diagnosis and improved surveillance through prenatal chromosomal analysis, ultrasound scan, maternal serum hCG, and serum AFP screening has created a complex situation, allowing confirmation of hydatidiform mole with a coexisting fetus.
424
Goldstein and S o m a
Since hCG and LH have identical alpha chains, most tests do not differentiate between the two gonadotropins. However, beta chains of hCG and LH are not the same. A specific beta subunit assay for hCG that allows precise hCG determination to a level approaching zero is available. Because the titers drop to a very low level, a nonspecific pregnancy test cannot be utilized because of cros s reactivity with LH. Recently the hCG-CTP test (EIA) has been developed. The polyclonal antibody being recognizable hCB-[3 subunit carboxyl terminal peptide is used, thereby the sensitivity of hCG-CTP test to detect hCG in serum and urine is less than 0.2 mIU/ml, and the crossreactivity for LH is extremely low and nearly negligible. Ascertainment of a partial mole has been a problem. Series of partial mole with follow up information have either emphasized triploidy of were based on morphologic classification without cytogenetics. DNA flow cytometry has been shown to be a rapid and inexpensive technique for determining nuclear ploidy. It can be applicable as an alternative to cytogenetics. If morphologic features are the basis of partial mole diagnosis, DNA ploidy can serve to separate mole subsets without bias. A combination of chromosomal or DNA and morphologic evaluation is required for accurate assessment of biological potential in molar disease. DNA fingerprint method is available for distinguishing partial mole from complete mole. Dr. Toshio Hata (Saitama, Japan) presented a case of choriocarcinoma with coexistent normal pregnancy. The patient was delivered of a premature female infant by cesarean section at 29 weeks because of extensive pulmonary metastases, thereby choriocarcinoma lesions were found in enlarged cystic ovaries. The placenta was grossly normal, but on microscopic examination, choriocarcinoma foci mixed with normal chorionic villi were also detected. To determine the genetic origin of choriocarcinoma occurring during pregnancy, DNA fingerprint method was performed. As a result, it was presumed that intraplacental choriocarcinoma might be derived form ovarian choriocarcinoma.