Gestational Trophoblastic Neoplasia
Pat Price, Karol Sikora in Treatment of Cancer, 2020
Gestational choriocarcinoma is the most aggressive form of gestational trophoblastic disease (GTD). Most choriocarcinomas have been shown to have grossly abnormal karyotypes with diverse ploidies and several chromosome rearrangements, none of which is specific for the disease. Heavy vaginal or intra-peritoneal bleeding is the most frequent immediate threat to life in patients with trophoblastic tumors. Furthermore, the levels of human chorionic gonadotrophin (hCG) produced by GTD are frequently identical to those found in normal pregnancy, although very high levels outside the range for a twin pregnancy may lead to suspicion of a trophoblastic tumor. GTD comprises two pre-malignant diseases, termed complete and partial hydatidiform mole (CHM and PHM), and the four malignant disorders, or gestational trophoblastic tumors: invasive mole, gestational choriocarcinoma, placental-site trophoblastic tumor, and epithelioid trophoblastic tumor. Most patients with low-risk disease have had a CHM or PHM as the antecedent pregnancy and require a history and physical examination followed by routine blood tests, including a serum hCG sample.
Endocrine tumors in pregnancy
Nadia Barghouthi, Jessica Perini in Endocrine Diseases in Pregnancy and the Postpartum Period, 2021
Gestational trophoblastic disease refers to a number of interrelated tumors arising from the placental villous trophoblastic tissue, including benign hydatidiform molar pregnancies and malignant conditions including invasive mole, choriocarcinoma, and placental site trophoblastic tumors. Treatment includes evacuation of pregnancy and serial monitoring of hCG levels. In the case of choriocarcinoma, chemotherapy and/or surgery may be required. Gestational trophoblastic disease refers to interrelated tumors arising from the placental villous trophoblastic tissue. Symptoms that raise suspicion for molar pregnancies include vaginal bleeding, uterine size out of proportion to gestational dating, and significantly elevated human chorionic gonadotropin levels. The result is focal and mild hyperplasia of trophoblastic elements and a mixture of normal and hydropic chorionic villi. Amniotic membranes and fetal tissue are both present. However, given the triploid nature, fetal development is typically severely hindered by congenital anomalies and is often nonviable.
Ultrasound Features of Gestational Trophoblastic Disease
Juan Luis Alcázar in Ultrasound Assessment in Gynecologic Oncology, 2018
This chapter reviews the ultrasound features of Gestational trophoblastic disease (GTD). GTD comprises a group of disorders arising from uncontrolled growth of placental trophoblastic tissue, with a spectrum of placental lesions including premalignant hydatiform mole and malignant invasive hydatiform mole, placental site trophoblastic tumor, epithelioid trophoblastic tumor, and choriocarcinoma. The diagnosis of GTD is mainly based on the human chorionic gonadotropin serum levels. Betel et al. reported that the sonographic features that predicted GTD were a myometrial epicenter, depth of myometrial invasion of more than one-third, placental venous lakes, maximum mass dimensions of more than 3.45 cm, and maximum endometrial thickness of less than 12 mm. The typical ultrasound appearance of a complete hydatiform mole is an enlarged uterus with the uterine cavity filled with multiple sonolucent areas of varying size and shape, the "snowstorm" appearance, without any embryonic or fetal structure.
NK and trophoblast cells interaction: cytotoxic activity on recurrent pregnancy loss
Published in Gynecological Endocrinology, 2019
Dmitriy I. Sokolov, Valentina A. Mikhailova, Alana O. Agnayeva, Dmitry O. Bazhenov, Evgeniya V. Khokhlova, Olesya N. Bespalova, Aleksandr M. Gzgzyan, Sergey A. Selkov
The trial objective was to determine the peripheral blood NK cells cytotoxic activity effect on trophoblast cells at recurrent pregnancy loss (RPL). The investigation involved non-pregnant women with PRL in proliferating and secretory menstrual cycle phases (PMCPh and SMCPh, respectively); women of 6–7 weeks pregnancy with RPL in past medical history; healthy fertile non-pregnant women in PMCPh and SMCPh, women of 6–7 weeks physiological pregnancy, nulliparity healthy women with regular menstrual function in PMCPh and SMCPh. NK cells cytotoxic activity was determined using peripheral blood mononuclear cells. The target cells were JEG-3 line trophoblasts. It has been established that NK cells cytotoxic activity effect on trophoblasts is lower in SMCPh than in PMCPh in non-pregnant fertile women. The NK cells cytotoxic activity was higher in SMCPh than in PMCPh in non-pregnant women with PRL and also higher than the same value in SMCPh in non-pregnant fertile women. The increased NK cells cytotoxic activity values in SMCPh in women with RPL may be the reason for miscarriage.
The Trophoblast Model of Cancer
Published in Nutrition and Cancer, 2015
John Beard, the British embryologist and histologist, first proposed his trophoblast model of cancer in 1902. The model has subsequently been expanded by Kelley, and in current times, Gonzalez and Isaacs. The trophoblast model of cancer can be stated as a specified, scientifically testable model, including its core predictions that 1) adult stem cells are ectopic trophoblasts that have migrated to other tissues early in embryogenesis; 2) pancreatic enzymes are the key signal that converts the trophoblast into the stable placenta; 3) cancer arises from trophoblasts that have escaped regulatory control; and 4) pancreatic enzymes can be used to treat cancer. The author reviewed the literature on the trophoblast model of cancer and the use of pancreatic enzymes for the treatment of cancer and organized its key tenets into a set of specified scientific hypotheses. The trophoblast model of cancer can be stated as a set of 11 core predictions and 3 adjunctive or nonessential components. The trophoblast model of cancer is a detailed, testable model that should be investigated within an overlapping set of fields including oncology, histology, physiology, molecular biology, and embryology.
Receptor expression by JEG-3 trophoblast cells in the presence of placenta secreted factors
Published in Gynecological Endocrinology, 2019
Dmitry O. Bazhenov, Kseniya N. Furaeva, Olga I. Stepanova, Larisa P. Viazmina, Anastasiya R. Sheveleva, Evgeniya V. Khokhlova, Valentina A. Mikhailova, Sergey A. Selkov, Dmitry I. Sokolov
Preeclampsia still remains one of the most severe pregnancy complications and is an actual problem in the obstetrics practice. At present, the joint impact of cytokines and other placenta secreted factors on trophoblast cell functional activity during preeclampsia complicated pregnancy remains unclear. The aim of the study is to estimate the surface receptors expression by trophoblast cells in the presence of placenta secreted factors during physiological pregnancy and at preeclampsia. Trophoblast cells of the JEG-3 line were incubated in the presence of supernatants obtained by cultivation of placentas from women with physiological pregnancy and with preeclampsia. Surface receptors expression by trophoblast cells was estimated by FACS Canto II flow cytometer. It was established that in the third trimester both under normal and pathological conditions, the placenta secreted factors impact on the cytokine receptor expression by trophoblast differs while the trophoblast response capacity to the migration and proliferation stimulating and inhibiting signals remains stable. JEG-3 line cells enhanced the expression of CD186, CD140a, Integrin β6, VE-cadherin, CD29, and CD140a in the case of incubation in the presence of placenta supernatants from the third-trimester pregnancy complicated with preeclampsia compared to incubation in the presence of placenta supernatants form the third trimester of physiological pregnancy.