Project description:Gene expressions obtained from the total RNA sequencing of 2 choriocarcinomas, 4 epithelioid trophoblastic tumors, and 4 placental site trophoblastic tumors were evaluated for differential gene expression, pathway alteration, fusion gene, infiltrating immune cell type, and PD-L1 expression level, and mutation analysis was performed using the RNA sequencing data.
Project description:Purpose was to determine whether varying gestational trophoblastic disease samples exhibit differences in RNA expression and fusion transcripts.
Project description:The term gestational trophoblastic disease (GTD) describes a range of pathologies derived from the villous trophoblasts of the placenta. These include benign entities such as partial and complete hydatidiform mole as well as invasive cancers such as gestational choriocarcinoma, placental site trophoblastic tumors, and epithelioid trophoblastic tumors. Collectively, the malignant forms of GTD are known as gestational trophoblastic neoplasia (GTN). The risk of GTN following a complete molar pregnancy ranges between 8-25%. Low risk patients are expected to have a high likelihood of response to single agent chemotherapy with methotrexate or actinomycin D, but the incidence of resistance to single agent chemotherapy among low risk patients remains 25-50%. We used gene expression microarrays to compare methotrexate sensitive trophoblastic cell lines to sublines that were conditioned to become methotrexate resistant.
Project description:The human placenta is covered by a single multinucleated fetal cell, the syncytiotrophoblast, which is bathed in maternal blood. During all pregnancies, membrane enclosed extracellular vesicles derived from the syncytiotrophoblast are extruded into the maternal blood.The large size of these extracellular vesicles (diameter larger than 10µm) is referred to as trophoblastic debris in this study. We have shown in the past that endothleial cells are involved in clearence of this trophoblastic debris and induction of immune tolerence by trophoblastic debris.This study aimed to characterise the transcriptional changes that occur in human vascular endothelial cells following exposure to trophoblastic debris from normal first trimester placentae. Microarrays were used to probe transcriptomic changes 2 and 21 hours after exposure of endothelial cells (Human microvascular endothelial cell line,HMEC-1) to trophoblastic debris from normal first trimester placentae
Project description:The human placenta is covered by a single multinucleated fetal cell, the syncytiotrophoblast, which is bathed in maternal blood. During all pregnancies, membrane enclosed extracellular vesicles derived from the syncytiotrophoblast are extruded into the maternal blood.The large size of these extracellular vesicles (diameter larger than 10µm) is referred to as trophoblastic debris in this study. We have shown in the past that endothleial cells are involved in clearence of this trophoblastic debris and induction of immune tolerence by trophoblastic debris.This study aimed to characterise the transcriptional changes that occur in human vascular endothelial cells following exposure to trophoblastic debris from normal first trimester placentae. Microarrays were used to probe transcriptomic changes 2 and 21 hours after exposure of endothelial cells (Human microvascular endothelial cell line,HMEC-1) to trophoblastic debris from normal first trimester placentae Trophoblastic debris were isolated by low speed centrifugation from three individual first trimester human placentae (three biological replicates). The protein content in trophoblastic debris was measured by BCA assay. HMEC-1 was co-cultured with trophoblastic debris (60ug/ml total debris protein contents) for either 2 or 21 hours before RNA extraction. Untreated HMEC-1 at 2 and 21 hours were used as controls.In total, 12 samples were analyzed.
Project description:As epithelioid trophoblastic tumor (ETT) shares similar clinical features with other gestational trophoblastic neoplasms (GTNs), it is likely to be clinically misdiagnosed and subsequently treated in an improper way. This study aimed to identify the sonographic features of ETT that are distinct from other GTNs, including placental site trophoblastic tumor (PSTT) and invasive mole/choriocarcinoma (IM/CC). Here, we retrospectively analyzed ultrasound images of 12 patients with ETT in comparison with those of 21 patients with PSTT and 24 patients with IM/CC. The results showed that maximal diameter and hemodynamic parameters were not significantly different among ETT, PSTT and IM/CC (P>0.05). However, a well-circumscribed border with hypoechogenic halo was identified in the gray-scale sonogram in all 12 cases of ETT, while only in 1 out of 21 cases of PSTT and 1 out of 16 cases of IM/CC (P<0.001 for ETT vs. PSTT or IM/CC). Moreover, a peripheral pattern of Doppler signals was observed in 11 out of 12 ETT lesions, showing relatively more Doppler signal spots around the tumor border than within the boundary, while a non-peripheral pattern of Doppler signals in all 21 PSTT cases and 14 out of 16 IM/CC cases: with minimal, moderate or remarkable signal spots within the tumor, but not along the tumor (P<0.001 for ETT vs. PSTT or IM/CC). These distinct sonographic features of ETT correlated with histopathologic observations, such as expansive growth pattern and vascular morphology. Thus, we draw the conclusions that the well-circumscribed border with peripheral Doppler signal may serve as a reliable sonographic feature to discriminate ETT from other types of GTNs. With further validation in a larger patient set in our ongoing multi-center study, this finding will be potentially developed into a non-invasive pre-operative GTN subtyping method for ETT.