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Review
. 2019 Nov 28:9:937.
doi: 10.3389/fonc.2019.00937. eCollection 2019.

A Review on the Pathogenesis and Clinical Management of Placental Site Trophoblastic Tumors

Xuan Feng  1   2   3 , Zhi Wei  1   2   3 , Sai Zhang  1   2   3 , Yan Du  1   2   3 , Hongbo Zhao  1   2   3
Affiliations
Review

A Review on the Pathogenesis and Clinical Management of Placental Site Trophoblastic Tumors

Xuan Feng et al. Front Oncol. .

Abstract

Placental site trophoblastic tumor (PSTT) is a rare type of gestational trophoblastic disease originating from the intermediate trophoblast. Compared with hydatidiform mole, invasive hydatidiform mole and choriocarcinoma, the diagnosis of PSTT is more complicated and lacks specific and sensitive tumor markers. Most PSTT patients demonstrate malignant potential, and the primary treatment of PSTT is hysterectomy. However, metastasis occasionally occurs and even causes death in a small number of PSTT patients. Most PSTT patients are young women hence fertility preservation is an important consideration. The major obstacle for PSTT patient prognosis is chemotherapy resistance. However, the current understanding of the pathogenesis of PSTT and clinical treatment remains elusive. In this review, we summarized the research progress of PSTT in recent years from three aspects: mechanism, clinical presentation, and treatment and prognosis. Well-conducted multi-center studies with sufficient sample sizes are of great importance to better examine the pathological progress and evaluate the prognosis of PSTT patients, so as to develop prevention and early detection programs, as well as novel treatment strategies, and finally improve prognosis for PSTT patients.

Keywords: clinical presentation; mechanism; placenta site trophoblastic tumor; prognosis; treatment.

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Figures

Figure 1
Figure 1
Origin of PSTT. (A) PSTT originates from extravillous trophoblasts, and then acquires the abilities of proliferation and migration. Afterwards, those cells migrate away from placenta and invade the decidual artery and uterine spiral artery to remodel the blood vessels which in turn provide nutrition for the embryo. The disruption of this well-regulated invasion process may lead to PSTT. (B) During delivery, placenta detaches from decidual, leaving small nodules and form placental site nodules in the myometrium. In the process of reabsorbing, some adverse trigger or stimuli may cause atypical mitosis and result in neoplasm.
Figure 2
Figure 2
Molecular mechanism of PSTT. PI3K/AKT and MAPK are important molecular pathways in PSTT. Over-expression of molecules, such as FBI-1 and P21 can activate kinases, such as PAK and AKT in gestational trophoblastic tumor cells and consequently cause changes in the adhesion-associated and cell cycle regulation proteins, resulting in alterations of biological behaviors including invasion and proliferation of PSTT.
Figure 3
Figure 3
Histopathological features of PSTT. Tumor cells present monomorphic population of large polyhedral cells with irregular hyperchromatic nuclei, which are at different stages of mitosis. Besides, there is eosinophilic or transparent substance in the cytoplasm that could be large amount of fibrin. Tumor cells grow like nest or bands into myometrium, with a handful of bleeding foci and mild inflammation or necrosis.
Figure 4
Figure 4
Imaging features of PSTT. (A) Ultrasound feature of PSTT: the mass shows as a mixed mass with intact capsule and presents as echogenic bulk. (B) Ultrasound feature of PSTT: formation of arteriovenous fistula can be observed. (C,D) MRI imaging of sagittal position: PSTT presents as uterine dilatation with short T1 and long T2 signals. (E,F) MRI imaging of axial position. (G) Enhancement imaging: the parauterine artery can be observed.
Figure 5
Figure 5
Schematic presentation of PSTT diagnosis, treatment, and prognosis.
See this image and copyright information in PMC

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