Discovery of a Cell

Abstract

Summary In 1976, a series of 12 cases describing a lesion that had previously not been well characterized was reported as “trophoblastic pseudotumor of the uterus.” Up until that time rare reports of the lesion had classified it most often as an unusual type of sarcoma associated with pregnancy. All patients in that series were alive and well except for one who died from complications of a uterine perforation occurring at the time of a diagnostic curettage. Thus, it appeared to be a benign neoplasm but subsequently it was found that some exhibited malignant behavior and the tumor was renamed “placental site trophoblastic tumor.” A variety of observations pointed to an origin in a distinctive cell of the placental site, designated “intermediate trophoblast,” which physiologically is seen in the normal implantation site. Subsequently, another subset of intermediate trophoblast cells originating from the chorion laeve have been shown to give rise to the placental site nodule/plaque, a well-circumscribed and usually microscopic incidental finding as well as the epithelioid trophoblastic tumor, its putative malignant counterpart. The initial description of “trophoblastic pseudotumor” opened a new area of research which brought to bear immunohistochemical and molecular genetic analyses that eventually has led to new insights in the diverse morphologic changes occurring in early placentation and also led to the development of a new classification of trophoblastic tumors and tumor-like lesions.

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

“…The above process is subject to strict temporal and spatial regulation in normal placentation (17). It is considered that PSTT is caused by hyperplasia of intermediate trophoblast, while hydatidiform mole and choriocarcinoma are results of abnormal or malignant proliferation of syncytiotrophoblast and cytotrophoblast (18, 19). Others propose that PSTT forms during the process of placenta detaching from the uterus, and the small nodules of the placental tissue remaining in the myometrium, and being reabsorbed over time.…”

Novel, genetically induced mouse model that recapitulates the histological morphology and immunosuppressive tumor microenvironment of metastatic peritoneal carcinomatosis

“…In fact, approximately 75% of patients with ovarian cancer have advanced stage disease by the time the symptoms become apparent. 2 Involving both pelvic and abdominal peritoneum, these tumors commonly spread along peritoneal surfaces including the mesentery, diaphragm, omentum and surfaces of solid organs such as liver and spleen. It has been reported that less than 25% of patients with stage III/IV HGSCs will be cured by current therapies and the median survival for stage IV is 23 months.…”

“…It has been reported that less than 25% of patients with stage III/IV HGSCs will be cured by current therapies and the median survival for stage IV is 23 months. 2 Thus, there is a great need for novel approaches to treat this tumor.…”

Association between RUNX3 gene polymorphisms in severe preeclampsia and its clinical features

“…[5] In early placental development, trophoblasts are considered as “pseudo-tumor cells” and share certain similar mechanisms with malignant cells in tumorigenesis and metastasis. [6,7] It is worth noting that genetic factors are believed to be involved in the development of severe preeclampsia (SPE). [8,9]…”