Disease relevance of Trophoblastic Neoplasms

• PURPOSE: To evaluate the results of etoposide, methotrexate, and dactinomycin alternating with cyclophosphamide and vincristine (EMA/CO) chemotherapy in women with high-risk gestational trophoblastic tumors (GTT) and to document the middle- and long-term toxicity of the regimen [1].
• The human choriocarcinoma cell lines BeWo and JAR, derived from trophoblastic tumors of the placenta, also strongly express NRF3 transcripts [2].
• OBJECTIVE: The purpose of this study was to evaluate the association of telomerase activity in complete hydatidiform moles with subsequent development of persistent gestational trophoblastic tumor [3].
• HCG is, however, not a unique marker for trophoblastic neoplasms, as a significant number of intracranial germinomas contain cells that are beta-HCG positive [4].
• Pregnancy-specific beta 1-glycoprotein, another oncoplacental antigen, has been used as a tumor marker for trophoblastic neoplasms, but not previously for human chorionic gonadotropin-producing tumors associated with precocious puberty [5].

High impact information on Trophoblastic Neoplasms

• The clinical course, human chorionic gonadotropin (HCG) levels, and serial circulating immune complex (CIC) levels in 21 patients with gestational trophoblastic neoplasia (GTN) were correlated for the evaluation of the relationship between CIC levels and trophoblastic tumor burden [6].
• EMA/CO for high-risk gestational trophoblastic tumors: results from a cohort of 272 patients [1].
• Combination but not single-agent methotrexate chemotherapy for gestational trophoblastic tumors increases the incidence of second tumors [7].
• Decreased expression of Ras GTPase activating protein in human trophoblastic tumors [8].
• Although TNF apparently serves important functions in cytotrophoblast during the course of placental development that might include promotion of proliferation and invasion, constitutive expression of this gene in neoplastic cells could account in part for the remarkable ability of trophoblastic tumors to overcome host defenses [9].

Chemical compound and disease context of Trophoblastic Neoplasms

• CONCLUSION: Selective uterine artery embolization is a safe and effective treatment for severe bleeding from residual uterine vascular malformations in patients with treated gestational trophoblastic tumors [10].
• Cytotoxicity of N6-subsituted adenosine analogs to cultured trophoblastic tumor cells [11].
• The management of gestational trophoblastic tumors with etoposide, methotrexate, and actinomycin D [12].
• Chemotherapy using 5-fluorouracil and nitrocaphanum in malignant trophoblastic tumor [13].
• Thirty-two patients with nonmetastatic gestational trophoblastic tumors were treated with methotrexate infusion and folinic acid and the results of this therapy were compared to our prior experience with the 8-day methotrexate-folinic acid regimen [14].

Biological context of Trophoblastic Neoplasms

• STUDY DESIGN: In this retrospective study 56 trophoblastic tumors were examined by means of immunocytochemical techniques to stain for the oncogene product for evidence of c-erb B-2 expression [15].
• Finally, we determined the precise methylation status of CpG sites of the TFPI-2 promoter in normal and tumor trophoblast cells using the bisulfite genomic sequencing method [16].
• Diagnostic and prognostic significance of circulating tumor suppressor gene p53 autoantibodies in patients with gestational trophoblastic tumors [17].
• The results indicate that TGF-alpha is present in trophoblasts throughout human gestation and may provide additional growth advantage to maintenance of the hyperproliferative condition in trophoblastic tumors [18].

Anatomical context of Trophoblastic Neoplasms

• Deglycosylated hCG, a very weak LH/hCG receptor agonist, was the most potent agonist in thyroid follicles (588 microU hTSH/mg protein). hCGs purified from urine of patients with trophoblastic tumors had greater TSH-like activity (37-84 microU hTSH/mg protein) than purified hCG [19].
• Decreased expression of p27Kip1 was observed in malignant trophoblastic neoplasms with a positive rate of 21.43%, which is significantly less than that in normal chorionic villi (80%) and in complete HM (73.33%) (P < 0.05) [20].

Gene context of Trophoblastic Neoplasms

• The increased expression of EGFR and c-erbB-3 in complete mole may also influence the development of persistent gestational trophoblastic tumor [21].
• The only marker that approaches the ideal is human chorionic gonadotropin (HCG) in gestational trophoblastic tumors [22].
• Recently, the importance of c-fms and its ligand CSF-1 in malignancies of non-hematopoietic origin, such as breast, ovarian, endometrial, pulmonary, and trophoblastic cancers has been recognized [23].
• Recently we showed the expression pattern of OPN in gestational trophoblastic tumors [24].
• Expression of CDKI p27Kip1 in trophoblastic neoplasm [20].

Analytical, diagnostic and therapeutic context of Trophoblastic Neoplasms

• METHOD: From 1979 to 1988, 152 patients with trophoblastic tumor were treated with combination chemotherapy using nitrocaphanum and 5-FU [13].
• Risk factors for the prediction of treatment failure in gestational trophoblastic tumors treated with EMA/CO regimen [25].
• Large doses of 5-fluorouracil, administered by slow intravenous drip, have proven to be very effective in the treatment of malignant trophoblastic tumors [26].
• Multimodality therapy with combination chemotherapy employing etoposide, high-dose methotrexate, actinomycin D, cyclophosphamide and vincristine (EMA-CO), and adjuvant radiotherapy and surgery, when indicated, has resulted in cure rates of 80-90% in patients with high-risk metastatic gestational trophoblastic tumors [27].
• Vinblastine, cisplatin and bleomycin (VPB) were utilized as salvage therapy in seven women with high-risk metastatic gestational trophoblastic tumors resistant to prior treatment with triple therapy (methotrexate, actinomycin D and cyclophosphamide) or the modified Bagshawe protocol [28].

References