Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (843 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A group of diseases arising from pregnancy that are commonly associated with hyperplasia of trophoblasts (trophoblast) and markedly elevated human chorionic gonadotropin. They include hydatidiform mole, invasive mole (hydatidiform mole, invasive), placental-site trophoblastic tumor (trophoblastic tumor, placental site), and choriocarcinoma. These neoplasms have varying propensities for invasion and spread.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Disease, Gestational Trophoblastic; Diseases, Gestational Trophoblastic; Gestational Trophoblastic Diseases; Trophoblastic Disease, Gestational; Trophoblastic Diseases, Gestational; Gestational Trophoblastic Neoplasia; Neoplasia, Gestational Trophoblastic; Trophoblastic Neoplasia, Gestational.
Where it fits in the MeSH classification
- Broader topics
- Trophoblastic Neoplasms
- Narrower topics
- Hydatidiform Mole
Related concepts
- Trophoblasts
- Chorionic Gonadotropin
- Hydatidiform Mole
- Invasive
- Trophoblastic Tumor
- Placental Site
- Choriocarcinoma
Research landscape
PubMed indexes 6,458 records tagged with the MeSH heading “Gestational Trophoblastic Disease” (counts retrieved 2026-10-29). 743 of them (11.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 3,571 records.
Reviews account for 679 records (10.5%) and meta-analyses for 34. Randomized controlled trials number 20 (0.3%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 3,571 |
| 2000-2009 | 1,040 |
| 2010-2019 | 1,104 |
| 2020 onward | 743 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 679 | 10.5% |
| Meta-analyses | 34 | 0.5% |
| Randomized controlled trials | 20 | 0.3% |
Method: PubMed query "Gestational Trophoblastic Disease"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cancer and oncology
Cancer research spans very different kinds of evidence. Laboratory studies in cell lines and animal models reveal mechanisms but often do not translate to patients. Early-phase trials mainly test safety and dosing, while phase 3 randomized trials and their meta-analyses are the usual basis for treatment conclusions. Outcomes also differ in meaning: tumour shrinkage, progression-free survival and overall survival are not interchangeable, and screening studies can be distorted by lead-time and overdiagnosis. When reading a result, check the cancer type and stage studied, the comparison treatment, and which outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Identification of microRNA signature in the progression of gestational trophoblastic disease | 2018 | Research article Design not recorded in structured metadata | 22 | cc by PMID 29367697 · DOI · PMC5833456 |
| Management and risk factors of recurrent gestational trophoblastic neoplasia: An update from 2004 to 2017 | 2020 | Research article Design not recorded in structured metadata | 17 | cc by PMID 32022487 · DOI · PMC7131839 |
| Molar pregnancy with a coexisting living fetus: a case series | 2022 | Research article Design not recorded in structured metadata | 14 | cc by PMID 36057566 · DOI · PMC9440514 |
| FIGO staging for gestational trophoblastic neoplasia: 2026 | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42473063 · DOI · PMC13505264 |
Identification of microRNA signature in the progression of gestational trophoblastic disease [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Gestational trophoblastic disease (GTD) encompasses a range of trophoblast-derived disorders.
- Closing excerpt
- The results presented here may offer new clues to the progression of GTD and may provide diagnostic biomarkers for GTN.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (232 words)
Gestational trophoblastic disease (GTD) encompasses a range of trophoblast-derived disorders. The most common type of GTD is hydatidiform mole (HM). Some of HMs can further develop into malignant gestational trophoblastic neoplasia (GTN). Aberrant expression of microRNA (miRNA) is widely reported to be involved in the initiation and progression of cancers. MiRNA expression profile also has been proved to be the useful signature for diagnosis, staging, prognosis, and response to chemotherapy. Till now, the profile of miRNA in the progression of GTD has not been determined. In this study, a total of 34 GTN and 60 complete HMs (CHM) trophoblastic tissues were collected. By miRNA array screening and qRT-PCR validating, six miRNAs, including miR-370-3p, -371a-5p, -518a-3p, -519d-3p, -520a-3p, and -934, were identified to be differentially expressed in GTN vs. CHM. Functional analyses further proved that miR-371a-5p and miR-518a-3p promoted proliferation, migration, and invasion of choriocarcinoma cells. Moreover, we demonstrated that miR-371a-5p was negatively related to protein levels of its predictive target genes BCCIP, SOX2, and BNIP3L, while miR-518a-3p was negatively related to MST1 and EFNA4. For the first time, we proved that miR-371a-5p and miR-518a-3p directly targeted to 3'-UTR regions of BCCIP and MST1, respectively. Additionally, we found that miR-371a-5p and miR-518a-3p regulated diverse pathways related to tumorigenesis and metastasis in choriocarcinoma cells. The results presented here may offer new clues to the progression of GTD and may provide diagnostic biomarkers for GTN.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29367697 · DOI · PMC5833456
Management and risk factors of recurrent gestational trophoblastic neoplasia: An update from 2004 to 2017 [2]
Abstract reading summary — source excerpts
- Opening excerpt
- ObjectiveWe investigated the clinical characteristics, treatments, and survival of patients with gestational trophoblastic neoplasia (GTN) who experienced recurrence.
- Closing excerpt
- An interval between antecedent pregnancy and chemotherapy >12 months, and an interval from first chemotherapy to achieving β-hCG normalization >14 weeks were predictors of recurrence.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (236 words)
ObjectiveWe investigated the clinical characteristics, treatments, and survival of patients with gestational trophoblastic neoplasia (GTN) who experienced recurrence. Factors predictive of recurrence were also investigated.MethodsPatients with GTN who recurred after completing chemotherapy at Peking Union Medical College Hospital Trophoblastic Disease Center were identified between January 2004 and December 2017. Logistic regression analysis was used to identify factors predictive of GTN recurrence.ResultsA total of 1827 patients with GTN achieved complete remission (CR) at our center, of whom 118 (6.5%) experienced recurrence during follow-up. The recurrence rates for patients initially treated at our center and those referred to us were 2.7% and 14.6%, respectively. The majority of recurrent patients received floxuridine-based multiagent chemotherapy (n = 64). Patients who underwent surgery achieved a significantly higher CR rate than those who did not (88.6% vs 61.1%, P = .001). Although 94.1% of recurrent patients reachieved CR, 33.3% of them recurred for a second time. The 5-year survival rate of the entire cohort was 80.4%. An interval between antecedent pregnancy and chemotherapy >12 months (OR: 6.600, 95% CI [3.217-13.540], P 14 weeks (OR: 2.226, 95% CI [1.080-4.588], P = .030) were predictors of recurrence.ConclusionsPatients with recurrent GTN are prone to recurring for a second time. Surgery plays a beneficial role in the management of recurrent GTN. An interval between antecedent pregnancy and chemotherapy >12 months, and an interval from first chemotherapy to achieving β-hCG normalization >14 weeks were predictors of recurrence.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32022487 · DOI · PMC7131839
Molar pregnancy with a coexisting living fetus: a case series [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundCoexistence of molar pregnancy with living fetus represents a challenge in diagnosis and treatment.
- Closing excerpt
- 1492).
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (260 words)
BackgroundCoexistence of molar pregnancy with living fetus represents a challenge in diagnosis and treatment. The objective of this study to present the outcome of molar pregnancy with a coexisting living fetus who were managed in our University Hospital in the last 5 years.MethodsWe performed a retrospective analysis of patients who presented with molar pregnancy with a coexisting living fetus to our Gestational Trophoblastic Clinic, Mansoura University, Egypt from September, 2015 to August, 2020. Clinical characteristics of the patients, maternal complications as well as fetal outcome were recorded. The patients and their living babies were also followed up at least 6 months after delivery.ResultsTwelve pregnancies were analyzed. The mean maternal age was 26.0 (SD 4.1) years and the median parity was 1.0 (range 0-3). Duration of the pregnancies ranged from 14 to 36 weeks. The median serum hCG was 165,210.0 U/L (range 7662-1,200,000). Three fetuses survived outside the uterus (25%), one of them died after 5 months because of congenital malformations. Histologic diagnosis was available for 10 of 12 cases and revealed complete mole associated with a normal placenta in 6 cases (60%) and partial mole in 4 cases (40%). Maternal complications occurred in 6 cases (50%) with the most common was severe vaginal bleeding in 4 cases (33.3%). There was no significant association between B-hCG levels and maternal complications (P = 0.3).ConclusionMaternal and fetal outcomes of molar pregnancy with a living fetus are poor. Counseling the patients for termination of pregnancy may be required.Trial registrationThe study was approved by Institutional Research Board (IRB), Faculty of Medicine, Mansoura University (number: R.21.10.1492).
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36057566 · DOI · PMC9440514
FIGO staging for gestational trophoblastic neoplasia: 2026 [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Gestational trophoblastic neoplasia (GTN) encompasses a wide range of diseases, which include choriocarcinoma, placental site trophoblastic tumor, epithelioid trophoblastic tumor, and post-molar persistent or rising levels of human chorionic gonadotrophin.
- Closing excerpt
- This article highlights the changes introduced in the 2026 system and provide explanatory notes to facilitate interpretation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (115 words)
Gestational trophoblastic neoplasia (GTN) encompasses a wide range of diseases, which include choriocarcinoma, placental site trophoblastic tumor, epithelioid trophoblastic tumor, and post-molar persistent or rising levels of human chorionic gonadotrophin. Standardization of the diagnostic criteria and investigative approaches for this uncommon, potentially lethal, yet highly treatable disease is important. Adoption of an evidence-based staging and scoring system is essential to guide patient management and enable comparison of treatment outcomes. An updated staging system for GTN has been proposed and adopted by the Committee on Women's Cancer of the International Federation of Gynecology and Obstetrics (FIGO) for this purpose. This article highlights the changes introduced in the 2026 system and provide explanatory notes to facilitate interpretation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42473063 · DOI · PMC13505264
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Gestational trophoblastic disease [5]
- Research article Gestational trophoblastic disease I: epidemiology, pathology, clinical presentation and diagnosis of gestational trophoblastic disease, and management of hydatidiform mole [6]
- Research article Gestational trophoblastic disease II: classification and management of gestational trophoblastic neoplasia [7]
- Research article Epidemiology and aetiology of gestational trophoblastic diseases [8]
- Research article Gestational trophoblastic neoplasia--pathogenesis and potential therapeutic targets [9]
- Research article Clinical practice. Molar pregnancy [10]
References
- Zhao JR, Cheng WW, Wang YX, Cai M, Wu WB, Zhang HJ. Identification of microRNA signature in the progression of gestational trophoblastic disease. . 2018. PMID 29367697 · DOI · PMC5833456
- Kong Y, Zong L, Cheng H, Jiang F, Wan X, Feng F, et al.. Management and risk factors of recurrent gestational trophoblastic neoplasia: An update from 2004 to 2017. . 2020. PMID 32022487 · DOI · PMC7131839
- Hemida R, Khashaba E, Zalata K. Molar pregnancy with a coexisting living fetus: a case series. . 2022. PMID 36057566 · DOI · PMC9440514
- Ngan HYS, Seckl MJ, Horowitz N, Cheung ANY, Braga A, Sekharan PK, et al.. FIGO staging for gestational trophoblastic neoplasia: 2026. . 2026. PMID 42473063 · DOI · PMC13505264
- Seckl MJ, Sebire NJ, Berkowitz RS. Gestational trophoblastic disease. Lancet. 2010. PMID 20673583 · DOI
- Lurain JR. Gestational trophoblastic disease I: epidemiology, pathology, clinical presentation and diagnosis of gestational trophoblastic disease, and management of hydatidiform mole. Am J Obstet Gynecol. 2010. PMID 20728069 · DOI
- Lurain JR. Gestational trophoblastic disease II: classification and management of gestational trophoblastic neoplasia. Am J Obstet Gynecol. 2011. PMID 20739008 · DOI
- Altieri A, Franceschi S, Ferlay J, Smith J, La Vecchia C. Epidemiology and aetiology of gestational trophoblastic diseases. Lancet Oncol. 2003. PMID 14602247 · DOI
- Shih IeM. Gestational trophoblastic neoplasia--pathogenesis and potential therapeutic targets. Lancet Oncol. 2007. PMID 17613426 · DOI
- Berkowitz RS, Goldstein DP. Clinical practice. Molar pregnancy. N Engl J Med. 2009. PMID 19369669 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.