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 (792 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 malignant metastatic form of trophoblastic tumors. Unlike the hydatidiform mole, choriocarcinoma contains no chorionic villi but rather sheets of undifferentiated cytotrophoblasts and syncytiotrophoblasts (trophoblasts). It is characterized by the large amounts of chorionic gonadotropin produced. Tissue origins can be determined by DNA analyses: placental (fetal) origin or non-placental origin (choriocarcinoma, non-gestational).
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: Choriocarcinomas.
Where it fits in the MeSH classification
- Broader topics
- Trophoblastic Neoplasms; Adenocarcinoma
- Narrower topics
- Choriocarcinoma, Non-gestational; Trophoblastic Tumor, Placental Site
- See also
- Choriocarcinoma, Non-gestational
Related concepts
- Hydatidiform Mole
- Chorionic Villi
- Trophoblasts
- Chorionic Gonadotropin
- Choriocarcinoma
- Non-Gestational
Research landscape
PubMed indexes 7,722 records tagged with the MeSH heading “Choriocarcinoma” (counts retrieved 2026-10-29). 398 of them (5.2%) were published from 2020 onward, and the busiest period so far is through 1999 with 5,357 records.
Reviews account for 610 records (7.9%) and meta-analyses for 1. Randomized controlled trials number 4 (0.1%) 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 | 5,357 |
| 2000-2009 | 1,137 |
| 2010-2019 | 830 |
| 2020 onward | 398 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 610 | 7.9% |
| Meta-analyses | 1 | 0.0% |
| Randomized controlled trials | 4 | 0.1% |
Method: PubMed query "Choriocarcinoma"[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 |
|---|---|---|---|---|
| Regulation of Mcl-1 by SRSF1 and SRSF5 in cancer cells | 2012 | Research article Design not recorded in structured metadata | 77 | cc by PMID 23284704 · DOI · PMC3524227 |
| Intensified therapies improve survival and identification of novel prognostic factors for placental-site and epithelioid trophoblastic tumours | 2019 | Research article Design not recorded in structured metadata | 63 | cc by PMID 30792530 · DOI · PMC6461960 |
| STOX1 overexpression in choriocarcinoma cells mimics transcriptional alterations observed in preeclamptic placentas | 2008 | Research article Design not recorded in structured metadata | 58 | cc by PMID 19079545 · DOI · PMC2592700 |
| Placental Site Trophoblastic Tumor Acquires Immune Functions by Incorporating Host Maternal Genes | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42338270 · DOI · PMC13336403 |
Regulation of Mcl-1 by SRSF1 and SRSF5 in cancer cells [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Up-regulation of the apoptosis-regulatory gene Mcl-1 (myeloid cell leukemia-1) occurs in different cancer types and is linked with drug resistance to cancer therapies.
- Closing excerpt
- The key findings from this study highlight the importance of the cellular context of different cancer cells for the function of multifunctional RBPs like SRSF1 and have implications for therapeutic approaches employed to target Mcl-1.
- 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 (196 words)
Up-regulation of the apoptosis-regulatory gene Mcl-1 (myeloid cell leukemia-1) occurs in different cancer types and is linked with drug resistance to cancer therapies. It is well known that Mcl-1 pre-mRNA undergoes alternative splicing events to produce two functionally distinct proteins, Mcl-1(S) (pro-apoptotic) and Mcl-l(L) (anti-apoptotic); the latter isoform is predominant in different cancers including breast and ovarian cancer cells. In the present study we report that the RNA-binding protein (RBP) and proto-oncogene SRSF1 (serine and arginine-rich splicing factor 1) influences splicing of Mcl-1 in both MCF-7 and MDA-MB-231 breast cancer cells and JAR choriocarcinoma cells; we also show for the first time that another RBP SRSF5 affects splicing of Mcl-1 in the MCF-7 cells. Moreover, we report that SRSF1 is involved in other aspects of Mcl-1 regulation with knockdown of SRSF1, by RNAi, resulting in a significant decrease in Mcl-1 protein levels in MCF-7 cells but an increase in JAR cells, respectively, by potentially affecting protein stability and translation of Mcl-l. The key findings from this study highlight the importance of the cellular context of different cancer cells for the function of multifunctional RBPs like SRSF1 and have implications for therapeutic approaches employed to target Mcl-1.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 23284704 · DOI · PMC3524227
Intensified therapies improve survival and identification of novel prognostic factors for placental-site and epithelioid trophoblastic tumours [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundPlacental-site trophoblastic (PSTT) and epithelioid trophoblastic tumours (ETT) are the rarest malignant forms of gestational trophoblastic disease (GTD).
- Closing excerpt
- Platinum-based and high-dose chemotherapy may help to improve survival in poor-prognosis patients.
- 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 (207 words)
BackgroundPlacental-site trophoblastic (PSTT) and epithelioid trophoblastic tumours (ETT) are the rarest malignant forms of gestational trophoblastic disease (GTD). Our prior work demonstrated that an interval of ≥48 months from the antecedent pregnancy was associated with 100% death rate, independent of the stage. Here, we assess whether modified treatments for these patients have increased survival and identify new prognostic factors.MethodsThe United Kingdom GTD database was screened to identify all PSTT/ETT cases diagnosed between 1973 and 2014. Data and survival outcomes from our prior patient cohort (1976-2006) were compared to our new modern cohort (2007-2014), when intensified treatments were introduced.ResultsOf 54,743 GTD patients, 125 (0.23%) were diagnosed with PSTT and/or ETT. Probability of survival at 5 and 10 years following treatment was 80% (95% CI 72.8-87.6%) and 75% (95% CI 66.3-84.3%), respectively. Univariate analysis identified five prognostic factors for reduced overall survival (age, FIGO stage, time since antecedent pregnancy, hCG level, mitotic index) of which stage IV disease (HR 6.18, 95% CI 1.61-23.81, p = 0.008) and interval ≥48 months since antecedent pregnancy (HR 14.57, 95% CI 4.17-50.96, p ConclusionPSTT/ETT with advanced FIGO stage or an interval ≥48 months from their last known pregnancy have poorer outcomes. Platinum-based and high-dose chemotherapy may help to improve survival in poor-prognosis patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30792530 · DOI · PMC6461960
STOX1 overexpression in choriocarcinoma cells mimics transcriptional alterations observed in preeclamptic placentas [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundMutations in STOX1 were proposed to be causal for predisposing to preeclampsia, a hypertensive disorder originating from placental defects, affecting up to 10% of human pregnancies.
- Closing excerpt
- Our cellular model could constitute an invaluable resource for studying specific aspects of this human disease.
- 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 (190 words)
BackgroundMutations in STOX1 were proposed to be causal for predisposing to preeclampsia, a hypertensive disorder originating from placental defects, affecting up to 10% of human pregnancies. However, after the first study published in 2005 three other groups have dismissed the polymorphism described in the first paper as a causal mutation.Methodology and principal findingsIn the present study, we have produced a choriocarcinoma cell line overexpressing STOX1. This overexpression results in transcriptional modification of 12.5% of the genes, some of them being direct targets as shown by chromatin immunoprecipitation. STOX1 overexpression correlates strongly and specifically with transcriptomic alterations in preeclamptic placentas (r = 0.30, p = 9.10(-7)). Numerous known key modulators of preeclampsia (such as Endoglin, Syncytin, human chorionic gonadotrophin -hCG-, and Glial Cell Missing Homolog -GCM1-) were modified in these transformed choriocarcinoma cells.ConclusionsOur results contribute to reconcile contradictory data concerning the involvement of STOX1 in preeclampsia. In addition, they strongly suggest that anomalies in STOX1 expression are associated with the onset of preeclampsia, thus indicating that this gene should be the target of future studies. Our cellular model could constitute an invaluable resource for studying specific aspects of this human disease.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 19079545 · DOI · PMC2592700
Placental Site Trophoblastic Tumor Acquires Immune Functions by Incorporating Host Maternal Genes [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Although it was proposed that cell fusion of cancer cells with leukocytes creates mobile hybrids with a metastatic phenotype, it has been difficult to genetically confirm cell fusion events in human cancer in vivo.
- Closing excerpt
- These findings indicate that PSTT sequentially incorporated exogenous genes from maternal cells to express immune-related molecules and suggest that cancer cells acquired B cell-related functions, including Ig production by cell fusion with host immune cells.
- 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 (199 words)
Although it was proposed that cell fusion of cancer cells with leukocytes creates mobile hybrids with a metastatic phenotype, it has been difficult to genetically confirm cell fusion events in human cancer in vivo. Here, we experienced 4 cases of placental site trophoblastic tumor (PSTT) that produced immunoglobulin (Ig). Three cases showed recurrence and responded well to pembrolizumab therapy. Among them, we could analyze temporal changes in the genetic profiles on one case of daughter-derived PSTT, which relapsed after pembrolizumab therapy. In this case, we found that PSTT incorporated the exogenous genes from host maternal cells. The rearrangement patterns of Ig genes and protein expressions sequentially increased. By analyzing single-nucleotide variants, PSTT incorporated daughter-non-inherited maternal alleles (DNIMA), including the Ig lambda and HLA-DQA2 loci. Protein expressions of TLR10 and SIGLEC10 increased during tumor progression concomitantly with DNIMA incorporation. DNIMA mapping indicates the incorporation of exogenous maternal genes was widely distributed through the whole chromosomes, suggesting the involvement of cell fusion in gene transfer mechanisms. These findings indicate that PSTT sequentially incorporated exogenous genes from maternal cells to express immune-related molecules and suggest that cancer cells acquired B cell-related functions, including Ig production by cell fusion with host immune cells.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42338270 · DOI · PMC13336403
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: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up [5]
- Research article Physiological and pathological aspects of the effect of human chorionic gonadotropin on the thyroid [6]
- Research article Kisspeptins and the placenta: regulation of trophoblast invasion [7]
- Research article Malignant potential of the dysgenetic gonad. Part 1 [8]
- Research article Placental site trophoblastic tumors and epithelioid trophoblastic tumors: Biology, natural history, and treatment modalities [9]
- Research article Placental site trophoblastic tumor: a 17-year experience at the New England Trophoblastic Disease Center [10]
References
- Gautrey HL, Tyson-Capper AJ. Regulation of Mcl-1 by SRSF1 and SRSF5 in cancer cells. . 2012. PMID 23284704 · DOI · PMC3524227
- Froeling FEM, Ramaswami R, Papanastasopoulos P, Kaur B, Sebire NJ, Short D, et al.. Intensified therapies improve survival and identification of novel prognostic factors for placental-site and epithelioid trophoblastic tumours. . 2019. PMID 30792530 · DOI · PMC6461960
- Rigourd V, Chauvet C, Chelbi ST, Rebourcet R, Mondon F, Letourneur F, et al.. STOX1 overexpression in choriocarcinoma cells mimics transcriptional alterations observed in preeclamptic placentas. . 2008. PMID 19079545 · DOI · PMC2592700
- Kagami K, Ono M, Mizumoto Y, Kanda T, Iizuka T, Daikoku T, et al.. Placental Site Trophoblastic Tumor Acquires Immune Functions by Incorporating Host Maternal Genes. . 2026. PMID 42338270 · DOI · PMC13336403
- Seckl MJ, Sebire NJ, Fisher RA, Golfier F, Massuger L, Sessa C, et al.. Gestational trophoblastic disease: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. Ann Oncol. 2013. PMID 23999759 · DOI
- Hershman JM. Physiological and pathological aspects of the effect of human chorionic gonadotropin on the thyroid. Best Pract Res Clin Endocrinol Metab. 2004. PMID 15157839 · DOI
- Hiden U, Bilban M, Knöfler M, Desoye G. Kisspeptins and the placenta: regulation of trophoblast invasion. Rev Endocr Metab Disord. 2007. PMID 17351756 · DOI
- Schellhas HF. Malignant potential of the dysgenetic gonad. Part 1. Obstet Gynecol. 1974. PMID 4608181
- Horowitz NS, Goldstein DP, Berkowitz RS. Placental site trophoblastic tumors and epithelioid trophoblastic tumors: Biology, natural history, and treatment modalities. Gynecol Oncol. 2017. PMID 27789086 · DOI
- Feltmate CM, Genest DR, Wise L, Bernstein MR, Goldstein DP, Berkowitz RS. Placental site trophoblastic tumor: a 17-year experience at the New England Trophoblastic Disease Center. Gynecol Oncol. 2001. PMID 11520134 · 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
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