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Serous Carcinomas

A plain-English summary of the published research on Serous Carcinomas, reviewed and approved by our editors — not a hand-curated clinical overview.

Research summary · reviewed
Educational only: This page is not medical advice. Coordinate decisions with your oncology team.

Reviewed Jun 2026 · OncoForge editorial · How we review →

AI extractedhuman reviewedsources checkedretractions suppressed· last updated Jun 2026

Evidence at a glanceHuman · observationalReported positive
2 published studies that name Serous Carcinomas2 human studies approved & graded (trial, observational, or meta-analysis)14 human clinical studies in the Serous Carcinomas corpus473 source documents in the Serous Carcinomas corpus

last checked June 14, 2026

Why this grade?

Human · observational — Human observational evidence only — no trials.

Computed deterministically from the studies’ types and reported outcomes — not written by AI, and not a claim that anything works.

What the guidelines say

NCI PDQESMONCCNASCO

We link the authoritative guidelines rather than reproduce them. Below, the treatments on this page are split into standard care, guideline or regulatory options, supportive care, and studied but not standard so established care is not mixed with experimental or supportive items.

Studied, not standard - investigational
  • prophylactic oophorectomy
  • risk-reducing salpingo-oophorectomy
  • risk-reducing salpingectomy with delayed oophorectomy
  • recombinant REG4 protein

Read the guidelines

Cancer-specific deep links aren’t curated yet — these search the authoritative sources for Serous Carcinomas.

Treatment map: Serous Carcinomas

Open as a full page →

Standard care plus every compound studied in the literature (each cited) and graded by evidence, organized by clinical readiness. A category, not a verdict that anything works — confirm anything here with your oncology team.

4
Interventions
0
Standard of care
0
Tested in people
0
Lab / animal
4
Named in lit.
2
Classes
Standard of care (0) Guideline option (0) Tested in people (0) Lab / animal only (0) Named in the literature (4)
Investigational & adjunct compounds — detail (4)
Named in the literature
prophylactic oophorectomy· BRCA1 and BRCA2risk-reducing salpingo-oophorectomy· biomarker-selectedrisk-reducing salpingectomy with delayed oophorectomy· biomarker-selectedrecombinant REG4 protein

"Tested in people" rows show the highest trial phase found in that compound's cited human studies (Phase I–IV; "phase not reported" = a human study with no phase tag). "Studied" = named in the cited literature for this cancer. "FDA ✓" = FDA-approved for this cancer; "off-label" = an FDA-approved drug used outside its approved indications (per openFDA). Not a claim that anything works.

Reported figures

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Snapshot

The essentials in ~60 seconds — every line is drawn from the cited sources below.

What it is
Serous carcinomas are an aggressive (type II) form of gynecologic cancer; endometrial serous carcinomas are often hormone‑independent, deeply invasive and widely metastatic. They are the predominant histology in peritoneal cancers in BRCA1/2 hereditary breast–ovarian cancer families, many extrauterine high‑grade serous carcinomas arise in the distal fallopian tube, and endometrial serous carcinomas may develop from endometrial intraepithelial carcinoma. [1][2][3][4]
Survival
Prognosis is generally poor; the 5‑year survival for all stages of ovarian cancer has been reported as 35–38%. [1][5]
Standard treatment
For prevention in high‑risk women, risk‑reducing salpingo‑oophorectomy is the standard approach and prophylactic oophorectomy has been reported to reduce ovarian cancer risk in BRCA1/2 carriers; evaluation of staged salpingectomy with delayed oophorectomy is underway. [6][2]
Key test
BRCA1/BRCA2 mutation testing to identify hereditary risk and guide preventive counseling and surgical decisions. [2][6]
Biggest challenge
Available screening methods appear insufficient for early detection of many ovarian cancers, and there is a gap in translating contemporary evidence into practical counseling for women with BRCA1/2 variants. [2][6]

Ask about Serous Carcinomas

Answers come only from the cited sources on this page — with the supporting evidence shown. If the sources here don't cover your question, it will say so. Educational information, not medical advice.

Key numbers & factors

Risk factors

  • ▲ increases riskBRCA1/BRCA2 mutations — BRCA1/BRCA2 mutations increase lifetime risk for peritoneal/tubo‑ovarian carcinoma; BRCA1 penetrance for ovarian cancer has been estimated in a higher range than BRCA2. [2]
  • ▲ increases riskJewish/Ashkenazi descent — HBOC syndrome and BRCA1/BRCA2 mutations are particularly prevalent in women of Jewish lineage, especially Ashkenazi descent. [2]

Biomarkers

  • BRCA1/BRCA2ActionableIdentifies hereditary risk and informs preventive surgical decisions and counseling. [2][6]
  • WT1 · Distinguishes uterine/endometrial (WT1‑negative) from most ovarian serous carcinomas (WT1‑reactive). [7][8]
  • p53 · p53 immunoreactivity/abnormal accumulation is common in endometrial serous carcinomas and associated lesions. [8][4]
  • DLL3 · High‑grade serous carcinomas lack DLL3 expression. [9]
  • REG4 · REG4 is highly expressed in certain ovarian cancer cell lines and increases tumor cell growth via EGFR/Akt/AP‑1 signaling in vitro. [5]
  • NEP/CD10 · Stromal NEP/CD10 is expressed in borderline and malignant ovarian tumors and its staining intensity is decreased in higher‑grade serous carcinomas. [10]
  • GATA4 · Expression of GATA4 is lost in most serous carcinomas (retained in most mucinous carcinomas). [11]
  • Loss of heterozygosity at 8p · Genomic alteration observed in serous carcinomas (found in 67% of samples in one report). [11]

9 sections — tap any heading to expand its cited detail. Key points are above.

Overview4 points
  • Serous carcinomas are the predominant histology among peritoneal cancers arising in hereditary breast-ovarian cancer (HBOC) kindreds associated with BRCA1 and BRCA2 mutations. [2]
  • Endometrial serous carcinomas (type II) are described as hormone independent, frequently deeply invasive and widely metastatic, and having a poor prognosis. [1]
  • Most extrauterine high-grade serous carcinomas have been determined to arise in the distal fallopian tube. [3]
  • Serous carcinomas of the endometrium are proposed to develop from "endometrial intraepithelial carcinoma," a lesion representing malignant transformation of the endometrial surface epithelium. [4]
Epidemiology3 points
  • Women who carry cancer-associated BRCA1 or BRCA2 mutations are at increased lifetime risk for peritoneal carcinoma, even after previous removal of the ovaries, fallopian tubes and uterus. [2]
  • Hereditary breast-ovarian cancer (HBOC) syndrome and BRCA1/BRCA2 mutations are reported to be particularly prevalent in women of Jewish lineage and especially those of Ashkenazi descent. [2]
  • The penetrance of BRCA1 mutations for ovarian cancer has been estimated in a range and the penetrance of BRCA2 mutations for ovarian cancer has been estimated in a lower range. [2]
Key biomarkers5 points
  • WT1 expression differs between uterine/endometrial serous carcinomas and extrauterine/ovarian serous carcinomas; WT1 immunoreactivity is reported to be absent in uterine papillary serous carcinomas while most ovarian serous carcinomas are WT1-reactive. [7][8]
  • p53 immunoreactivity is reported in the majority of endometrial serous carcinomas and only a small fraction of endometrioid carcinomas. [8]
  • High-grade serous carcinomas lacked DLL3 expression. [9]
Show 2 lab & early-research findings
  • REG4 mRNA was found to be expressed at a high level in CAOV3, SKOV3/DDP, HO8910, and HO8910-PM ovarian cancer cell lines compared with other cell lines. [5]
  • In ovarian cancer cell lines, treatment with recombinant REG4 (50 nM) significantly increased SKOV3 cell growth; REG4 has been reported to be a potent activator of the epidermal growth factor receptor/Akt kinase/activator protein-1 (EGFR/Akt/AP-1) signaling pathway, leading to increased expression of Bcl-2, Bcl-xl and survivin. [5]
Biology & pathways5 points
  • Global gene expression profiles differ between type I (endometrioid) and type II (serous) endometrial carcinomas; one study identified 315 genes that statistically differentiate the two groups. [1]
  • Loss of heterozygosity (LOH) at 8p was detected in 67% of serous carcinoma samples. [11]
  • Expression of the transcription factor gene GATA4 was lost in most serous carcinomas but retained in the majority of mucinous carcinomas. [11]
  • Neutral endopeptidase (NEP/CD10) is expressed in the stroma of borderline and malignant ovarian tumors including serous carcinomas, and stromal NEP staining intensity was decreased in higher-grade serous carcinomas. [10]
  • Serous carcinoma and endometrial intraepithelial carcinoma are associated with p53 mutations and abnormal accumulation of p53 protein. [4]
Standard management3 points
  • Risk-reducing salpingo-oophorectomy remains the standard for prevention, conferring reduction in tubo-ovarian cancer risk and improved overall survival. [6]
  • Prophylactic oophorectomy has been reported to reduce the risk for ovarian cancer in women from hereditary breast–ovarian cancer (HBOC) kindreds and in BRCA1 and BRCA2 mutation carriers. [2]
  • Evaluation of risk-reducing salpingectomy with delayed oophorectomy as a staged surgical strategy is underway to balance oncologic safety with preservation of hormonal function. [6]
Treatments & compounds studied4 treatments

Procedures & devices

  • prophylactic oophorectomy: BRCA1 and BRCA2Prophylactic oophorectomy has been reported to reduce the risk for ovarian cancer in women from HBOC kindreds and BRCA1/BRCA2 mutation carriers, leaving a residual risk for peritoneal carcinomatosis of well less than 5%. [2]
  • risk-reducing salpingo-oophorectomy: biomarker-selectedRisk-reducing salpingo-oophorectomy is described as a preventive surgical strategy that reduces tubo-ovarian cancer risk and is associated with improved overall survival in women with BRCA pathogenic variants. [6]
  • risk-reducing salpingectomy with delayed oophorectomy: biomarker-selectedRisk-reducing salpingectomy with delayed oophorectomy has been evaluated as a staged surgical approach for women with BRCA pathogenic variants aiming to balance oncologic risk reduction with preservation of hormonal function. [6]

Other

Show 1 lab & early-research entry
  • recombinant REG4 protein: Preclinical laboratory studies reported that recombinant REG4 (50 nM) increased growth of SKOV3 ovarian cancer cells. [5]
Prognosis4 points
  • In one series, ovarian carcinomas associated with germline BRCA1 or BRCA2 mutations were reported to be invasive serous carcinomas. [12]
  • In that series, BRCA-associated serous ovarian carcinomas had high proportions of grade 3 features, including 50% with Gynecologic Oncology Group grade 3 and 84% with nuclear grade 3. [12]
  • Type II (serous) endometrial carcinomas are associated with a poor prognosis. [1]
  • The 5-year survival rate for all stages of ovarian cancer has been reported as 35–38%. [5]
What we don't know yet2 points
  • Available screening methods appear to be insufficient for early detection of many ovarian cancers. [2]
  • A clinically relevant gap remains in translating contemporary evidence into a practical counseling framework for women with BRCA1/2 pathogenic variants. [6]
Staging & risk1 point
  • Each ovarian cancer in the study cohort was staged according to the International Federation of Gynecology and Obstetrics (FIGO) staging system. [5]

Sources

Every statement above is drawn from these reviewed sources. This page reports what they describe. Sources last checked June 14, 2026.

  1. Clinical trialDistinctive gene expression profiles by cDNA microarrays in endometrioid and serous carcinomas of the endometrium · 2004
  2. Clinical trialPeritoneal carcinoma in women with genetic susceptibility: implications for Jewish populations · 2004
  3. Review articleUntangling the Labyrinth: An Integrated View of the Mesothelial and Epithelial Linings of the Female Adnexa Based on Newly Characterized Anatomic and Histologic Junctions · 2026
  4. Clinical trialTheories of endometrial carcinogenesis: a multidisciplinary approach · 2000
  5. StudyThe role of the REG4 gene and its encoding product in ovarian epithelial carcinoma · 2015
  6. Review articleContemporary risk assessment and risk-reducing strategies for tubo-ovarian cancer in women with BRCA pathogenic variants · 2026
  7. Clinical trialWT1 immunoreactivity in uterine papillary serous carcinomas is different from ovarian serous carcinomas · 2002
  8. Clinical trialDifferential expression of WT1 and p53 in serous and endometrioid carcinomas of the endometrium · 2004
  9. Clinical trialAssessment of delta-like ligand 3 (DLL3) immunostaining in neuroendocrine tumors of the gynecological tract and comparing expression with other high-grade gynecological malignancies · 2026
  10. Clinical trialNeutral endopeptidase/CD10 expression in the stroma of epithelial ovarian carcinoma · 2003
  11. Clinical trialComparison of serous and mucinous ovarian carcinomas: distinct pattern of allelic loss at distal 8p and expression of transcription factor GATA-4 · 2001
  12. Clinical trialHistopathologic features of genetically determined ovarian cancer · 2002

What supports this page

The kinds of sources behind this page, strongest at the top. Faint rungs show what is not here yet.

Guideline
2
Meta-analysis
4
Systematic review
2
Randomized trial
0
Clinical trial
32
Observational
2
Case report
27
Review
403
Preclinical
0
Other
1

Living document — last change June 14, 2026: Cancer page updated. 3 recent updates logged.

Pooled evidence across studies

PubMed
  • Overall HER2 IHC/FISH concordance: 92.5% (91–94 across studies) · HercepTest™ + HER2 IQFISH pharmDx (FISH)
    2 studies · 100% agree · consistent38740270

Numbers pooled deterministically across 2 published studies that passed our figure-accuracy checks — a quick synthesis, not a formal meta-analysis. Updated 9/7/2026.

What recent studies report in Serous Carcinomas

These are reviewed studies whose abstracts concern Serous Carcinomas. Each describes only what that study reported. This is not a claim by OncoForge that any compound helps or harms Serous Carcinomas. Most are early lab, animal, or small human studies, and findings often conflict.

2 studies2 humanMechanism (2)

Tracking 2 published studies of Serous Carcinomas: 2 in humans.

Reported direction across studies: 2 positive.

These counts summarize what the studies reported; they are not a measure of whether anything works for Serous Carcinomas.

Human · observationalMechanismReported positiveModerate evidenceTier 3 · early humann = 65

Performance of HER2 DAKO HercepTest and Ventana 4B5 immunohistochemical assays on detecting HER2 gene-amplification in uterine serous carcinomas

Human pathology · Jun 2024 · comparative diagnostic study (IHC assays compared with FISH)

uterine serous carcinomauterine serous carcinomas

This study compared two HER2 immunohistochemistry assays (DAKO HercepTest and Ventana PATHWAY 4B5) against HER2 FISH (HER2 IQFISH pharmDx) in 65 uterine serous carcinomas. Both IHC assays showed high specificity (100%) for IHC 3+ cases and high overall IHC/FISH concordance, but notable false-negative rates among IHC 0-1+ cases (19% HercepTest, 25% 4B5). The authors note comparable sensitivity between assays and suggest considering reflex FISH for some low-IHC cases.

Reported effects: complete concordance HercepTest vs 4B5 68%, n=65 · IHC/FISH concordance by HercepTest 94%, n=48 · +9 more

Studied with: HER2 IQFISH pharmDx (FISH).

Key findings
  • Complete concordance between HercepTest and 4B5 assays was achieved in 44/65 tumors (68%).
  • Overall HER2 IHC/FISH concordance was 94% (45/48) by HercepTest and 91% (42/46) by 4B5.
  • All HER2 IHC 3+ cases with HercepTest (n = 6) and 4B5 (n = 4) were gene-amplified, corresponding to specificities of 100%.
  • Among IHC 2+ cases, 41% (7/17) by HercepTest and 42% (8/19) by 4B5 had HER2 gene amplification.
  • Sensitivity at a cut-off of IHC 3+ was 38% for HercepTest and 25% for 4B5 (P = 0.50); at a cut-off of IHC 2+ sensitivity was 81% for HercepTest and 75% for 4B5 (P > 0.99).
  • Among HER2 IHC 0-1+ cases, 3/42 cases by HercepTest and 4/42 cases by 4B5 showed amplified FISH results, corresponding to overall false negative rates of 19% for HercepTest and 25% for 4B5.
Limitations: Relatively small sample size (65 tumors).; FISH denominators differ (48 and 46) implying not all cases had paired FISH results or some data missing.; Tissue-based diagnostic study with no patient clinical outcome or treatment-response data reported.; Findings are specific to uterine serous carcinoma and may not generalize to other tumor types..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early human

The role of the REG4 gene and its encoding product in ovarian epithelial carcinoma

BMC cancer · Jun 2015 · cell line experiments plus human tissue expression and survival analysis

ovarian epithelial carcinomaovarian cancermucinous ovarian tumorsserous carcinomas

This study looked at REG4 in ovarian epithelial carcinoma using SKOV3 cells and ovarian tissue samples. In cells, adding REG4 or making cells overexpress REG4 reduced apoptosis and increased proliferation, migration, invasion, and G2/S cell-cycle progression. In patient tissues, REG4 was more highly expressed in tumor samples than in normal ovarian tissue, and higher REG4 expression was linked with worse survival outcomes.

Key findings
  • REG4 overexpression and recombinant REG4 inhibited apoptosis in SKOV3 cells.
  • REG4 increased proliferation, migration, invasion, and G2/S progression in SKOV3 cells.
  • Wnt5a, p70s6k, survivin, and VEGF increased, while Bax decreased with REG4 overexpression.
  • REG4 mRNA and protein were higher in ovarian tumor tissues than in normal ovarian tissue.
  • Higher REG4 expression was associated with poorer cumulative and relapse-free survival.
Limitations: Primarily cell-line and tissue-expression study; no therapeutic intervention in patients.; Observational survival association cannot establish causality.; Abstract does not report sample sizes, effect sizes, or detailed statistical estimates.; Findings are based on one ovarian cancer cell line (SKOV3) and may not generalize to all ovarian cancers..

REG4 was studied as a biomarker and functional regulator in ovarian cancer, not as a repurposed drug or natural compound.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Browse all studies mentioning Serous Carcinomas →

What the research shows for Serous Carcinomas

A plain-language summary of the reviewed studies OncoForge tracks for Serous Carcinomas. It reports what those studies described, not a claim that any compound or therapy helps or harms Serous Carcinomas. Most of this evidence is early, and findings often conflict.

  • Studies report REG4 was examined in ovarian epithelial carcinoma using the SKOV3 cell line: adding REG4 protein or forcing REG4 overexpression in these cultured cells reduced apoptosis and increased proliferation, migration, invasion, and G2/S cell-cycle progression.
  • Studies report the research also included analysis of ovarian tumor tissue samples from patients to assess REG4, although the provided summary gives limited detail about the specific tissue-level findings.
  • Studies report that the body of evidence is primarily preclinical (cell-line experiments) with limited human observational biomarker data, and the reported findings are of limited strength and require independent replication.
  • Studies report no clinical trials or interventional studies targeting REG4 in serous ovarian carcinomas were described in the provided material.

Supportive & alternative options discussed

  • Hyperthermia (heat): Also discussed as a supportive option for ovarian/serous carcinoma care in some settings, typically as an adjunct to other treatments rather than based on the studies above.
  • Exercise / prehabilitation: Also discussed as a supportive option to help maintain physical function and quality of life for people with ovarian/serous carcinomas; this brief's studies did not test exercise.
  • Mind–body (MBSR / CBT): Also discussed as a supportive option for coping, symptom management, and quality of life in ovarian/serous carcinoma, but not evaluated in the studies summarized here.
  • Acupuncture: Also discussed as a supportive option for symptom relief (for example, nausea or pain) in ovarian/serous carcinoma care; it was not assessed in the studies above.
  • Ketogenic / metabolic therapy: Also discussed by some as a supportive or adjunctive dietary approach for cancer care broadly, but the studies summarized here did not evaluate ketogenic diets.
  • Mistletoe (VAE): Also discussed in some regions as a complementary therapy for cancer symptom support, but it was not part of the research summarized in these studies.

What we don’t know yet

  • Whether REG4 expression in patient tumors predicts clinical outcomes (prognosis or treatment response) is not established by these studies.
  • It is unknown whether the effects seen in SKOV3 cells (reduced apoptosis and increased invasiveness) occur in patients' tumors in vivo.
  • No interventional data exist on modifying REG4 in patients — safety, dosing, and clinical benefit have not been studied.
  • Details about the patient tissue analysis (sample size, statistical associations, and potential confounders) are limited or not provided here; replication in larger cohorts is needed.
  • Evidence from additional cell lines, animal models, and independent laboratories is lacking to confirm generalizability of the findings.
The evidence is preliminary — mainly laboratory cell-line experiments with limited observational tissue analysis — and does not establish clinical benefit or guide treatment decisions.

Clinical trials in Serous Carcinomas

79 ongoing · 101 completed · tracked from ClinicalTrials.gov. Recruiting is not the same as proven, and completed is not the same as positive — read the results. Not a recommendation.

Completed
43 stopped (terminated / withdrawn / suspended)

Search all trials on ClinicalTrials.gov →

Getting care & support

Nonprofit / Gov

Practical, vetted help for Serous Carcinomas — advocacy, paying for treatment, second opinions, and caregivers.

If you’re struggling emotionally, you don’t have to wait.

Advocacy & community

No dedicated organization for this specific cancer is curated yet — these general organizations can help in the meantime.

Financial help

  • PAN Foundation ↗ — Copay assistance funds by diagnosis (funds open and close as money allows). · status changes often — check the fund’s site
  • HealthWell Foundation ↗ — Copay and premium assistance funds by disease. · status changes often — check the fund’s site
  • CancerCare — financial assistance ↗ — Limited grants plus free financial counseling. · status changes often — check the fund’s site
  • Family Reach ↗ — Help with everyday living costs (rent, transport, food) during treatment. · status changes often — check the fund’s site
  • NeedyMeds ↗ — Searchable directory of drug patient-assistance and discount programs. · status changes often — check the fund’s site
What you’ll typically need to apply
  • Your diagnosis and, if you have it, the specific drug/treatment name (from your care team).
  • Insurance details — your member ID card, or a note that you're uninsured (some funds require active insurance, some don't).
  • Proof of income and household size (recent pay stubs, a tax return, or a benefits letter) — most funds are income-based.
  • Your prescriber's contact information; some programs need the clinic to submit part of the application.
  • Apply early and re-check: funds open and close as money is available, so a closed fund may reopen.

General guidance — each program sets its own eligibility. Confirm requirements on the program’s site.

Second opinions

Caregiver support

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