Primary fallopian tube carcinoma presenting as an isolated sigmoid colon metastasis: a case report

Introduction

Background

Primary fallopian tube carcinoma (PFTC) is a rare and challenging malignancy, often categorized alongside ovarian and peritoneal cancers under the broader spectrum of epithelial ovarian carcinoma (EOC) (1). Recent molecular and pathological evidence suggests that most high-grade serous carcinomas (HGSCs), traditionally labeled as ovarian, actually originate from the fimbrial epithelium of the fallopian tube, with serous tubal intraepithelial carcinoma (STIC) serving as the key precursor lesion (2,3). This paradigm shift suggests that the true incidence of PFTC has likely been underestimated. Despite these insights, PFTC remains difficult to diagnose because its early symptoms are nonspecific. The classic Latzko’s triad—intermittent serous vaginal discharge, colicky abdominal pain relieved by discharge, and a palpable pelvic mass—occurs in fewer than 15% of cases (4,5). Consequently, many cases are discovered incidentally during surgery or confirmed only through postoperative pathological examination.

Rationale and knowledge gap

Given its rarity and nonspecific manifestations, PFTC is particularly challenging to diagnose preoperatively, especially in patients who present without gynecologic symptoms or imaging abnormalities. Atypical initial presentations—such as palpable lymphadenopathy or metastases to the breast, or brain—have been reported (6-8). However, these patients often have a prior malignancy, detectable adnexal abnormalities, or gross tubal or ovarian lesions identified intraoperatively. Such features typically provide essential clues to the tumor’s primary origin. In contrast, cases in which isolated metastatic disease constitutes the first and only clinically detectable lesion. At the same time, the PFTC, which is identifiable solely at the microscopic level, is exceedingly rare. To our knowledge, the present report describes the first case of PFTC presenting as an isolated sigmoid colon metastasis in the setting of completely normal uterine and adnexal imaging and negative serum tumor markers.

Objective

In this paper, we present a rare case of high-grade serous PFTC manifesting as an isolated sigmoid colon metastasis despite routine pelvic imaging and negative tumor markers. By detailing the diagnostic challenges and the decisive histopathological and immunohistochemical findings that established the correct primary site, we aim to enhance clinical recognition of atypical PFTC presentations and emphasize the critical role of comprehensive histopathological and immunohistochemical assessment in identifying tumor origin. We present this article in accordance with the CARE reporting checklist (available at https://gpm.amegroups.com/article/view/10.21037/gpm-25-32/rc).

Case presentation

A 52-year-old postmenopausal woman (gravida 2, para 2) presented with a 3-month history of paroxysmal left lower abdominal pain accompanied by diarrhea. She had no personal or family history of malignancy. Transvaginal ultrasound showed no abnormalities in the uterus or bilateral adnexa. She was initially diagnosed with acute gastroenteritis and received multiple courses of symptomatic treatment, which led to only transient relief. Two months before referral, her abdominal pain worsened, prompting an emergency department visit. Pelvic computed tomography (CT) revealed sigmoid colon wall thickening with a 2.5 cm × 2.0 cm soft-tissue mass and adjacent peritoneal thickening suggestive of tumor involvement (Figure 1). The uterus and adnexa appeared normal. At a tertiary hospital, serum cancer antigen 125 (CA125), carbohydrate antigen 19-9 (CA19-9), and carcinoembryonic antigen (CEA) levels were all within normal limits. Gastroenteroscopy demonstrated chronic atrophic gastritis without other abnormalities. One week later, the patient underwent laparoscopic exploration, resection of the intra-abdominal mass, segmental sigmoid colectomy, and excision of a suspected peritoneal implant on the left abdominal wall. Intraoperatively, the uterus and adnexa were grossly normal.

Figure 1 Abdominal and pelvic CT showing a 2.5 cm × 2 cm heterogeneously enhancing soft tissue mass near the thickened sigmoid colon and adjacent peritoneal thickening. The arrows indicate the sigmoid colon mass. CT, computed tomography.

Postoperative histopathology confirmed high-grade serous adenocarcinoma in the sigmoid colon lesion, with tumor involvement confined to the serosal layer (Figure 2A,2B). Immunohistochemistry demonstrated positivity for paired box 8 (PAX8), cytokeratin 7 (CK7), and Wilms tumor 1 (WT1), with mutant-type p53 expression, and negativity for cytokeratin 20 (CK20), caudal-type homeobox 2 (CDX2), and special AT-rich sequence-binding protein 2 (SATB2) (Figure 2C-2E), indicating a Müllerian origin. A subsequent pathology review confirmed the diagnosis of high-grade serous adenocarcinoma, with positive staining for PAX8, WT1, epithelial membrane antigen (EMA), and mutant p53 (Figure 2C-2F). Collectively, these findings supported a gynecologic primary. Further histopathological examination of the fallopian tube subsequently identified a microscopic focus of HGSC confined to the fimbrial end, as shown in Figure 2G,2H. The patient was referred to our department for further evaluation 1 month after surgery.

Figure 2 Histologic and immunohistochemical examinations of the colon and fallopian tube lesions. (A) Postoperative pathological analysis of the colon lesion showing serous carcinoma of gynecological origin (H&E staining, 200×). (B) Higher magnification of the colon lesion confirms serous carcinoma of gynecological origin (H&E staining, 400×). (C) Immunohistochemistry for p53 showing positive staining (200×). (D) Immunohistochemistry for PAX8 showing positive staining (200×). (E) Immunohistochemistry for WT1 showing positive staining (200×). (F) Immunohistochemistry for EMA showing positive staining (200×). (G) The white arrow indicates the fallopian tube lesion, pathologically confirmed as high-grade serous adenocarcinoma. The black arrow indicates normal fallopian tube tissue (H&E staining, 100×). (H) Higher magnification of the fallopian tube lesion confirms high-grade serous adenocarcinoma (H&E staining, 400×). EMA, epithelial membrane antigen; H&E, hematoxylin and eosin; PAX8, paired box 8; WT1, Wilms tumor 1.

Comprehensive assessment to localize the primary tumor was unrevealing. Serum CA125 and human epididymis protein 4 (HE4) levels remained within normal limits. Repeat abdominopelvic CT and transvaginal ultrasound showed no uterine or adnexal abnormalities. ¹⁸F-fluorodeoxyglucose (¹⁸F-FDG) positron emission tomography (PET)/CT demonstrated no pathological uptake. Second-look laparoscopy revealed a normal uterus and adnexa with no visible tumor implants or ascites (Figure 3A,3B). Pelvic washings were obtained for cytology. The patient subsequently underwent laparoscopic total hysterectomy, bilateral salpingo-oophorectomy, total omentectomy, and pelvic and para-aortic lymphadenectomy.

Figure 3 Laparoscopic and gross specimen views of the uterus and bilateral adnexa. (A) Laparoscopic exploration shows no visible abnormalities in the uterus, bilateral adnexa, or pelvic cavity. (B) Gross specimen of the resected uterus, fallopian tubes, and ovaries.

Histological examination of the surgical specimens ultimately identified a primary HGSC confined to the fimbrial end of the right fallopian tube (Figure 2G). The microscopic tumor, measuring approximately 1 mm, showed destructive solid invasion consistent with stromal infiltration (Figure 2H). No cancer was identified in the uterus, ovaries, left fallopian tube, omentum, or lymph nodes. Peritoneal cytology was negative. Due to the minute size of the lesion, additional immunohistochemistry or molecular analysis was not feasible. Based on these findings, the patient was diagnosed with primary fallopian tube HGSC with sigmoid colon metastasis. According to the 2014 International Federation of Gynecology and Obstetrics (FIGO) and tumor-node-metastasis (TNM) staging criteria for ovarian carcinoma, the postoperative surgical stage was TIIbN0M0, corresponding to stage IIB (1).

Homologous recombination deficiency (HRD) genetic testing revealed no BRCA1 or BRCA2 germline mutations; however, the genomic instability score was 67, indicating HRD positivity. The patient was referred to the Oncology and Radiotherapy Center and received adjuvant chemotherapy consisting of carboplatin 500 mg plus docetaxel 80 mg every 3 weeks for six cycles. At the 1-year follow-up, there was no evidence of recurrence or metastasis. Figure 4 summarizes the timeline of this case report.

Figure 4 Timeline of the treatment route the patient received. CT, computed tomography; HGSC, high-grade serous carcinoma.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Key findings

This case reports an infrequent presentation of PFTC presented as a mass sigmoid colon mimicking primary colon carcinoma, despite completely normal uterine and adnexal imaging and negative serum tumor markers. Following hysterectomy and bilateral salpingo-oophorectomy, pathological examination revealed that the tumor originated from a microscopic HGSC (approximately 1 mm) located in the fimbrial end of the right fallopian tube.

Strengths and limitations

Early diagnosis is unquestionably associated with better prognosis in patients with PFTC. In this case, a comprehensive diagnostic evaluation—including detailed intra-abdominal exploration, extensive imaging, and thorough histopathological and immunohistochemical assessment—enabled the identification of an exceptionally small (approximately 1 mm) primary lesion in the fimbrial end of the fallopian tube. Moreover, this case provides valuable insight into an infrequent clinical manifestation of PFTC, thereby adding meaningful evidence to the limited literature and enhancing clinicians’ understanding of atypical manifestations. However, several limitations should be acknowledged. First, as a single case report, the generalizability of our findings is inherently limited. Second, due to the microscopic size of the primary lesion, it was not possible to perform direct molecular analyses—such as additional immunohistochemical markers or genetic testing—on the tubal tumor itself, limiting our ability to explore further and validate the underlying pathogenesis.

Comparison with similar research

Metastatic tumors to the colorectum account for approximately 1% of all colorectal malignancies, and ovarian cancer represents about 6% of metastatic colorectal tumors in women (9). Only a small number of cases describing colorectal metastases from ovarian or fallopian tube carcinoma have been reported. Deliveliotou et al. described the only documented case of isolated sigmoid colon metastasis originating from PFTC, in which the patient developed a serosal recurrence 3 years after hysterectomy and bilateral salpingo-oophorectomy for PFTC (10). Aqsa et al. reported sigmoid colon metastasis 3 years after ovarian cancer surgery, presenting as an isolated intraluminal fungating mass and later confirmed pathologically as metastatic ovarian carcinoma (11). Similarly, Kim et al. documented a case of sigmoid colon metastasis identified 8 years after ovarian cancer surgery, radiologically mimicking a primary colorectal carcinoma due to its intraluminal fungating appearance (12). A history of malignancy may therefore serve as an essential diagnostic clue when evaluating suspected metastatic colorectal lesions. However, in the present case, determining the primary tumor site was particularly challenging because the patient had no prior malignancy and initially presented with a solitary sigmoid colon mass mimicking primary colorectal cancer. In contrast, preoperative imaging of the uterus and adnexa, as well as serum tumor markers, was entirely normal.

Explanations of findings

Secondary metastasis to the colon may arise through direct invasion and peritoneal seeding from adjacent malignancies, or via hematogenous or lymphatic dissemination, as typically seen in metastatic breast cancer, lung cancer, or melanoma (13,14). In PFTC, colonic involvement most often results from direct invasion or peritoneal dissemination, with the serosal surface usually affected first, and tumor infiltration progressing inward through the bowel wall (10). In this case, histopathological examination demonstrated that tumor invasion was only confined to the colonic serosa, consistent with direct invasion or peritoneal dissemination. The extremely small primary fimbrial carcinoma—measuring only 1 mm—likely contributed to its absence on preoperative imaging and even intraoperative assessment. Moreover, early-stage PFTC typically presents with minimal tumor burden, and commonly used serum tumor markers have limited sensitivity and specificity in this setting. Together, these factors explain the negative tumor marker results in this patient and highlight the difficulty of preoperatively diagnosing early PFTC before detailed pathological evaluation.

Implications and actions needed

This case underscores the substantial difficulty of diagnosing PFTC preoperatively. Clinicians should adopt a comprehensive diagnostic approach, integrating medical history, imaging examinations, serum tumor markers, and a comprehensive histopathological and immunohistochemical evaluation. Tumor markers such as CA125, HE4, and estrogen receptor (ER)/progesterone receptor (PR) have limited sensitivity and specificity in early PFTC (15-17), and imaging modalities [ultrasound, CT, magnetic resonance imaging (MRI)] often lack distinctive features, frequently mimicking hydrosalpinx, tubo-ovarian abscess, or ovarian carcinoma (5,18). When pathology suggests a Müllerian origin despite normal imaging findings, surgical removal of the adnexa followed by comprehensive immunohistochemical and pathological evaluation of the ovaries, tubes, and fimbriae is critical for identifying the primary site. The immunophenotype of high-grade serous PFTC is typically characterized as CK7⁺/CK20⁻, PAX8⁺, and diffuse WT1⁺ expression, often accompanied by ER/PR positivity (19-21). whereas primary colorectal adenocarcinoma usually exhibits CK7⁻/CK20⁺ and CDX2⁺ staining (22). In this case, diffuse positivity for CK7, PAX8, and WT1, with negativity for CK20 and CDX2, strongly indicated a Müllerian origin. Combined with characteristic histomorphology, this confirmed the fallopian tube as the primary origin.

Although PFTC is uncommon, the incidence of its serous subtype increased more than fourfold between 2001 and 2014 (23). This trend may partly reflect the growing understanding of EOC pathogenesis. Studies have shown that tubal ligation confers a protective effect against ovarian cancer (24), supporting the widely accepted theory proposed by Kurman and Shih, which suggests that high-grade serous ovarian carcinoma (HGSOC) originates from the fallopian tubes (3). Subsequent extensive retrospective studies further demonstrated that tubal ligation or opportunistic salpingectomy markedly reduces the incidence of ovarian carcinoma (25). BRCA1/2 mutations markedly increase the risk of developing STIC, now recognized as the precursor lesion for most high-grade serous ovarian and peritoneal carcinomas (5). The earliest event typically involves TP53 mutations in the secretory epithelial cells of the fimbrial end, resulting in “p53 signatures”. These lesions may undergo clonal expansion, progress to STIC, and ultimately evolve into invasive PFTC, or exfoliate and disseminate to the ovary and peritoneum, forming primary ovarian or peritoneal carcinoma (3,26,27). In the present case, the metastatic tumor exhibited aberrant p53 staining consistent with the biology of HGSC. However, the tiny size of the fimbrial lesion (1 mm) prevented further immunohistochemistry and molecular analysis to confirm clonal relatedness between the primary and metastatic sites directly.

Based on the importance of molecular aspects, the patients’ genetic profile, and family history, the management of PFTC should involve a dedicated multidisciplinary team, including gynecologic oncologists, gynecologic surgeons, radiation oncologists, radiologists, geneticists, psychologists, and pathologists. The prognosis largely depends on the stage at diagnosis, the histological subtype, and the extent of optimal cytoreduction achieved during surgery (1). Standard treatment includes cytoreductive surgery followed by platinum-based combination chemotherapy (28). Targeted therapies such as PARP inhibitors and anti-angiogenic agents (e.g., bevacizumab) have been shown to improve outcomes and increase survival in high-risk patients (29,30). Because BRCA1/2 mutations and HRD occur at higher frequencies in HGSCs and often correlate with a stronger family history, genetic counseling and germline or somatic testing are recommended for all patients, regardless of age or family background (31). Such testing not only informs the selection of targeted treatments but also supports risk assessment and preventive strategies for family members at risk.

Conclusions

In conclusion, we report a rare case of isolated colon metastasis from a microscopic HGSC of the fallopian tube fimbria mimicking a primary colon cancer. It underscores the diagnostic challenges of PFTC, which is often missed or misdiagnosed preoperatively due to its nonspecific symptoms. Accurate diagnosis is crucial for effective treatment strategies; thus, the absence of macroscopic disease on imaging or during surgery should not rule out PFTC. Comprehensive immunohistochemical and pathological analyses remain fundamental for identifying primary lesions of malignancies with atypical presentations.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://gpm.amegroups.com/article/view/10.21037/gpm-25-32/rc

Peer Review File: Available at https://gpm.amegroups.com/article/view/10.21037/gpm-25-32/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://gpm.amegroups.com/article/view/10.21037/gpm-25-32/coif). Z.L. serves as an unpaid editorial board member of Gynecology and Pelvic Medicine from June 2024 to December 2025. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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