2
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Thoracic spinal metastasis as recurrence of borderline Brenner tumor without local recurrence: A case report

      case-report

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Highlights

          • Brenner tumor is a rare epithelial ovarian neoplasm.

          • Metastasis may occur even after diagnosis as a borderline Brenner tumor.

          • We report the first case of thoracic spinal metastasis of a recurrent Brenner tumor.

          Abstract

          Background

          Brenner tumor is a rare epithelial ovarian neoplasm that accounts for 2–3% of all ovarian neoplasms. Herein, we report the first case of thoracic spinal metastasis of recurrent Brenner tumor without local recurrence.

          Case Description.

          A 70-year-old female presented with a feeling of abdominal distension. Computed tomography revealed cystic lesions in her bilateral ovaries. Blood examination revealed high CA-125 [74.9 U/ml]. We excised bilateral ovaries, uterus, and omentum. Borderline Brenner tumor was diagnosed [Ki-67 labeling index: 10 %]. Follow-up abdominal echo and CA-125 examination revealed no local recurrence. 26 months later she developed paraplegia. Magnetic resonance imaging revealed tumor in the 5th-9th thoracic vertebra and compression of spinal cord at the 6th thoracic vertebra level. Her paraplegia was progressive. We performed semi-urgent partial resection of tumor and release of spinal cord compression. Spinal metastasis from Brenner tumor was diagnosed [Ki-67 labeling index: 50–60 %]. She received adjuvant radiation of 30 Gy in 10 fractions to the 4th-10th thoracic vertebra. After radiation and rehabilitation, she was discharged home on foot. She received adjuvant radiation and chemotherapy but died 11 months after spinal surgery. An autopsy has not been performed on her, and the cause of death is unknown.

          Conclusion

          We report the first case of thoracic metastasis of recurrent Brenner tumor without local recurrence.

          Related collections

          Most cited references17

          • Record: found
          • Abstract: found
          • Article: not found

          The origin and pathogenesis of epithelial ovarian cancer: a proposed unifying theory.

          Ovarian cancer is the most lethal gynecologic malignancy. Efforts at early detection and new therapeutic approaches to reduce mortality have been largely unsuccessful, because the origin and pathogenesis of epithelial ovarian cancer are poorly understood. Despite numerous studies that have carefully scrutinized the ovaries for precursor lesions, none have been found. This has led to the proposal that ovarian cancer develops de novo. Studies have shown that epithelial ovarian cancer is not a single disease but is composed of a diverse group of tumors that can be classified based on distinctive morphologic and molecular genetic features. One group of tumors, designated type I, is composed of low-grade serous, low-grade endometrioid, clear cell, mucinous and transitional (Brenner) carcinomas. These tumors generally behave in an indolent fashion, are confined to the ovary at presentation and, as a group, are relatively genetically stable. They lack mutations of TP53, but each histologic type exhibits a distinctive molecular genetic profile. Moreover, the carcinomas exhibit a shared lineage with the corresponding benign cystic neoplasm, often through an intermediate (borderline tumor) step, supporting the morphologic continuum of tumor progression. In contrast, another group of tumors, designated type II, is highly aggressive, evolves rapidly and almost always presents in advanced stage. Type II tumors include conventional high-grade serous carcinoma, undifferentiated carcinoma, and malignant mixed mesodermal tumors (carcinosarcoma). They displayTP53 mutations in over 80% of cases and rarely harbor the mutations that are found in the type I tumors. Recent studies have also provided cogent evidence that what have been traditionally thought to be primary ovarian tumors actually originate in other pelvic organs and involve the ovary secondarily. Thus, it has been proposed that serous tumors arise from the implantation of epithelium (benign or malignant) from the fallopian tube. Endometrioid and clear cell tumors have been associated with endometriosis that is regarded as the precursor of these tumors. As it is generally accepted that endometriosis develops from endometrial tissue by retrograde menstruation, it is reasonable to assume that the endometrium is the source of these ovarian neoplasms. Finally, preliminary data suggest that mucinous and transitional (Brenner) tumors arise from transitional-type epithelial nests at the tubal-mesothelial junction by a process of metaplasia. Appreciation of these new concepts will allow for a more rationale approach to screening, treatment, and prevention that potentially can have a significant impact on reducing the mortality of this devastating disease.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Ovarian Cancer Is an Imported Disease: Fact or Fiction?

            The cell of origin of ovarian cancer has been long debated. The current paradigm is that epithelial ovarian cancer (EOC) arises from the ovarian surface epithelium (OSE). OSE is composed of flat, nondescript cells more closely resembling the mesothelium lining the peritoneal cavity, with which it is continuous, rather than the various histologic types of ovarian carcinoma (serous, endometrioid, and clear cell carcinoma), which have a Müllerian phenotype. Accordingly, it has been argued that the OSE undergoes a process termed "metaplasia" to account for this profound morphologic transformation. Recent molecular and clinicopathologic studies not only have failed to support this hypothesis but also have provided evidence that EOC stems from Müllerian-derived extraovarian cells that involve the ovary secondarily, thereby calling into question the very existence of primary EOC. This new model of ovarian carcinogenesis proposes that fallopian tube epithelium (benign or malignant) implants on the ovary to give rise to both high-grade and low-grade serous carcinomas, and that endometrial tissue implants on the ovary and produces endometriosis, which can undergo malignant transformation into endometrioid and clear cell carcinoma. Thus, ultimately EOC is not ovarian in origin but rather is secondary, and it is logical to conclude that the only true primary ovarian neoplasms are germ cell and gonadal stromal tumors analogous to tumors in the testis. If this new model is confirmed, it has profound implications for the early detection and treatment of "ovarian cancer."
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Transitional cell tumors of the ovary: a comparative clinicopathologic, immunohistochemical, and molecular genetic analysis of Brenner tumors and transitional cell carcinomas.

              Transitional cell tumors of the ovary include 2 distinct clinicopathologic categories: Brenner tumors and transitional cell carcinomas (TCCs). Their molecular genetic alterations have not been fully investigated. We have performed a clinicopathologic, immunohistochemical, and molecular genetic analysis of 19 transitional cell tumors including 13 Brenner tumors (5 benign, 7 borderline, and 1 malignant) and 6 TCCs. Immunoreactivity for epidermal growth factor receptor (EGFR), Ras, Cyclin D1, p16, Rb, and p53, as well as fluorescence in situ hybridization analysis for EGFR were assessed in all cases. Screening for mutations in K-Ras, B-Raf, CTNNB1, PIK3CA, and p53 genes was also performed. The mean patient age was 58 years (range, 32 to 85 y). Abdominal enlargement and pain were the usual complaints. Treatment was known in 14 patients: 10 had hysterectomy with bilateral salpingo-oophorectomy, which was accompanied by omentectomy in 7; and 4 had only unilateral or bilateral salpingo-oophorectomy, 1 with omentectomy. Four patients had brachytherapy. Six borderline Brenner tumors were stage IA and 1 stage IIA. The malignant Brenner tumor was stage IA. One TCC was stage IA, one IC, 2 IIIC and the stage was unknown in 2 cases. Follow-up information was available only in 5 of the nonbenign cases. Two patients who had borderline Brenner tumors were alive and well at 3 and 10.9 years. The patient who had a malignant Brenner tumor died of pulmonary thromboembolism shortly postoperatively, and 2 patients with TCCs died of tumor 1.8 and 13 years, postoperatively. Brenner tumors and TCCs differed mainly in the expression of EGFR, p16, and p53. Benign Brenner tumors showed a low immunoexpression for all markers. Borderline Brenner tumors failed to immunoreact for p16, Rb, and p53; and showed weak immunostaining for Cyclin D1, moderate for Ras, and strong for EGFR. The malignant Brenner tumor was also negative for p16, Rb, and p53, and strongly positive for Cyclin D1, Ras, and EGFR. In contrast, TCCs had p53 mutations with p53 and p16 protein overexpression and showed a negative immunoreaction for EGFR, Cyclin D1, and Ras. Our results suggest that Brenner tumors and TCCs follow different tumorigenic pathways, whereas borderline and malignant Brenner tumors are low-grade neoplasms with activation of the PI3K/AKT pathway through EGFR, TCCs are high-grade tumors that have p53 mutations and p16 and p53 protein overexpression.
                Bookmark

                Author and article information

                Contributors
                Journal
                Gynecol Oncol Rep
                Gynecol Oncol Rep
                Gynecologic Oncology Reports
                Elsevier
                2352-5789
                13 December 2022
                December 2022
                13 December 2022
                : 44
                : 101120
                Affiliations
                [a ]Department of Neurosurgery, Kyoto Okamoto Memorial Hospital, Sayamanishinoguchi 100, Kumiyama-cho, Kuse-gun, Kyoto 613-0034 Japan
                [b ]Department of Gynecology, Kyoto Okamoto Memorial Hospital, Sayamanishinoguchi 100, Kumiyama-cho, Kuse-gun, Kyoto 613-0034 Japan
                [c ]Department of Pathology, Kyoto Okamoto Memorial Hospital, Sayamanishinoguchi 100, Kumiyama-cho, Kuse-gun, Kyoto 613-0034 Japan
                [d ]Department of Radiotherapy, Kyoto Okamoto Memorial Hospital, Sayamanishinoguchi 100, Kumiyama-cho, Kuse-gun, Kyoto 613-0034 Japan
                Author notes
                [* ]Corresponding author. fujita-kyf@ 123456umin.ac.jp
                Article
                S2352-5789(22)00200-4 101120
                10.1016/j.gore.2022.101120
                9797606
                36589509
                5aa7e921-844e-499c-9e03-6a06c72fe843
                © 2022 The Author(s)

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 5 October 2022
                : 16 November 2022
                : 22 November 2022
                Categories
                Case Report

                brenner tumor,thoracic spinal metastasis,recurrence,bt, brenner tumor,ct, computed tomography

                Comments

                Comment on this article

                scite_
                0
                0
                0
                0
                1
                Smart Citations
                This paper has been withdrawn 1 time
                0
                0
                0
                0
                Citing PublicationsSupportingMentioningContrasting
                View Citations

                See how this article has been cited at scite.ai

                scite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.

                Similar content148

                Most referenced authors130