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 Table of Contents  
REVIEW ARTICLE
Year : 2021  |  Volume : 10  |  Issue : 5  |  Page : 225-226

Serous tubal intraepithelial carcinoma: Emerging trend in ovarian neoplasm: A must know for a pathologist


Department of Pathology, Dr. D. Y. Patil Medical College, Hospital and Research Center, Pune, Maharashtra, India

Date of Submission28-Apr-2021
Date of Acceptance23-Jul-2021
Date of Web Publication28-Oct-2021

Correspondence Address:
Banyameen Iqbal
Department of Pathology, Dr. D. Y. Patil Medical College, Hospital and Research Center, Pimpri, Pune - 411 018, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ccij.ccij_46_21

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  Abstract 


Among all gynecological malignancies, ovarian cancer is associated with the highest rate of mortality. Most ovarian carcinomas have been suggested to originate from the ovarian surface epithelium or postovulatory inclusion cysts formed after follicular rupture and repair. Over the past decade, a new model has emerged to explain the origin of epithelial tumors of the ovary and the fallopian tube now appears to play a central role; however, there is now compelling evidence that many epithelial pelvic cancers, especially high-grade serous carcinomas of the ovary/peritoneum, begin in the mucosa of the fallopian tube as serous tubal intraepithelial carcinoma.

Keywords: Fallopian tube, ovary, serous tubal intraepithelial carcinoma


How to cite this article:
Iqbal B. Serous tubal intraepithelial carcinoma: Emerging trend in ovarian neoplasm: A must know for a pathologist. Clin Cancer Investig J 2021;10:225-6

How to cite this URL:
Iqbal B. Serous tubal intraepithelial carcinoma: Emerging trend in ovarian neoplasm: A must know for a pathologist. Clin Cancer Investig J [serial online] 2021 [cited 2021 Dec 6];10:225-6. Available from: https://www.ccij-online.org/text.asp?2021/10/5/225/329480




  What Should Be Known? Top


Among all gynecological malignancies, ovarian cancer is associated with the highest rate of mortality. It is estimated that there will be >1,40,000 deaths per year worldwide.[1] Although many surgical techniques and chemotherapies have been developed for ovarian carcinoma, the prognosis remains poor, with a 5-year survival rate of 45%.[2] Most ovarian carcinomas have been suggested to originate from the ovarian surface epithelium or postovulatory inclusion cysts formed after follicular rupture and repair.[3] According to the incessant ovulation hypothesis, every ovulation creates a wound, and the surface ovarian epithelial cells are then repaired by increased proliferation. This may increase the likelihood for DNA damage and carcinogenic mutations.[4] However, this hypothesis is inconsistent with the observation that the patients with polycystic ovarian syndrome who have decreased ovulatory cycles appear to have an increased ovarian cancer risk.[5] Nevertheless, attempts to define a precursor lesion from this tissue have always failed.

Over the past decade, a new model has emerged to explain the origin of epithelial tumors of the ovary and the fallopian tube now appears to play a central role. Pathologists have always paid little attention to the fallopian tube; however, there is now compelling evidence that many epithelial pelvic cancers, especially high-grade serous carcinomas (HGSCs) of the ovary/peritoneum, begin in the mucosa of the fallopian tube as serous tubal intraepithelial carcinoma (STIC). This is independent of the fact, whether or not the patient has BRCA mutation and has an increased risk of breast and ovarian cancers. Pelvic HGSC can be diagnosed in an early stage, now if the pathologists focus their attention to fallopian tubes and look for STIC lesions. These lesions are in the mucosa of the fimbriae of fallopian tubes. These tubal tumors are microscopic, high grade, and resemble HGSC are usually noninvasive and harbor p53 mutations as in advanced stages of HGSC. STIC is found in almost 60% of women with ovarian or peritoneal HGSC only if the tubes are carefully processed for complete microscopic examination.[6]

These features suggest that all these pelvic HGSC first start in the mucosa of the fallopian tube as STIC and shed these tumor cells which then get implanted on the ovary and peritoneum where they progress to form large tumors.[7] One more hypothesis suggests that these benign mucosal cells from the fallopian tube get shed onto the ovary during ovulation and get entrapped in the ovarian tissue near the ruptured ovarian follicle which later on form epithelial inclusion glands and cysts in the ovary, which may later transform into HGSC.

Molecular studies are identifying the sequence of events which lead to the transformation to STIC in fallopian tubes and HGSC in the ovary. P53 appears to play a major role. In women, who do not have BRCA germline mutations, there may be a risk-reducing role for removing fallopian tubes during abdominal surgery done for any other indication or for performing salpingectomy instead of tubal ligation for sterilization.[8]


  How Are Serous Tubal Intraepithelial Carcinoma Lesions Diagnosed Top


Traditionally, the technique of taking one cross section from the middle of the fallopian tube and not from the nonfimbriated end for histopathologic examination should be discouraged because these STIC lesions are present in the fimbriated end of the fallopian tube and can be missed on traditional grossing techniques. After proper grossing, a pathologist should be aware of the diagnostic criteria for tubal carcinoma, in particular STIC.

Currently, the diagnosis of these STIC lesions depends on a combination of morphology and immunohistochemistry. The morphologic criteria are severe nuclear atypia, mitosis, and loss of polarity of the mucosa of the tube (i.e. stratification, piling up, and tufting). There should also be a loss of normal specialized features of tubal mucosa such as cilia, terminal bars, and peg cells. The immunohistochemical criteria are aberrant P53 and MIB1 staining. Aberrant P53 staining is defined as either diffuse, strong nuclear expression, or complete absence of any staining in any nuclei. Normal mucosal epithelium should exhibit patchy week nuclear P53 expression. Aberrant MIB1 staining simply means that the percent of cells that exhibit nuclear expression in the lesion is noticeably higher than the small percent of cells in the adjacent normal mucosa (some authors suggest 10% or more is sufficient to call aberrant). When both the criteria are met the diagnosis of STIC can be made. If invasion into the underlying stroma is present, then a diagnosis of invasive tubal HGSC can be made. Occasionally, some tubal proliferations may show partial criteria but not all criteria for STIC; some suggest naming them as serous tubal intraepithelial lesion. Their management still remains to be ascertained.


  Difficulties in Diagnosis Top


It is possible for metastasis from either primary gynecological tumor outside the tube (endometrium and cervix) or primary nongynecological tumors (colorectal and breast) to grow in the fallopian tube and mimic STIC. Primary gynecological tumors should be PAX8 positive, whereas nongynecological carcinomas are PAX8 negative. In addition, STIC should be WT1 positive, whereas nonserous carcinomas of the gynecological organs are WT1 negative. PAX8 and WT1 are useful when trying to differentiate STIC from metastatic carcinoma of other sites.


  Differential Diagnosis Top


The differential diagnosis of STIC includes a variety of benign proliferations, metaplasias and reactive alterations to inflammation, hemorrhage (endometriosis), or prior treatment (radiation and chemotherapy).

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D. Global cancer statistics. CA Cancer J Clin 2011;61:69-90.  Back to cited text no. 1
    
2.
Siegel R, Ward E, Brawley O, Jemal A. Cancer statistics, 2011: The impact of eliminating socioeconomic and racial disparities on premature cancer deaths. CA Cancer J Clin 2011;61:212-36.  Back to cited text no. 2
    
3.
Mok SC, Kwong J, Welch WR, Samimi G, Ozbun L, Bonome T, et al. Etiology and pathogenesis of epithelial ovarian cancer. Dis Markers 2007;23:367-76.  Back to cited text no. 3
    
4.
Landen CN, Birrer MJ, Sood AK. Early events in the pathogenesis of epithelial ovarian cancer. J Clin Oncol 2008;26:995-1005.  Back to cited text no. 4
    
5.
Schildkraut JM, Schwingl PJ, Bastos E, Evanoff A, Hughes C. Epithelial ovarian cancer risk among women with polycystic ovary syndrome. Obstet Gynecol 1996;88:554-9.  Back to cited text no. 5
    
6.
Tone AA, Salvador S, Finlayson SJ, Tinker AV, Kwon JS, Lee CH, et al. The role of the fallopian tube in ovarian cancer. Clin Adv Hematol Oncol 2012;10:296-306.  Back to cited text no. 6
    
7.
Kurman RJ, Shih IeM. The origin and pathogenesis of epithelial ovarian cancer: A proposed unifying theory. Am J Surg Pathol 2010;34:433-43.  Back to cited text no. 7
    
8.
Kessler M, Fotopoulou C, Meyer T. The molecular fingerprint of high grade serous ovarian cancer reflects its fallopian tube origin. Int J Mol Sci 2013;14:6571-96.  Back to cited text no. 8
    




 

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