Serous Tubal Intraepithelial Carcinoma (STIC)-like Lesions Arising in Ovarian Serous Cystadenofibroma

Craig, Elaine; Clarke, R.; Rushton, Gary; McCluggage, W. Glenn

doi:10.1097/pgp.0000000000000195

Cited by 9 publications

(3 citation statements)

References 24 publications

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“…The term ‘STIC‐like’ lesion was used in the same year in a study co‐authored by one of us (W.G.M.) in a report of two cases of ovarian serous cystadenofibromas with focal involvement of the epithelial lining of the neoplasms by a high‐grade serous proliferation with mutation‐type p53 staining without invasion of the underlying stroma 12 . The term ‘STIC‐like’ lesion has also been used for cases of fallopian tube mucosal involvement without ‘invasion’ by uterine serous carcinoma (USC) 13 .…”

Section: Figurementioning

confidence: 99%

‘STIC‐like’ lesions in ovarian low‐grade serous carcinoma: a diagnostic pitfall

Machuca-Aguado

McCluggage

2023

Histopathology

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Section: Figurementioning

confidence: 99%

‘STIC‐like’ lesions in ovarian low‐grade serous carcinoma: a diagnostic pitfall

Machuca-Aguado

McCluggage

2023

Histopathology

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“…With genetic screening and risk-reducing salpingooophorectomy (RRSO), early HGSCs with TP53 mutations have been reported in the fallopian tubes of asymptomatic vulnerable women with germline BRCA1/2 mutations (BRCA m ) [4][5][6][7][8][9][10][11][12][13][14]. A pathologic dissection protocol ('SEE-FIM'), introduced in 2005, focused on the distal fallopian tube (fimbria), and a range of serous cancer precursors (serous tubal intraepithelial lesions, STIL) and serous tubal intraepithelial carcinomas (STIC) with TP53 mutations have been described (Figure 1A-C) [15][16][17].…”

Section: The Tubal Theory Of Ovarian Carcinogenesismentioning

confidence: 99%

Genomic catastrophe, the peritoneal cavity and ovarian cancer prevention

Yoon

Chapel

Goebel

et al. 2022

The Journal of Pathology

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The current theory of carcinogenesis for the deadliest of ‘ovarian’ cancers—high‐grade serous carcinoma (HGSC)—holds that the malignancy develops first in the fallopian tube and spreads to the ovaries, peritoneum, and/or regional lymph nodes. This is based primarily on the observation of early forms of serous neoplasia (serous tubal intraepithelial lesions [STILs], and serous tubal intraepithelial carcinomas [STICS]) in the fimbria of women undergoing risk reduction surgery. However, these lesions are uncommon in the general population, confer a low risk (5%) of HGSC following their removal in at‐risk women with germ‐line BRCA1/2 mutations, and require 4 or more years to recur as intraperitoneal HGSC. These features suggest that isolated STILs and STICs behave as precursors, with uncertain cancer risk rather than carcinomas. Their evolution to HGSC within, or after, escape from the tube could proceed stepwise with multiple biologic events; however, it is unclear whether tubal or ovarian HGSCs encountered in the setting of advanced disease evolved in the same fashion. The latter scenario could also be explained by a ‘catastrophic’ model in which STICs suddenly develop with invasive and metastatic potential, overwhelming or obscuring the site of origin. Moreover, a similar model might explain the sudden emergence of HGSC in the peritoneal cavity following escape of precursor cells years before. Long‐term follow‐up data from opportunistic or prophylactic salpingectomy should shed light on where malignant transformation occurs, as well as the timeline from precursor to metastatic HGSC. © 2022 The Pathological Society of Great Britain and Ireland.

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“…The observation that many cancers were associated with large cystic masses could be interpreted to mean that the lesions develop within pre-existing cysts such as endosalpingosis, endometriomas or adenofibromas [23]. However, there was little direct evidence (except in rare instances) that HGSCs arise from these preexisting conditions [26]. Two studies performing an exhaustive examination of the ovarian cortical inclusion cysts of women with BRCA mutations failed to identify any evidence of a precursor with TP53 mutation [27,28].…”

Section: Unanswered Questionsmentioning

confidence: 99%

Back to the Future? The Fallopian Tube, Precursor Escape and a Dualistic Model of High-Grade Serous Carcinogenesis

Soong

Kolin

Teschan

2018

Cancers

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Beginning with the discovery of the BRCA-associated ovarian cancer susceptibility genes and subsequent detailed examination of risk-reducing salpingo-oophorectomy (RRSO) specimens, a new paradigm of ovarian carcinogenesis has unfolded with attention to the distal fallopian tube. The primary focus has been an early cancer or neoplasm in the fallopian tube which is seen in virtually all incidentally discovered high-grade serous cancers in asymptomatic women. This high-frequency of tubal involvement in early serous neoplasm (usually in the form of serous tubal intraepithelial carcinoma—STIC) has galvanized attention to this organ as a primary source of this disease. However, an enduring mystery has been the relatively low frequency of STIC in the fallopian tubes of women with advanced malignancy. This paradox, a high frequency of tubal involvement early on and a low frequency of involvement later in the disease process, has spurred interest in other potential sources, such as the ovarian surface epithelium or cortical inclusions and the secondary Mullerian system. However, because essentially all high-grade serous carcinomas are linked by TP53 mutations, and because fallopian tubes frequently contain early serous proliferations (ESPs) with these mutations, attention has turned to the possibility that the nonmalignant but TP53 mutated tubal epithelium could be responsible for an eventual malignancy. Recent data have shown evidence of a lineage continuity between ESPs and concurrent serous carcinomas prompting the concept of “precursor escape”. This creates a second component of the paradigm by which cells from early precursors are shed from the tube and undergo subsequent malignant transformation, emerging suddenly as widespread intraperitoneal malignancy. This dualistic model thus provides a unique pathway by which the future outcome (wide spread high-grade serous carcinomas—HGSC) is ultimately explained by going back in time to an early serous proliferation. This paradigm also brings the peritoneal cavity into focus, raising new questions about the potential co-variables or exposures that might facilitate the occasional malignant transformation of an ESP in the peritoneal cavity or on the peritoneal surface.

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Serous Tubal Intraepithelial Carcinoma (STIC)-like Lesions Arising in Ovarian Serous Cystadenofibroma

Cited by 9 publications

References 24 publications

‘STIC‐like’ lesions in ovarian low‐grade serous carcinoma: a diagnostic pitfall

‘STIC‐like’ lesions in ovarian low‐grade serous carcinoma: a diagnostic pitfall

Genomic catastrophe, the peritoneal cavity and ovarian cancer prevention

Back to the Future? The Fallopian Tube, Precursor Escape and a Dualistic Model of High-Grade Serous Carcinogenesis

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