Fallopian Tube Intraluminal Tumor Spread From Noninvasive Precursor Lesions

2013 ◽  
Vol 37 (8) ◽  
pp. 1123-1130 ◽  
Author(s):  
Jonathan G. Bijron ◽  
Cornelis A. Seldenrijk ◽  
Ronald P. Zweemer ◽  
Joost G. Lange ◽  
René H.M. Verheijen ◽  
...  
2014 ◽  
Vol 132 (2) ◽  
pp. 322-327 ◽  
Author(s):  
K. Bahar-Shany ◽  
H. Brand ◽  
S. Sapoznik ◽  
J. Jacob-Hirsch ◽  
Y. Yung ◽  
...  

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Amy L. Gross ◽  
Robert J. Kurman ◽  
Russell Vang ◽  
Ie-Ming Shih ◽  
Kala Visvanathan

The lack of proven screening tools for early detection and the high mortality of ovarian serous carcinoma (OSC), particularly high grade, have focused attention on identifying putative precursor lesions with distinct morphological and molecular characteristics. The finding of occult invasive and intraepithelial fallopian tube carcinomas in prophylactically removed specimens from asymptomatic high-risk BRCA 1/2-mutation carriers supports the notion of an origin for OSC in the fallopian tube. The intraepithelial carcinomas have been referred to as serous intraepithelial carcinomas (STICs) but our own findings (unpublished data) and recent reports have drawn attention to a spectrum of changes that fall short of STICs that we have designated serous tubal intraepithelial lesions (STILs).


2001 ◽  
Vol 11 (4) ◽  
pp. 283-289 ◽  
Author(s):  
L. B. Jordan ◽  
M. Abdul-Kader ◽  
A. Al-Nafussi

Abstract.Jordan LB, Abdul-Kader M, Al-Nafussi A. Uterine serous papillary carcinoma: Histopathologic changes within the female genital tract.The histopathologic features of 25 patients with uterine serous papillary carcinoma (USPC) were presented, with particular emphasis on the changes seen in the remaining müllerian epithelium. The mean age at presentation was 68.9 years; 52% of patients were stage III at the time of presentation and 40% died of their disease within 24 months of diagnosis. Histologic assessment revealed: 1) pure serous carcinoma in 56% of patients and mixed differentiation of serous and endometrioid in the remainder; 2) malignant epithelium reminiscent of that of USPC and akin to carcinoma in situ, frequently seen in the remaining endometrium, cervix, and, less commonly, the fallopian tube; 3) residual endometrium that, when identified (11/25 cases), was atrophic in all cases; 4) various types of cervical involvement in 17 cases (68%) ; 5) tumor within the fallopian tube in three cases (12%); and 6) carcinoma with in situ-like features in five cases (20%). In conclusion, it appears that USPC is frequently associated with malignant epithelial changes (as with carcinoma in situ) in the remaining müllerian epithelium. This finding suggests either a field change or, more likely, a transepithelial tumor spread. The latter theory is preferable, because this type of spread is frequently seen on serosal surfaces in cases of serous ovarian carcinoma. Uterine serous papillary carcinoma is, therefore, biologically more akin to its ovarian counterpart.


2015 ◽  
Vol 34 (1) ◽  
pp. 57-64 ◽  
Author(s):  
Mary C. Tolcher ◽  
Elizabeth M. Swisher ◽  
Fabiola Medeiros ◽  
Joema F. Lima ◽  
Jodi L. Hilderbrand ◽  
...  

2008 ◽  
Vol 110 (3) ◽  
pp. 408-417 ◽  
Author(s):  
Shannon Salvador ◽  
Allan Rempel ◽  
Robert A. Soslow ◽  
Blake Gilks ◽  
David Huntsman ◽  
...  

2019 ◽  
Vol 41 (5) ◽  
pp. 646-655 ◽  
Author(s):  
Jose A Colina ◽  
Peter Varughese ◽  
Subbulakshmi Karthikeyan ◽  
Amrita Salvi ◽  
Dimple A Modi ◽  
...  

AbstractHigh-grade serous ovarian cancer (HGSOC) is thought to progress from a series of precursor lesions in the fallopian tube epithelium (FTE). One of the preneoplastic lesions found in the FTE is called a secretory cell outgrowth (SCOUT), which is partially defined by a loss of paired box 2 (PAX2). In the present study, we developed PAX2-deficient murine cell lines in order to model a SCOUT and to explore the role of PAX2 loss in the etiology of HGSOC. Loss of PAX2 alone in the murine oviductal epithelium (MOE) did not induce changes in proliferation, migration and survival in hypoxia or contribute to resistance to first line therapies, such as cisplatin or paclitaxel. RNA sequencing of MOE PAX2shRNA cells revealed significant alterations in the transcriptome. Silencing of PAX2 in MOE cells produced a messenger RNA expression pattern that recapitulated several aspects of the transcriptome of previously characterized human SCOUTs. RNA-seq analysis and subsequent qPCR validation of this SCOUT model revealed an enrichment of genes involved in estrogen signaling and an increase in expression of estrogen receptor α. MOE PAX2shRNA cells had higher estrogen signaling activity and higher expression of putative estrogen responsive genes both in the presence and absence of exogenous estrogen. In summary, loss of PAX2 in MOE cells is sufficient to transcriptionally recapitulate a human SCOUT, and this model revealed an enrichment of estrogen signaling as a possible route for tumor progression of precursor lesions in the fallopian tube.


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