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1 ainly located in the upper tract (uterus and fallopian tubes).
2 ectopic pregnancy is embryo retention in the fallopian tube.
3 ht to originate in the distal portion of the fallopian tube.
4 s such as the respiratory epithelium and the fallopian tube.
5 g the testes, epididymis, uterus, ovary, and fallopian tube.
6 t was also present on time epithelium of the fallopian tube.
7 receptor (FSHR) expression in the ovary and fallopian tube.
8 lls but not from the proximal portion of the fallopian tube.
9 and in the general population arise from the fallopian tube.
10 death and sloughing of ciliated cells of the Fallopian tube.
11 the ovary, namely the secretory cells of the fallopian tube.
12 tasis in an ex vivo infection model of human fallopian tubes.
13 e revealing the influence of estrogen on the fallopian tubes.
14 0 and are also predisposed to cancers of the fallopian tubes.
15 od, lymph nodes, vagina, cervix, uterus, and fallopian tubes.
16 mullerian duct-derived epithelium of normal fallopian tubes.
17 salpingography to depict normal and diseased fallopian tubes.
18 s in the toxicity of N. gonorrhoeae to human fallopian tubes.
19 tudy patients with surgically proved dilated fallopian tubes.
20 the lower genital tract into the uterus and fallopian tubes.
21 epithelia in brain ventricles, airways, and Fallopian tubes.
22 production and ciliated cell death in human fallopian tubes.
23 be caused by pelvic adhesions affecting the fallopian tubes.
24 essed by normal endocervix, endometrium, and fallopian tube (60, 64, and 29% of specimens, respective
25 mon biologic origin, likely to be the distal fallopian tube among all cases.High-grade serous carcino
27 to 40 years of age, had at least one patent fallopian tube and a normal uterine cavity, and had a ma
28 ealed highest expression of this molecule in fallopian tube and cervical tissues, followed by endomet
32 f open chromatin and histone modification in fallopian tube and ovarian surface epithelial cells (FTS
34 velop from intraepithelial carcinomas in the fallopian tube and, as a result, disseminate as carcinom
35 sets to gene expression sets of eight normal fallopian tubes and 499 high-grade serous malignant ovar
37 ith highest expression in the upper tissues (fallopian tubes and endometrium), followed by cervix and
39 is commonly result in ascending infection to fallopian tubes and subsequent immune-mediated tubal pat
40 ing genital infections cause inflammation of fallopian tubes and subsequent scarring and occlusion.
41 are relatively common in women with ovarian, fallopian tube, and peritoneal carcinoma (OC) causing a
48 taining the relevant cell types of the human fallopian tube as well as a luminal architecture that cl
49 op high-grade serous cancers, removal of the fallopian tube at an early age prevents cancer formation
53 and BRCA2 carriers after RRBSO with ovarian, fallopian tube, breast, and peritoneal cancer published
54 factors for PID, confirmed PID, and occluded fallopian tubes but not with acute C. trachomatis infect
55 by normal vagina and ectocervix and inflamed fallopian tube, but variably expressed by normal endocer
58 cinoma of the peritoneum (four patients), or fallopian tube cancer (two patients) who previously had
59 V epithelial ovarian, primary peritoneal, or fallopian tube cancer and were not selected for EGFR exp
60 ients with recurrent ovarian, peritoneal, or fallopian tube cancer have limited therapeutic options.
61 e epithelial ovarian, primary peritoneal, or fallopian tube cancer, and a clinical complete response
66 l resemblance to human serous cancers, these fallopian tube cancers highly express genes that are kno
68 II trial included the following: ovarian and fallopian tube cancers or primary carcinoma of the perit
69 -one breast, ovarian, primary peritoneal, or fallopian tube cancers were detected after receipt of ge
70 0 (16%) had peritoneal cancer, four (6%) had fallopian tube cancers, and three (5%) had uterine papil
74 tations among Ashkenazi Jewish patients with fallopian tube carcinoma (FTC) or primary peritoneal car
75 s isolated from a previous transgenic murine fallopian tube carcinoma model, and confirmed that loss
76 t epithelial ovarian, primary peritoneal, or fallopian tube carcinoma with a maximum of two prior che
77 endometrioid ovarian, primary peritoneal, or fallopian tube carcinoma, had received at least two prev
78 d for all women with ovarian, peritoneal, or fallopian tube carcinoma, regardless of age or family hi
80 ed from UW, there was a higher proportion of fallopian tube carcinomas (13.3% vs 5.7%; P < .001); sta
81 the level of genomic aberration observed in fallopian tube carcinomas compared with high-grade serou
82 a genome-wide copy number analysis of occult fallopian tube carcinomas identified through risk-reduci
83 ubal intraepithelial carcinomas (STICs), and fallopian tube carcinomas), ovarian cancers, and metasta
84 ade that primary ovarian epithelial tumours, fallopian tube carcinomas, and primary peritoneal carcin
87 for temporal resolution, spatial resolution, fallopian tube conspicuity, and free spill conspicuity.
91 s end, the adhesion molecules induced on the fallopian tube endothelium during infection with C. trac
93 g were investigated by using cultured bovine fallopian tube epithelial (BFTE) cells inoculated with C
95 SEC) cultures are useful for studying normal fallopian tube epithelial biology, as well as for develo
97 talized ovarian surface epithelial cells and fallopian tube epithelial cells via a single-run mass sp
102 op new and robust model systems to study the fallopian tube epithelium as the cell of origin of "ovar
103 experimental model systems for studying the fallopian tube epithelium in high-risk women as well as
104 ad molecular profiles more similar to normal fallopian tube epithelium than ovarian surface epitheliu
110 difference in ciliary beat frequency between fallopian tubes exposed to peritoneal fluids of women wi
111 ions of genital chlamydial infection include fallopian tube fibrosis and tubal factor infertility.
112 his article, we discuss the emergence of the fallopian tube fimbria as a field of origin for high-gra
113 %) of 147 women with PID and from ovaries or fallopian tubes from 5 (22.7%) of 22 women with PID, but
115 ous ovarian carcinomas (SOCs) arise from the fallopian tube (FT) epithelium rather than the ovarian s
118 om multiple extra-ovarian origins, including fallopian tube, gastrointestinal tract, cervix and endom
119 26 patients with nonuniform sampling of the fallopian tubes (group 1) and 19 patients with complete
122 mors of the ovary and Walthard cell nests of Fallopian tubes have been considered to represent urothe
123 primary samples of normal, nondiseased human fallopian tubes, (ii) transformation of FTSECs with defi
124 ome of the fimbrial and proximal ends of the fallopian tube in BRCA1/2 mutation carriers and non-carr
126 blinded readers correctly identified dilated fallopian tubes in 31 of 41 study patients and correctly
128 s in accordance with known cyclic changes of fallopian tubes in response to ovarian hormones and may
131 rly identical findings were found in macaque fallopian tubes infected in situ repeatedly with C. trac
133 ated by salpingectomy, in which the affected Fallopian tube is removed, or salpingotomy, in which the
134 for finding an extraovarian mass, since the fallopian tube is the most common location for ectopic p
135 ber analyses of laser capture microdissected fallopian tube lesions (p53 signatures, serous tubal int
136 e show that PRKCI is also expressed in early fallopian tube lesions, called serous tubal intraepithel
139 Main outcome measures were nonovarian, non-fallopian tube, nonbreast, positive intra-abdominal peri
142 hlamydial upper genital tract infection, the fallopian tubes of 40 female Macaca nemestrina were inoc
144 s a possible origin of HGSOC either from the fallopian tube or from the ovarian surface epithelium.
145 st and BRCA-associated gynecologic (ovarian, fallopian tube or primary peritoneal) cancer when BRCA2
146 ed each adnexa for the presence of a dilated fallopian tube or thickened tubal wall and mucosal folds
147 ith an 80% reduction in the risk of ovarian, fallopian tube, or peritoneal cancer in BRCA1 or BRCA2 c
148 o estimate the reduction in risk of ovarian, fallopian tube, or peritoneal cancer in women with a BRC
149 observed until either diagnosis of ovarian, fallopian tube, or peritoneal cancer, death, or date of
151 logy and Obstetrics stage IIB to IV ovarian, fallopian tube, or peritoneal epithelial carcinoma.
152 ly confirmed epithelial cancer of the ovary, fallopian tube, or peritoneum (any stage, grade 2 to 3 i
154 with platinum-resistant epithelial ovarian, fallopian tube, or primary peritoneal cancer received IM
155 atients with suboptimal stage III or IV EOC, fallopian tube, or primary peritoneal cancer were random
156 resistant or -refractory epithelial ovarian, fallopian tube, or primary peritoneal cancer were random
157 Patients with recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer were random
158 , high-grade serous or endometrioid ovarian, fallopian tube, or primary peritoneal cancer, or those w
160 ential sites: the surfaces of the ovary, the fallopian tube, or the mesothelium-lined peritoneal cavi
164 matory disease (PID) and surgical specimens (fallopian tubes, ovaries, or both) from 22 women with PI
166 populations: Primary (cells in the ovary or fallopian tube), Peritoneal (viable cells in peritoneal
167 al and serial sectioning of both ovaries and fallopian tubes, peritoneal and omental biopsies, and co
169 uring hysterosalpingography (0.04-0.55 cGy), fallopian tube recanalization (0.2-2.75 cGy), computed t
174 on acts to drive malignant transformation in fallopian tube secretory cells that are the site of orig
176 e have developed a system for studying human fallopian tube secretory epithelial cell (FTSEC) transfo
179 rade serous carcinoma (HGSC) originates from fallopian tube secretory epithelial cells (FTSECs).
180 h factors for GAB2-induced transformation of fallopian tube secretory epithelial cells and clonogenic
184 ylation levels between fimbrial and proximal fallopian tube segments are threefold higher in BRCA mut
185 erous carcinoma, which often arises from the fallopian tubes, showed a weaker genetic correlation wit
186 In positive endocervix, endometrium, and fallopian tube specimens, HD-5 was located in apically o
187 is and identified bacterial 16S sequences in Fallopian-tube specimens from 11 (24%) of 45 consecutive
188 omas are first observed in the stroma of the fallopian tube, suggesting that these epithelial cancers
189 ic aberrations that transform ovarian and/or fallopian tube surface epithelial cells, allowing for th
190 an origin arise in the fimbriated end of the fallopian tube, this site cannot account for all of thes
192 describes the isolation of FTSECs from human fallopian tube tissue, conditions for primary FTSEC cult
194 gly1 null mutant causes much more damage to fallopian tube tissues than its isogenic wild-type paren
196 ese Dicer-Pten double-knockout mice, primary fallopian tube tumors spread to engulf the ovary and the
197 ale breast (six cases), ovary (three cases), fallopian tube (two cases), pancreas (three cases), blad
198 + T cells both longitudinally within the RT (Fallopian tube, uterine endometrium, endocervix, ectocer
199 NA expression of TLRs 1 to 6 was observed in fallopian tubes, uterine endometrium, cervix, and ectoce
200 male reproductive tissues, prostate, testis, fallopian tube, uterus, and placenta, as well as in pros
201 e loops between organ modules for the ovary, fallopian tube, uterus, cervix and liver, with a sustain
202 ns and isolated cell cultures from the human fallopian tube, uterus, cervix, and vaginal mucosa were
203 0.139), site of tumor origin (ovaries versus fallopian tubes versus peritoneum) (P = 0.170), and prim
206 to 40 years of age with at least one patent fallopian tube were randomly assigned to ovarian stimula
207 anatomy of the ovary, functional cysts, and fallopian tubes were correlated with findings at histopa
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