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1        In contrast to full-length SRC-1, the endometriotic 70-kDa SRC-1 C-terminal fragment prevents
2  bind to inflammatory targets of TTP in both endometriotic and endometrial epithelial cell lines.
3                          Silencing of TTP in endometriotic and endometrial epithelial cells revealed
4                      Using human fluorescent endometriotic cell lines and chimeric mouse model as pre
5 t lymphangiogenic factor, is up-regulated in endometriotic cells and contributes to increased lymphan
6 MIF protein secretion and mRNA expression in endometriotic cells in response to E(2).
7 esponse of 12Z immortalized human epithelial endometriotic cells to TNF-alpha.
8 OA neurons are influenced by the presence of endometriotic cysts in the abdominal cavity.
9 id not cause any histological changes in the endometriotic cysts of recipients.
10                                          The endometriotic cysts were found to be significantly large
11 clear atypia in the epithelial lining of all endometriotic cysts, histologically corresponding to aty
12 ning of 42 and 50% of peritoneal and ovarian endometriotic cysts, respectively, which were histologic
13 ecrosis factor (TNF)-alpha is central to the endometriotic disease process.
14 posure to seminal plasma could contribute to endometriotic disease progression in women.
15                                    Use of an endometriotic epithelial cell line (12Z) in which the mi
16 NF-alpha-induced signaling pathways in human endometriotic epithelial cells results in decreased expr
17 n of endometrial epithelial, endothelial and endometriotic epithelial cells with IL-33 led to the pro
18                                       In 12Z endometriotic epithelial cells, CDD-2693 and CDD-3167 si
19  of all the above endometriotic genes in 12Z endometriotic epithelial cells.
20 epithelial-mesenchymal transition (EMT) from endometriotic epithelial cells.
21                                 The secreted endometriotic exosomes create an immunosuppressive gradi
22                      We showed that secreted endometriotic exosomes isolated from supernatants of sho
23 ecrease resistance to invasion by cancer and endometriotic foci in other estrogen-responsive tissues.
24 of small molecule kinase inhibitors to block endometriotic gene expression directly.
25 NF-alpha-induced expression of all the above endometriotic genes in 12Z endometriotic epithelial cell
26 dy early angiogenesis in vivo and to monitor endometriotic growth and the efficacy of systemic antian
27           Here, we report that primary human endometriotic H-38 cells express high levels of GPR30 wi
28 is, we now report that Icon largely destroys endometriotic implants by vascular disruption without ap
29 evealed five patients with surgically proved endometriotic implants in the ileum at enteroclysis (thr
30                      Barium studies revealed endometriotic implants in the terminal ileum within 10 c
31       Recent evidence indicates that ectopic endometriotic implants recruit their own unique neural a
32 le-contrast barium enema studies, associated endometriotic implants were found in the rectosigmoid co
33 hat host-derived TGFB1 deficiency suppresses endometriotic lesion development and provides proof of p
34 tigated the physiologic function of TGFB1 in endometriotic lesion development, using Tgfb1-null mutan
35 ed to the peritoneal environment early after endometriotic lesion establishment and remain present in
36 hese results suggest that TSLP modulates the endometriotic lesion microenvironment and promotes a Th2
37 Cs, HUVECs, and hESCs) representative of the endometriotic lesion microenvironment increased cytokine
38      Furthermore, treatment increased murine endometriotic lesion proliferation.
39 ly is one of the fundamental requirements of endometriotic lesion survival in the peritoneal cavity.
40 44-3p/miR-451a cluster is expressed in human endometriotic lesion tissue, the level of expression cor
41  demonstrated expression of miR-451 in human endometriotic lesion tissue.
42  of the miR-144-3p/miR-451a cluster in human endometriotic lesion tissue.
43 creased lymphatic vessels development in the endometriotic lesion, enlarged retroperitoneal lymph nod
44 ells are a disease-inducing component of the endometriotic lesion, we explored the response of 12Z im
45                     This gradient guards the endometriotic lesions against clearance by a cytotoxic a
46 y proved endometrioma and no associated deep endometriotic lesions and 317 healthy subjects for a cas
47 ential expression of IL-17A in human ectopic endometriotic lesions and matched eutopic endometrium fr
48     Recent studies have detected TSLP within endometriotic lesions and shown that its concentrations
49 898 will prevent neovascularization of human endometriotic lesions and that ABT-898 treatment will no
50 trate that neutrophils reside within patient endometriotic lesions and that patient lesions possess a
51 functional cytokine that is abundant in both endometriotic lesions and the peritoneal fluid in women
52 The oxidative stress conditions found within endometriotic lesions are likely to contribute to the tr
53 positive endothelial cells incorporated into endometriotic lesions but not eutopic endometrium, as re
54         Caplostatin suppressed the growth of endometriotic lesions by 59% compared with controls.
55  that RNABPs TTP and HuR are dysregulated in endometriotic lesions compared to matched eutopic patien
56 ession was elevated in the stroma of patient endometriotic lesions compared with control endometrial
57 ression levels were higher in macrophages of endometriotic lesions compared with control endometrial
58                                              Endometriotic lesions from ABT-898-treated mice exhibite
59                                 Furthermore, endometriotic lesions from IL-33 treated mice were highl
60                         In a large cohort of endometriotic lesions from individuals with endometriosi
61 m of affected women and secreted products of endometriotic lesions have given insight into the pathog
62 ent gene expression to promote the growth of endometriotic lesions in mice.
63                                              Endometriotic lesions increased circulating endothelial
64                                              Endometriotic lesions induce a state of chronic peritone
65 ese findings indicate that vasculogenesis in endometriotic lesions is dependent on estrogen, which ad
66 t in the cervix, the uterus, and periovarian endometriotic lesions of the affected macaque.
67 e the first evidence, to our knowledge, that endometriotic lesions produce IL-17A and that the remova
68                                We found that endometriotic lesions produce significantly higher level
69 EPHA2 and EPHA4 expressions are increased in endometriotic lesions relative to normal eutopic endomet
70                                      Because endometriotic lesions require new blood supply for survi
71 s) to test our hypothesis that the growth of endometriotic lesions results in alterations in immune a
72          We demonstrate the establishment of endometriotic lesions that exhibit similarities to those
73 ouse model of endometriosis in which ectopic endometriotic lesions were deficient for both of these m
74                                              Endometriotic lesions were induced in irradiated FVB/N m
75 ere higher, but numbers of recruited EPCs in endometriotic lesions were significantly lower when comp
76                                              Endometriotic lesions were surgically induced in irradia
77 nsplantation, gene KO was induced by DOX and endometriotic lesions were thereafter removed.
78  the loss of FKBP52 encourages the growth of endometriotic lesions with increased inflammation, cell
79 ABT-898 inhibits neovascularization of human endometriotic lesions without affecting mouse fecundity.
80 ression between patient eutopic endometrium, endometriotic lesions, and control endometrial samples.
81 romoting factor markedly expressed in active endometriotic lesions, and estradiol (E(2)) in ectopic e
82 red well with the location of the transgenic endometriotic lesions, and lesion size correlated with t
83 ssues are frequently being used to represent endometriotic lesions, despite the unequivocal differenc
84 olute bulk data from endometrial cancers and endometriotic lesions, illuminating the cell types domin
85  and platelets in close contact infiltrating endometriotic lesions, suggesting potential cell-cell in
86 nagement, and many aspects of the biology of endometriotic lesions, the pathophysiological mechanisms
87 e euthanized to assess neovascularization of endometriotic lesions, using CD31(+) immunofluorescence.
88 bition of COX-2 suppresses vasculogenesis in endometriotic lesions, which may contribute to an impair
89 te, forming a "protective shield" around the endometriotic lesions.
90 nflammation, the establishment and growth of endometriotic lesions.
91 expression on nerve fibers innervating human endometriotic lesions.
92 essels contributes to the vascularization of endometriotic lesions.
93 essels contributes to the vascularization of endometriotic lesions.
94 f11-/- knockout mice with surgically induced endometriotic lesions.
95 gral part in the establishment and growth of endometriotic lesions.
96 ous expression of TF by endothelial cells in endometriotic lesions.
97 athways forming PGE2 are highly expressed in endometriotic lesions.
98 mportant role in the formation and growth of endometriotic lesions.
99 isk reduction was greatest for women who had endometriotic lesions.
100 xtensively discussed in the establishment of endometriotic lesions.
101 P-TFII, VEGF-C, and lymphangiogenesis in the endometriotic microenvironment, which opens up new horiz
102 on of the 70-kDa SRC-1 C-terminal isoform in endometriotic mouse tissue.
103 hypothesize the Schwann cells involvement in endometriotic pain.
104 with surgically induced endometriosis and in endometriotic stromal cells biopsied from patients with
105 eted vimentin-positive poorly differentiated endometriotic stromal tissue and infiltrating macrophage
106 ons positively correlated with the amount of endometriotic tissue and peaked 1 to 4 days after induct
107                                      Ectopic endometriotic tissue exhibits decelerated DNAm age, simi
108 lytic isoform is highly elevated both in the endometriotic tissue of mice with surgically induced end
109 on, survival, and growth of endometrium-like/endometriotic tissue outside the uterine cavity, causing
110                       We studied the role of endometriotic tissue-secreted exosomes in the pathophysi
111  thereby increasing the invasion activity of endometriotic tissues for establishment of ectopic lesio
112 ls, enhanced ERbeta activity was detected in endometriotic tissues, and the inhibition of enhanced ER

 
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