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1 n process occurs along the pain neuroaxis in endometriosis.
2 -beta1 through the ID1 pathway in women with endometriosis.
3 between macrophages and nerves in peritoneal endometriosis.
4 or nonsteroidal targets for the treatment of endometriosis.
5 ts in oncology and women's health, including endometriosis.
6 eased clinical pregnancy rates in women with endometriosis.
7 Rbeta function stimulated the progression of endometriosis.
8 um, GLI1 expression is reduced in women with endometriosis.
9 ian tube, gastrointestinal tract, cervix and endometriosis.
10 ial implants, contributing to development of endometriosis.
11 ontribute to the development and severity of endometriosis.
12 dulatory role of IL-10 in the development of endometriosis.
13 lation may be involved in the development of endometriosis.
14 y foods were associated with a lower risk of endometriosis.
15 rrier to the identification and treatment of endometriosis.
16 pelvic pain (CPP) who are suspected to have endometriosis.
17 une factors, which are altered in women with endometriosis.
18 on factor KLF11/Klf11 in the pathogenesis of endometriosis.
19 se and hindlimb vibration) and in a model of endometriosis.
20 nd the scope and capability for treatment of endometriosis.
21 oods are associated with a decreased risk of endometriosis.
22 t a subset of clear cell cancers evolve from endometriosis.
23 nd cell migration in the invasive disease of endometriosis.
24 CH and mirex were positively associated with endometriosis.
25 g of the genetic factors that play a role in endometriosis.
26 bjects with and without the invasive disease endometriosis.
27 25(OH)D level was inversely associated with endometriosis.
28 nting de novo disease-associated fibrosis in endometriosis.
29 ysis, and 168 of these reported a history of endometriosis.
30 effective therapeutic approach in women with endometriosis.
31 sions and the peritoneal fluid in women with endometriosis.
32 a considerable impact on the development of endometriosis.
33 vated 2,4OH-BP levels may be associated with endometriosis.
34 nd central hyperalgesia in mice with induced endometriosis.
35 and 738, respectively, reported a history of endometriosis.
36 r IL-1 receptor type 2 (IL1R2) in women with endometriosis.
37 may play a major role in the pathogenesis of endometriosis.
38 rial cells that are hallmarks of progressive endometriosis.
39 nd likely participate in the pathogenesis of endometriosis.
40 onal axis promotes pathogenic progression of endometriosis.
41 fic subtypes of ovarian cancer in women with endometriosis.
42 lead to surgery, such as uterine fibroids or endometriosis.
43 rotein axis in regulation of inflammation in endometriosis.
44 cells in a mouse model of surgically induced endometriosis.
45 lity-preserving, and effective treatment for endometriosis.
46 as a clinical compound for the treatment of endometriosis.
47 ophilin cochaperone in the etiology of human endometriosis.
48 of pelvic pain, one of the core symptoms of endometriosis.
49 down-regulation of FKBP52 in cases of human endometriosis.
50 tudy the unique aspects of P(4) signaling in endometriosis.
51 possibility that DCs may also play a role in endometriosis.
52 on and rectum and evaluation of rectosigmoid endometriosis.
53 somatic stimulation in treating symptoms of endometriosis.
54 together explain up to 5.19% of variance in endometriosis.
55 ng their contribution to the pathogenesis of endometriosis.
56 se and the reduced fertility associated with endometriosis.
57 entified 19 independent common risk loci for endometriosis.
58 mechanism to the complex pathophysiology of endometriosis.
59 ressed the estrogen-dependent progression of endometriosis.
60 ding protein 3 (IGFBP-3) was associated with endometriosis.
61 term nonestrogen or nonsteroidal therapy for endometriosis.
62 matched eutopic endometrium from women with endometriosis.
63 A in the pathogenesis and pathophysiology of endometriosis.
64 ts in the lesion survival and progression of endometriosis.
65 on are associated with relief of pain due to endometriosis.
66 e information is available in the context of endometriosis.
67 reased in the peritoneal fluid of women with endometriosis.
68 lay an essential role in the pathogenesis of endometriosis.
69 ciated with improved outcomes for women with endometriosis?
70 es, showed a weaker genetic correlation with endometriosis (0.25, 95% CI = 0.11-0.39), despite the ab
72 vs. 1.5+/-0.5 mm(2), n=4 and 4, P<0.0001 for endometriosis; 67.6+/-15.1 vs. 22.7+/-14.6 mm(2), n=5 an
74 nsecutive patients suspected of having bowel endometriosis above the rectosigmoid junction underwent
75 longer than 6 months without or with minimal endometriosis, adhesions, or pelvic inflammatory disease
80 0.01) with moderate or large effect sizes in endometriosis, although these variants may exist in non-
81 ted with incident laparoscopically confirmed endometriosis among 70,556 US women in Nurses' Health St
82 s17561 has also been associated with risk of endometriosis, an epidemiologic risk factor for ovarian
84 nd evidence for shared genetic risks between endometriosis and all histotypes of ovarian cancer, exce
88 ferative diseases of the endometrium such as endometriosis and cancer are common and E2 dependent.
89 udies have demonstrated associations between endometriosis and certain histotypes of ovarian cancer,
90 percentage of 42 of the association between endometriosis and CHD could be explained by greater freq
94 lay an important role in the pathogenesis of endometriosis and endometriosis-associated angiogenesis,
95 nome-wide significantly associated with both endometriosis and fat distribution (waist-to-hip ratio a
96 de transcriptional profiling to characterize endometriosis and found that it exhibits a gene expressi
97 tive study to assess the association between endometriosis and histological subtypes of ovarian cance
98 atistically significant associations between endometriosis and IGF-1 (incidence rate ratio (IRR) = 0.
99 iotic tissue of mice with surgically induced endometriosis and in endometriotic stromal cells biopsie
102 ncreased in peritoneal fluid from women with endometriosis and levels correlated with TGF-beta1 conce
103 pressed in eutopic endometrium of women with endometriosis and likely participate in the pathogenesis
104 h placebo in women with surgically diagnosed endometriosis and moderate or severe endometriosis-assoc
106 that the epidemiological association between endometriosis and ovarian adenocarcinoma may be attribut
107 rge number of genetic variants contribute to endometriosis and ovarian cancer (all histotypes combine
110 sociation between laparoscopically confirmed endometriosis and subsequent CHD among 116 430 women in
111 ved endothelial cells in the pathogenesis of endometriosis and support the potential clinical use of
112 was increased in peritoneum from women with endometriosis and TGF-beta1 increased concentrations of
113 significant evidence of involvement in both endometriosis and WHRadjBMI (in/near KIFAP3, CAB39L, WNT
117 Only follicular fluid from patients with endometriosis, and not controls, produced ROS and damage
121 taglandin E2 (PGE2) are higher in women with endometriosis, and this increased PGE2 plays important r
122 Severe pelvic pain is often associated with endometriosis, and this pain can be diminished with ther
126 ports role for ID1 in the pathophysiology of endometriosis, as an effector of TGFbeta1 dependent upre
127 ole in the pathogenesis of endometriosis and endometriosis-associated angiogenesis, and the angiogene
129 ed controlled trial; 67 patients with severe endometriosis-associated pain (maximum pain: 7.6 +/- 2.0
135 e measured in sera from surgically confirmed endometriosis cases (n = 248) first diagnosed between 19
138 typing large numbers of surgically-confirmed endometriosis cases and controls, and/or sequencing high
139 ase severity (P=0.0046) when moderate/severe endometriosis cases are tested against minimal/mild case
140 nistered into the peritoneum of baboons with endometriosis, cells in lesions selectively underwent ap
141 evere (n = 136) endometriosis (rAFS: revised endometriosis classification of the American Fertility S
143 ted levels of EPCs in the blood of mice with endometriosis compared with control subject that underwe
144 dy, a population-based case-control study of endometriosis conducted among 18- to 49-year-old female
147 ncer, rheumatoid arthritis, atherosclerosis, endometriosis, diabetic retinopathy, and age-related mac
148 association between POPs and the odds of an endometriosis diagnosis and the consistency of findings
149 ved only between 2,4OH-BP and the odds of an endometriosis diagnosis in the operative cohort (OR = 1.
150 tervals (CIs) for each POP in relation to an endometriosis diagnosis, with separate models run for ea
152 rations of BP derivatives and the odds of an endometriosis diagnosis; ORs increased across quartiles
154 re pelvic pains are symptoms associated with endometriosis (ENDO), a common condition among women tha
155 grade serous ovarian cancers (HGSOCs) and in endometriosis epithelial cells (EECs), the likely precur
156 ently conditioned with serum from women with endometriosis exhibited a tolerogenic phenotype, includi
157 iosis, women with laparoscopically confirmed endometriosis had a higher risk of myocardial infarction
161 , randomized, 6-month phase 3 trials (Elaris Endometriosis I and II [EM-I and EM-II]) to evaluate the
163 yl levels to classify women with and without endometriosis illustrates the potential benefits of thes
164 hat KLF11 expression was diminished in human endometriosis implants and further investigated its path
165 believed that these nascent nerve fibers in endometriosis implants influence dorsal root neurons wit
167 1 and IGFBP-3 and laparoscopically confirmed endometriosis in a case-control study nested within the
171 sistent organochlorine pollutants (POPs) and endometriosis in women, with differences attributed to m
193 interactions, providing novel evidence that endometriosis is an estrogen-dependent neuroinflammatory
203 ng autism, breast cancer, colorectal cancer, endometriosis, ischaemic stroke, leukemia, lymphoma and
204 1 or IGFBP-3 plays a role in the etiology of endometriosis, it is minimal and perhaps only among youn
205 have been associated with deep infiltrating endometriosis, its contribution to the disease pathophys
206 w-derived DCs (BMDCs) incorporated into both endometriosis lesions and into B16 melanoma tumors and e
210 aling pathway (including COX-2, EP2, EP4) in endometriosis lesions, dorsal root ganglia (DRG), spinal
216 P2/EP4: (i) decreases growth and survival of endometriosis lesions; (ii) decreases angiogenesis and i
217 i) decreases angiogenesis and innervation of endometriosis lesions; (iii) suppresses proinflammatory
218 molecular environment of the endometrium and endometriosis lesions; and (v) restores endometrial func
220 hat seminal plasma enhances the formation of endometriosis-like lesion via a direct effect on endomet
221 ndometrial tissue resulted in development of endometriosis-like lesions in 63% of ovariectomized estr
222 radiol significantly inhibited the growth of endometriosis-like lesions in a dose-dependent manner.
223 iosis that transient hypoxia in transplanted endometriosis-like lesions results in the up-regulation
224 considered to be involved in the etiology of endometriosis, neither the extent of their participation
228 common variants between fat distribution and endometriosis (P = 3.7 x 10(-3)), which was stronger whe
230 mparisons to assess how fat distribution and endometriosis pathogenesis research fields can inform ea
231 targeted proteomics of peritoneal fluid from endometriosis patients and find growth-factor-driven ADA
232 RNA binding protein (RNABP) HuR/TTP axis in endometriosis patients compared to menstrual stage match
235 with a significant positive association with endometriosis [per 1-SD increase in log-transformed gamm
238 xcised moderate (n = 67) or severe (n = 136) endometriosis (rAFS: revised endometriosis classificatio
239 %, and 10%, respectively, and the cumulative endometriosis recurrence rate was 1%, 6%, and 8%, respec
241 divides type I tumors into three groups: i) endometriosis-related tumors that include endometrioid,
242 s the SNP with the strongest association for endometriosis risk (P = 1.84 x 10-5, OR = 1.244 (1.126-1
243 ive novel loci significantly associated with endometriosis risk (P<5 x 10(-8)), implicating genes inv
244 io appeared to be positively associated with endometriosis risk among women aged <40 years at blood d
245 re was no evidence of an association between endometriosis risk and distance to road or exposure to P
249 er, our results suggest that SNPs increasing endometriosis risk in this region act through CDC42, but
253 oci in our meta-analysis that associate with endometriosis:, RNF144B-ID4 on 6p22.3 (rs6907340; P = 2.
255 ars and confirm a strong correlation between endometriosis severity and infertility (n = 1182, P<0.00
256 and Mmp9(-)/(-) mice with surgically induced endometriosis showed that activation of tumor necrosis f
257 a C57BL/6 mouse model of surgically induced endometriosis significantly decreased the size of endome
258 at might lead to malignant transformation of endometriosis so as to help identify subsets of women at
262 ay were 18% less likely to be diagnosed with endometriosis than those reporting 2 servings per day (r
263 cted vitamin D level had a 24% lower risk of endometriosis than women in the lowest quintile (rate ra
264 In summary, we developed a mouse model of endometriosis that exhibits similarities to human perito
265 demonstrate in an established mouse model of endometriosis that transient hypoxia in transplanted end
268 tant recurrent miscarriages and remission of endometriosis, these findings have clinical implications
269 yses restricting cases to those with ovarian endometriosis (third vs. lowest quartile: OR = 2.5; 95%
271 pared between women with deeply infiltrative endometriosis undergoing CO2 laser ablative surgery with
272 al-medium-specific POPs were associated with endometriosis, underscoring the importance of methodolog
273 ted a genome-wide association scan (GWAS) of endometriosis using 25.5 million sequence variants detec
274 ential role of protein-modifying variants in endometriosis using exome-array genotyping in 7164 cases
275 igated the role of IL-33 in the pathology of endometriosis using patient samples, cell lines and a sy
276 we developed and validated a mouse model of endometriosis using syngeneic menstrual endometrial tiss
279 ospective cohort, laparoscopically confirmed endometriosis was associated with increased risk of CHD.
280 ser laparoscopic excision of moderate-severe endometriosis was comparable in women with or without bo
283 th an increase in the odds of a diagnosis of endometriosis was examined in 600 women who underwent la
285 at the serum level of IL-10 in patients with endometriosis was significantly higher than that in heal
286 on between serum beta-HCH concentrations and endometriosis was stronger in analyses restricting cases
287 identify genetic factors that contribute to endometriosis we conducted a two-stage genome-wide assoc
289 By using human tissues and a mouse model of endometriosis, we demonstrate that macrophages in lesion
291 2,486 incident cases of surgically confirmed endometriosis were identified over 710,230 person-years
294 vations suggest a model for the pathology of endometriosis where BLyS-responsive plasma cells interac
295 licular fluid from patients with the disease endometriosis, which affects 10% of women and is associa
296 olymorphisms (SNPs) robustly associated with endometriosis, which together explain up to 5.19% of var
298 berrant molecular and cellular mechanisms in endometriosis with the intention of providing much-neede
300 analyses using data from the Women's Risk of Endometriosis (WREN) study, a population-based case-cont
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