ライフサイエンスコーパス: endometriosis

1 nd central hyperalgesia in mice with induced endometriosis.

2 nd likely participate in the pathogenesis of endometriosis.

3 rotein axis in regulation of inflammation in endometriosis.

4 of pelvic pain, one of the core symptoms of endometriosis.

5 together explain up to 5.19% of variance in endometriosis.

6 ng their contribution to the pathogenesis of endometriosis.

7 se and the reduced fertility associated with endometriosis.

8 mechanism to the complex pathophysiology of endometriosis.

9 ressed the estrogen-dependent progression of endometriosis.

10 ding protein 3 (IGFBP-3) was associated with endometriosis.

11 term nonestrogen or nonsteroidal therapy for endometriosis.

12 haracterization of neutrophil involvement in endometriosis.

13 matched eutopic endometrium from women with endometriosis.

14 A in the pathogenesis and pathophysiology of endometriosis.

15 on are associated with relief of pain due to endometriosis.

16 e information is available in the context of endometriosis.

17 reased in the peritoneal fluid of women with endometriosis.

18 lay an essential role in the pathogenesis of endometriosis.

19 -beta1 through the ID1 pathway in women with endometriosis.

20 between macrophages and nerves in peritoneal endometriosis.

21 or nonsteroidal targets for the treatment of endometriosis.

22 (THC) in a mouse model of surgically-induced endometriosis.

23 gate possible benefits of THC for women with endometriosis.

24 ts in oncology and women's health, including endometriosis.

25 eased clinical pregnancy rates in women with endometriosis.

26 Rbeta function stimulated the progression of endometriosis.

27 useful tool in the diagnosis of extragenital endometriosis.

28 ian tube, gastrointestinal tract, cervix and endometriosis.

29 ial implants, contributing to development of endometriosis.

30 contributing to pain as cardinal symptom in endometriosis.

31 ontribute to the development and severity of endometriosis.

32 dulatory role of IL-10 in the development of endometriosis.

33 lation may be involved in the development of endometriosis.

34 y foods were associated with a lower risk of endometriosis.

35 rrier to the identification and treatment of endometriosis.

36 pelvic pain (CPP) who are suspected to have endometriosis.

37 une factors, which are altered in women with endometriosis.

38 on factor KLF11/Klf11 in the pathogenesis of endometriosis.

39 se and hindlimb vibration) and in a model of endometriosis.

40 nd the scope and capability for treatment of endometriosis.

41 oods are associated with a decreased risk of endometriosis.

42 t a subset of clear cell cancers evolve from endometriosis.

43 nd cell migration in the invasive disease of endometriosis.

44 CH and mirex were positively associated with endometriosis.

45 re reduced in nonhuman primates induced with endometriosis.

46 g of the genetic factors that play a role in endometriosis.

47 bjects with and without the invasive disease endometriosis.

48 affects quality of life in young women with endometriosis.

49 25(OH)D level was inversely associated with endometriosis.

50 nting de novo disease-associated fibrosis in endometriosis.

51 ysis, and 168 of these reported a history of endometriosis.

52 effective therapeutic approach in women with endometriosis.

53 sions and the peritoneal fluid in women with endometriosis.

54 a considerable impact on the development of endometriosis.

55 vated 2,4OH-BP levels may be associated with endometriosis.

56 and 738, respectively, reported a history of endometriosis.

57 ar mechanisms involved in the development of endometriosis.

58 e-sensitizing factor in pain associated with endometriosis.

59 acrophages in producing pain associated with endometriosis.

60 and suggest overlapping genetic origins with endometriosis.

61 There is no cure for endometriosis.

62 rses the pain behavior observed in mice with endometriosis.

63 zons in understanding the pathophysiology of endometriosis.

64 r UL diagnosis among those with a history of endometriosis.

65 somatic stimulation in treating symptoms of endometriosis.

66 tient samples, we provide evidence of EMT in endometriosis.

67 entified 19 independent common risk loci for endometriosis.

68 ts in the lesion survival and progression of endometriosis.

69 n process occurs along the pain neuroaxis in endometriosis.

70 um, GLI1 expression is reduced in women with endometriosis.

71 ciated with improved outcomes for women with endometriosis?

72 es, showed a weaker genetic correlation with endometriosis (0.25, 95% CI = 0.11-0.39), despite the ab

73 howed the strongest genetic correlation with endometriosis (0.51, 95% CI = 0.18-0.84).

74 Endometriosis, a major reproductive pathology affecting

75 nsecutive patients suspected of having bowel endometriosis above the rectosigmoid junction underwent

76 Endometriosis affects approximately 10% of young, reprod

77 0.01) with moderate or large effect sizes in endometriosis, although these variants may exist in non-

78 ted with incident laparoscopically confirmed endometriosis among 70,556 US women in Nurses' Health St

79 s17561 has also been associated with risk of endometriosis, an epidemiologic risk factor for ovarian

80 tained 310 premenopausal women with incident endometriosis and 615 matched controls.

81 onses were received; 340 with a diagnosis of endometriosis and 69 with no diagnosis.

82 nd evidence for shared genetic risks between endometriosis and all histotypes of ovarian cancer, exce

83 and cellular aspects of the pathogenesis of endometriosis and associated clinical symptoms.

84 , no genetic enrichment was observed between endometriosis and BMI (P = 0.79).

85 reatment of estrogen-dependent diseases like endometriosis and breast cancer.

86 ferative diseases of the endometrium such as endometriosis and cancer are common and E2 dependent.

87 udies have demonstrated associations between endometriosis and certain histotypes of ovarian cancer,

88 percentage of 42 of the association between endometriosis and CHD could be explained by greater freq

89 ld partially explain the association between endometriosis and CHD.

90 or translational application, for example in endometriosis and contraception.

91 Both endometriosis and CPP have significant negative impact.

92 nome-wide significantly associated with both endometriosis and fat distribution (waist-to-hip ratio a

93 atistically significant associations between endometriosis and IGF-1 (incidence rate ratio (IRR) = 0.

94 Though endometriosis and infertility are clearly associated, th

95 intervention is needed to reduce the risk of endometriosis and infertility.

96 Knowledge of infiltrating endometriosis and its ultrasonographic features will ena

97 ncreased in peritoneal fluid from women with endometriosis and levels correlated with TGF-beta1 conce

98 pressed in eutopic endometrium of women with endometriosis and likely participate in the pathogenesis

99 h placebo in women with surgically diagnosed endometriosis and moderate or severe endometriosis-assoc

100 that the epidemiological association between endometriosis and ovarian adenocarcinoma may be attribut

101 rge number of genetic variants contribute to endometriosis and ovarian cancer (all histotypes combine

102 men (aged 12-25 y) with surgically confirmed endometriosis and pelvic pain enrolled in a double-blind

103 elevated in peritoneal fluid from women with endometriosis and positively correlate with their pain s

104 assess the association between self-reported endometriosis and risk of ovarian cancer.

105 sociation between laparoscopically confirmed endometriosis and subsequent CHD among 116 430 women in

106 was increased in peritoneum from women with endometriosis and TGF-beta1 increased concentrations of

107 significant evidence of involvement in both endometriosis and WHRadjBMI (in/near KIFAP3, CAB39L, WNT

108 ated in the peritoneal fluid from women with endometriosis, and exposure of HPMCs to TGF-beta1 exacer

109 h vs. those without a confirmed diagnosis of endometriosis, and if there was any change in diagnostic

110 Only follicular fluid from patients with endometriosis, and not controls, produced ROS and damage

111 orders, including advanced prostatic cancer, endometriosis, and precocious puberty.

112 taglandin E2 (PGE2) are higher in women with endometriosis, and this increased PGE2 plays important r

113 Similarly, age at menopause, endometriosis, and tubal ligation were only associated w

114 a key neurotrophic and sensitizing factor in endometriosis, and we propose that therapies that modify

115 Adolescents with endometriosis are a particularly underserved population

116 Women with endometriosis are at increased risk of infertility.

117 Two major clinical symptoms of endometriosis are chronic intolerable pelvic pain and su

118 to patients' quality of life, the causes of endometriosis are not fully understood and validated dia

119 pose one-tenth of reproductive-aged women to endometriosis are poorly understood.

120 itoneal immune microenvironment of mice with endometriosis as demonstrated by changes in pro-inflamma

121 polycystic ovary syndrome, uterine fibroids, endometriosis) as well as contraception.

122 ports role for ID1 in the pathophysiology of endometriosis, as an effector of TGFbeta1 dependent upre

123 expression of IGF-1 in an in vitro model of endometriosis-associated macrophages and confirmed expre

124 ed controlled trial; 67 patients with severe endometriosis-associated pain (maximum pain: 7.6 +/- 2.0

125 omega-3 (n-3) fatty acid supplementation on endometriosis-associated pain in adolescents.

126 agnosed endometriosis and moderate or severe endometriosis-associated pain.

127 phages into lesions, plays a pivotal role in endometriosis-associated pain.

128 utic options for the treatment of women with endometriosis-associated pain.

129 c pain during a 6-month period in women with endometriosis-associated pain.

130 rine endometrial tissue in other body areas, endometriosis can cause severe abdominal pain and/or inf

131 hat macrophage depletion in a mouse model of endometriosis can reverse abnormal changes in pain behav

132 e measured in sera from surgically confirmed endometriosis cases (n = 248) first diagnosed between 19

133 cohort including 2,019 surgically confirmed endometriosis cases and 14,471 controls.

134 ion case-control data sets, totalling 17,045 endometriosis cases and 191,596 controls.

135 typing large numbers of surgically-confirmed endometriosis cases and controls, and/or sequencing high

136 ase severity (P=0.0046) when moderate/severe endometriosis cases are tested against minimal/mild case

137 nistered into the peritoneum of baboons with endometriosis, cells in lesions selectively underwent ap

138 evere (n = 136) endometriosis (rAFS: revised endometriosis classification of the American Fertility S

139 In the endometriosis cohort there was a mean diagnostic delay o

140 dy, a population-based case-control study of endometriosis conducted among 18- to 49-year-old female

141 To address this, we used two endometriosis datasets genotyped on common arrays with f

142 local chronic inflammation and concomitantly endometriosis development.

143 ved only between 2,4OH-BP and the odds of an endometriosis diagnosis in the operative cohort (OR = 1.

144 ophorectomy and earlier age at surgery after endometriosis diagnosis.

145 rations of BP derivatives and the odds of an endometriosis diagnosis; ORs increased across quartiles

146 All endometriosis drug approvals to date have been contracep

147 a noncontraceptive treatment for women with endometriosis either as a primary nonhormonal treatment

148 grade serous ovarian cancers (HGSOCs) and in endometriosis epithelial cells (EECs), the likely precur

149 red from the pelvic peritoneum of women with endometriosis exhibit significantly higher glycolysis, l

150 ently conditioned with serum from women with endometriosis exhibited a tolerogenic phenotype, includi

151 iosis, women with laparoscopically confirmed endometriosis had a higher risk of myocardial infarction

152 Since then, surgical techniques to treat endometriosis have been improved and the effect of PN ob

153 erstood and validated diagnostic markers for endometriosis have not been identified.

154 Treatment of endometriosis HPMCs with the pyruvate dehydrogenase kina

155 , randomized, 6-month phase 3 trials (Elaris Endometriosis I and II [EM-I and EM-II]) to evaluate the

156 In a syngeneic mouse model of endometriosis, IL-33 injections caused systemic inflamma

157 hat KLF11 expression was diminished in human endometriosis implants and further investigated its path

158 1 and IGFBP-3 and laparoscopically confirmed endometriosis in a case-control study nested within the

159 lso reduced in the endometrium of women with endometriosis in correlation with diminished ARID1A, and

160 egy that could be useful to treat peritoneal endometriosis in humans.

161 , PM10), and timing of exposure with risk of endometriosis in the Nurses' Health Study II.

162 adulthood were not associated with incident endometriosis in this cohort of women.

163 Using an experimental mouse model of endometriosis in which ectopic endometriotic lesions wer

164 er illustrates the findings for infiltrating endometriosis involving the bowel and urinary tract on a

165 Endometriosis is a chronic inflammatory condition in wom

166 Endometriosis is a chronic inflammatory, gynecological d

167 Endometriosis is a chronic pain condition affecting ~176

168 Endometriosis is a chronic painful disease highly preval

169 Endometriosis is a chronic, estrogen-dependent condition

170 Endometriosis is a chronic, inflammatory disease charact

171 Endometriosis is a common cause of both cyclic and chron

172 Endometriosis is a common cause of CPP in adolescents wh

173 Endometriosis is a common cause of pelvic pain and infer

174 Endometriosis is a common gynaecological disease associa

175 Endometriosis is a common gynaecological disease of wome

176 Endometriosis is a common gynecological condition with c

177 Endometriosis is a common incurable inflammatory disorde

178 Endometriosis is a debilitating condition that is catego

179 Endometriosis is a debilitating, estrogen-dependent, pro

180 Endometriosis is a frequently occurring disease in women

181 Endometriosis is a gynecological disorder affecting 6%-1

182 Endometriosis is a heritable hormone-dependent gynecolog

183 Endometriosis is a highly prevalent gynecological diseas

184 Endometriosis is a pathologic condition affecting approx

185 Endometriosis is a prevalent gynecologic disease associa

186 Endometriosis is an estrogen-dependent inflammatory diso

187 interactions, providing novel evidence that endometriosis is an estrogen-dependent neuroinflammatory

188 Endometriosis is an incurable gynecological disorder cha

189 Endometriosis is an inflammatory condition in which endo

190 Endometriosis is an inflammatory condition that is assoc

191 Endometriosis is chronic disorder with high socioeconomi

192 Endometriosis is considered an estrogen-dependent diseas

193 The etiology of endometriosis is poorly understood, and few modifiable r

194 Endometriosis is the presence of endometrial tissue outs

195 Diagnosis and treatment of endometriosis is, on average, delayed by 7-10 years from

196 ng autism, breast cancer, colorectal cancer, endometriosis, ischaemic stroke, leukemia, lymphoma and

197 1 or IGFBP-3 plays a role in the etiology of endometriosis, it is minimal and perhaps only among youn

198 have been associated with deep infiltrating endometriosis, its contribution to the disease pathophys

199 peritoneal fluid lactate concentrations and endometriosis lesion size in a mouse model.

200 ey dictate the growth and vascularization of endometriosis lesions and more recently have been shown

201 to investigate the molecular composition of endometriosis lesions and pinpoints metabolic markers th

202 ing pain and the establishment of innervated endometriosis lesions outside the uterus.

203 SI-MS imaging data allowed classification of endometriosis lesions with overall accuracies of 89.4%,

204 aling pathway (including COX-2, EP2, EP4) in endometriosis lesions, dorsal root ganglia (DRG), spinal

205 ought to play a role in the establishment of endometriosis lesions.

206 ays important role in survival and growth of endometriosis lesions.

207 ity for the establishment and maintenance of endometriosis lesions.

208 P2/EP4: (i) decreases growth and survival of endometriosis lesions; (ii) decreases angiogenesis and i

209 i) decreases angiogenesis and innervation of endometriosis lesions; (iii) suppresses proinflammatory

210 molecular environment of the endometrium and endometriosis lesions; and (v) restores endometrial func

211 in transforming growth factor beta1 impairs endometriosis-like lesion growth in mice.

212 hat seminal plasma enhances the formation of endometriosis-like lesion via a direct effect on endomet

213 Endometriosis occurs in approximately 10% of women and i

214 As most endometriosis occurs on organ surfaces facing the perito

215 Endometriosis of the bowel and urinary tract are types o

216 y (IHC) staining in endometrial tissues from endometriosis or control patients.

217 common variants between fat distribution and endometriosis (P = 3.7 x 10(-3)), which was stronger whe

218 iation of rs519664[T] in TTC39B on 9p22 with endometriosis (P=4.8 x 10(-10); OR=1.29).

219 mparisons to assess how fat distribution and endometriosis pathogenesis research fields can inform ea

220 ve stress have been postulated as factors in endometriosis pathogenesis.

221 cal inflammatory environment associated with endometriosis pathogenesis.

222 r, whether and how neutrophils contribute to endometriosis pathophysiology remain poorly understood.

223 targeted proteomics of peritoneal fluid from endometriosis patients and find growth-factor-driven ADA

224 metrial tissue outside the uterine cavity in endometriosis patients are primarily driven by hormone-d

225 RNA binding protein (RNABP) HuR/TTP axis in endometriosis patients compared to menstrual stage match

226 e that systemic circulating neutrophils from endometriosis patients display distinct transcriptomic d

227 remains unknown, it is well established that endometriosis patients exhibit immune dysfunction.

228 opic and ectopic endometrial tissues from 89 endometriosis patients.

229 systemic circulation and peritoneal fluid of endometriosis patients; however, whether and how neutrop

230 with a significant positive association with endometriosis [per 1-SD increase in log-transformed gamm

231 ors included genetic liability to 3 factors (endometriosis, polycystic ovary syndrome, type 2 diabete

232 he mouse SRC-1 gene has an essential role in endometriosis progression.

233 xcised moderate (n = 67) or severe (n = 136) endometriosis (rAFS: revised endometriosis classificatio

234 %, and 10%, respectively, and the cumulative endometriosis recurrence rate was 1%, 6%, and 8%, respec

235 s work has linked endometrial ARID1A loss to endometriosis-related endometrial non-receptivity.

236 Endometriosis-related pain has a marked negative impact

237 nctive presacral neurectomy (PN) for chronic endometriosis-related pelvic pain.

238 divides type I tumors into three groups: i) endometriosis-related tumors that include endometrioid,

239 Internationally, people with endometriosis report significant negative impact across

240 ur syngeneic, immunocompetent mouse model of endometriosis revealed that neutrophils are rapidly recr

241 s the SNP with the strongest association for endometriosis risk (P = 1.84 x 10-5, OR = 1.244 (1.126-1

242 ive novel loci significantly associated with endometriosis risk (P<5 x 10(-8)), implicating genes inv

243 io appeared to be positively associated with endometriosis risk among women aged <40 years at blood d

244 re was no evidence of an association between endometriosis risk and distance to road or exposure to P

245 Our data suggested increased endometriosis risk associated with serum concentrations

246 The involvement of KDR in endometriosis risk highlights the importance of the VEGF

247 We investigated endometriosis risk in relation to environmental exposure

248 er, our results suggest that SNPs increasing endometriosis risk in this region act through CDC42, but

249 stent and strong association with increasing endometriosis risk.

250 on between these air pollution exposures and endometriosis risk.

251 organochlorine pesticides (OCPs), may affect endometriosis risk.

252 n the meta-analysis are also associated with endometriosis risk; an epidemiological meta-analysis acr

253 oci in our meta-analysis that associate with endometriosis:, RNF144B-ID4 on 6p22.3 (rs6907340; P = 2.

254 Endometriosis (RR = 1.27, 95% CI: 0.70, 2.31; P = 0.43)

255 ars and confirm a strong correlation between endometriosis severity and infertility (n = 1182, P<0.00

256 Autotransplanted mouse model of endometriosis showed lenvatinib treatment abrogated the

257 and Mmp9(-)/(-) mice with surgically induced endometriosis showed that activation of tumor necrosis f

258 a C57BL/6 mouse model of surgically induced endometriosis significantly decreased the size of endome

259 at might lead to malignant transformation of endometriosis so as to help identify subsets of women at

260 In young women with endometriosis, supplementation with vitamin D led to sig

261 andomized controlled studies of conservative endometriosis surgery with or without adjunctive PN were

262 Here we report the discovery of a new endometriosis susceptibility locus on 4q12 (rs17773813[G

263 descent to examine the mechanism underlying endometriosis susceptibility.

264 unknown whether phytocannabinoids may modify endometriosis symptoms and development.

265 Here we identify an endometriosis-targeting peptide that is internalized by

266 ay were 18% less likely to be diagnosed with endometriosis than those reporting 2 servings per day (r

267 cted vitamin D level had a 24% lower risk of endometriosis than women in the lowest quintile (rate ra

268 In summary, we developed a mouse model of endometriosis that exhibits similarities to human perito

269 and urinary tract are types of extragenital endometriosis that manifest with nonspecific symptoms, b

270 phages are central to the pathophysiology of endometriosis: they dictate the growth and vascularizati

271 yses restricting cases to those with ovarian endometriosis (third vs. lowest quartile: OR = 2.5; 95%

272 , in the eutopic endometrium from women with endometriosis throughout the menstrual cycle.

273 ession Omnibus database (GEO), which contain endometriosis tissues and normal endometrial tissues.

274 dherin (CDH1) and up-regulation of CXCL12 in endometriosis tissues.

275 pared between women with deeply infiltrative endometriosis undergoing CO2 laser ablative surgery with

276 al-medium-specific POPs were associated with endometriosis, underscoring the importance of methodolog

277 ted a genome-wide association scan (GWAS) of endometriosis using 25.5 million sequence variants detec

278 ential role of protein-modifying variants in endometriosis using exome-array genotyping in 7164 cases

279 igated the role of IL-33 in the pathology of endometriosis using patient samples, cell lines and a sy

280 we developed and validated a mouse model of endometriosis using syngeneic menstrual endometrial tiss

281 To determine phenotype-specificity, endometriosis was also generated in Klf9-/- animals.

282 Self-reported endometriosis was associated with a significantly increa

283 as strong evidence that genetic liability to endometriosis was associated with an increased risk of i

284 ospective cohort, laparoscopically confirmed endometriosis was associated with increased risk of CHD.

285 ser laparoscopic excision of moderate-severe endometriosis was comparable in women with or without bo

286 This GWAS of endometriosis was conducted with high diagnostic certain

287 Endometriosis was induced in BALB/c-Rag2(-/-)Il2rg(-/-)

288 at the serum level of IL-10 in patients with endometriosis was significantly higher than that in heal

289 on between serum beta-HCH concentrations and endometriosis was stronger in analyses restricting cases

290 identify genetic factors that contribute to endometriosis we conducted a two-stage genome-wide assoc

291 In a preclinical mouse model of endometriosis we demonstrated overexpression of the PGE2

292 By using human tissues and a mouse model of endometriosis, we demonstrate that macrophages in lesion

293 nes/pathways involved in the pathogenesis of endometriosis, we recruited 3 raw microarray datasets (G

294 2,486 incident cases of surgically confirmed endometriosis were identified over 710,230 person-years

295 cases of incident laparoscopically confirmed endometriosis were reported.

296 licular fluid from patients with the disease endometriosis, which affects 10% of women and is associa

297 olymorphisms (SNPs) robustly associated with endometriosis, which together explain up to 5.19% of var

298 genetic variants underlying the aetiology of endometriosis, WHRadjBMI and BMI using GWAS data.

299 When compared with women without endometriosis, women with laparoscopically confirmed end

300 analyses using data from the Women's Risk of Endometriosis (WREN) study, a population-based case-cont