ライフサイエンスコーパス: vulva

1 elvic malignancies (prostate, cervix, penis, vulva).

2 e named these genes sqv-1 to sqv-8 (squashed vulva).

3 ulate cell fate patterning in the C. elegans vulva.

4 the pharynx in the hypodermis, hindgut, and vulva.

5 es have feminized gonads and often develop a vulva.

6 neurons, body wall muscle, spermatheca, and vulva.

7 with abnormal somatic gonad, germ line, and vulva.

8 e tail before the spicule tips penetrate the vulva.

9 on if a previous thrust failed to breach the vulva.

10 ulval cells helps determine the shape of the vulva.

11 ulval primordium and are essential to form a vulva.

12 ns nervous system and also in the developing vulva.

13 mid-body region, leading to formation of the vulva.

14 rity protein PAR-1 in the development of the vulva.

15 y shown to promote formation of a functional vulva.

16 ining pA-D is required for expression in the vulva.

17 in the mechanisms that pattern the nematode vulva.

18 the anterior and the posterior sides of the vulva.

19 cells, which also connect the uterus to the vulva.

20 uv1 cells), which connect the uterus to the vulva.

21 es several tissues, including the uterus and vulva.

22 osterior structures are induced instead of a vulva.

23 s in the central body region to generate the vulva.

24 that mediates induction of the hermaphrodite vulva.

25 stead, a protrusion forms at the site of the vulva.

26 the induction of the Caenorhabditis elegans vulva.

27 e anchor cell, which links the uterus to the vulva.

28 ke the connection between the uterus and the vulva.

29 uterine cell fates, the AC also induces the vulva.

30 mal cells that are competent to generate the vulva.

31 ed women with squamous cell carcinoma of the vulva.

32 as of the cervix, ovary, uterus, vagina, and vulva.

33 search of the hermaphrodite surface for the vulva.

34 penis, prostate, rectum, testis, vagina, and vulva.

35 e contractions during attempts to breach the vulva.

36 mple taken from the lesion and contralateral vulva.

37 ent difficulty in locating the hermaphrodite vulva.

38 posite orientations in the two halves of the vulva.

39 tation displayed in the anterior half of the vulva.

40 e specification in the posterior half of the vulva.

41 in inhibiting LIN-12/Notch signalling in the vulva.

42 of egl-18/elt-6 function specifically in the vulva.

43 cancers of the cervix (3.3%), vagina (8.3%), vulva (1.5%), and penis (8.3%).

44 As a model, we used the nematode vulva, a highly conserved, essential organ, the developm

45 ced RAS signalling and engendered protruding vulva, a phenotype previously linked to the RASopathy-ca

46 of the Caenorhabditis elegans hermaphrodite vulva, a signal from the anchor cell activates the LET-2

47 lyzing the cells that form the hermaphrodite vulva, a specialized hypodermal passageway used for egg

48 ck layer of vulval tissue at the apex of the vulva and a physical blockage of the exit to the vulva f

49 sufficient for expression in the developing vulva and adult seam cells.

50 re essential for the proper organogenesis of vulva and appear to be temporally regulated, the mechani

51 s of cell fates and fusion in the developing vulva and are apparent direct transcriptional targets of

52 of the heart, haemorrhages, prenatal death, vulva and clitoral defects and keratoconjunctivitis sicc

53 Because human SCCs of the vulva and head and neck exhibited hallmarks of B cell in

54 e expression by RNAi suppressed the aberrant vulva and hypodermis development phenotypes of let-7(n28

55 SQV-4 is expressed in the vulva and in oocytes, among many other cells, and SQV-4

56 SQV-1 and SQV-7 are both expressed in the vulva and in oocytes, where they likely act in vulval mo

57 s hermaphrodites requires development of the vulva and its precise connection with the uterus.

58 germline proliferation, the formation of the vulva and male tail, and the metaphase to anaphase trans

59 rrest showed mutant phenotypes such as burst vulva and molting defects.

60 igration defects, the AC fails to invade the vulva and no lumen is formed in vulF.

61 men should have a thorough inspection of the vulva and perianal region, and women with abnormalities-

62 red with more radical surgical approaches in vulva and possibly vaginal melanomas.

63 chanically sense passage of eggs through the vulva and release tyramine to inhibit egg laying, in par

64 pmental arrest, morphological defects of the vulva and tail, and reduced fecundity.

65 The Caenorhabditis elegans vulva and the Drosophila eye are two classic paradigms f

66 l called the utse, and its attachment to the vulva and the epidermal seam cells.

67 ite development, the anchor cell induces the vulva and the uterine pi cells whose daughters connect t

68 lack of temporal synchronization between the vulva and the uterus is not due to precocious or acceler

69 To form a functional connection between the vulva and the uterus, the anchor cell must fuse with the

70 Development of the vulva and the ventral uterus is coordinated by the induc

71 velops with a temporal delay relative to the vulva and, thus, is not present when the connection norm

72 1 cervical carcinoma, 1 Bowen disease of the vulva, and 1 multiple Epstein-Barr virus(+) leiomyosarco

73 basement membranes between the gonad and the vulva, and in mutants in unc-6 netrin or its receptor un

74 elatinous mass that covers the hermaphrodite vulva, and its deposition decreases the mating success o

75 pment of the excretory system, hermaphrodite vulva, and male spicules.

76 sion in the epidermal seam cells, uterus and vulva, and may help to coordinate the terminal developme

77 een in HPV-related precursors of the vagina, vulva, and penis further support the notion that junctio

78 dividual sites of the genital tract (cervix, vulva, and rectum) with that from one swab with secretio

79 y, timing developmental events in the gonad, vulva, and sex myoblasts, in addition to its well-establ

80 es vulval cell fate, resulting in a deformed vulva, and the P12 hypodermal precursor often differenti

81 those in cellular sampling of the cervix and vulva, and their correlation with rigorously confirmed c

82 The primary tumor was limited to the vulva, and there were no groin lymph nodes that were cli

83 sis and management of cancers of the cervix, vulva, and vagina are reviewed.

84 anules in oocytes, with the uterine wall and vulva, and with membrane systems in the spermathecal val

85 The cell lineages that form each half of the vulva are identical, except that they occur in opposite

86 The status of the vulva as an overachiever is in part due to its inherent

87 cation events in the epithelial cells of the vulva as well as the mesodermal cells in the uterus of t

88 pharynx in cells surrounding the rectum and vulva, as well as in the germ line.

89 they do not perform the subsequent steps of vulva attachment via spicule insertion and sperm transfe

90 ell and, instead, remains at the apex of the vulva, blocking the connection between the vulval and ut

91 necessary for transcription of lin-3 in the vulva but not in the anchor cell.

92 als, three VPCs are induced to form a single vulva, but, in fog; fbf mutants, four or five VPCs are t

93 r cell signal induces Pn.p cells to form the vulva by activating a conserved receptor tyrosine kinase

94 ecordings of fluorescent keratin 13 in human vulva carcinoma-derived A431 cells.

95 e expressed differentially in the developing vulva cells, providing a potential readout for different

96 ale tail presses against the hermaphrodite's vulva, cholinergic and glutamatergic reciprocal innervat

97 The mature vulva comprises seven cell types (vulA, vulB1, vulB2, vu

98 estricts repetitive intromission attempts to vulva cues was unclear.

99 Ventral cord and vulva development are analyzed in a large sample of nema

100 Comparative studies of vulva development between Caenorhabditis elegans and oth

101 number and directionality of changes in the vulva development characters.

102 s, vulva development is similar to wild-type vulva development except that it occurs precociously, in

103 ctivated protein kinase pathway required for vulva development in Caenorhabditis elegans.

104 Recent studies of vulva development in the nematode Pristionchus pacificus

105 In lin-28 mutants, vulva development is similar to wild-type vulva developm

106 Caenorhabditis elegans vulva development provides an in vivo model to genetical

107 pe voltage-gated calcium channels to promote vulva development, and acts downstream or parallel to LE

108 we analyzed more than 40 characteristics of vulva development, including cell fates, fate induction,

109 During nematode vulva development, precursor cells acquire one of three

110 n several developmental processes, including vulva development, somatic gonad development, and male t

111 d lin-2, lin-7, and lin-10) are required for vulva development.

112 vulval epithelium, a step crucial for proper vulva development.

113 interaction between ceMIB and lin-18/RYK in vulva development.

114 nc-62 are also required for several steps in vulva development.

115 The vulva develops from a subset of ectodermal vulval precur

116 The Caenorhabditis elegans vulva develops from the progeny of three vulval precurso

117 necessary for sensation of the hermaphrodite vulva during mating.

118 ail and insert them into the hermaphrodite's vulva during mating.

119 o that the male can respond to hermaphrodite vulva efficiently.

120 Panagrolaimidae, the number of cells in the vulva equivalence group is limited by apoptosis and decr

121 of twelve ventral epidermal cells form the 'vulva equivalence group'; although all six cells are com

122 multiple mutants in which the uterus and the vulva fail to make a functional connection, resulting in

123 ts were isolated in which the uterus and the vulva fail to make a proper connection.

124 nt patient with an invasive carcinoma of the vulva for which postoperative inguinopelvic radiotherapy

125 teral hypodermal seam cells, adjacent to the vulva, for wild-type vulva formation and egg laying.

126 cells, adjacent to the vulva, for wild-type vulva formation and egg laying.

127 any non-hypodermal cells with known roles in vulva formation or egg laying.

128 Vulva formation requires the heterochronic gene lin-29,

129 lated by Hox gene lin-39: cell migration and vulva formation.

130 t cell lineages in the posterior half of the vulva from a default orientation displayed in the anteri

131 a and a physical blockage of the exit to the vulva from the uterus.

132 The anchor cell induces the vulva from ventral epithelial cells via the LIN-3 growth

133 Mutations in C. elegans sqv (squashed vulva) genes affect both vulval morphogenesis and embryo

134 sqv (squashed vulva) genes comprise a set of eight independent loci in

135 f eight Caenorhabditis elegans sqv (squashed vulva) genes, the vulval extracellular space fails to ex

136 g surgery [grade 3]; recurrent cancer of the vulva [grade 4]) and six serious adverse events were rep

137 rait they produce does not, and the nematode vulva has become a model organ for detecting such "devel

138 The Caenorhabditis elegans vulva has been a valuable paradigm for defining componen

139 f only 22 nuclei, the Caenorhabditis elegans vulva has done very well for itself.

140 epleting PAR-1 during the development of the vulva has no detectable effect on fate specification or

141 uamous cell carcinoma (SCC) of the cervix or vulva have limited therapeutic options, and the potentia

142 n biological roles of Cb-glp-1, e.g., in the vulva, have diverged from those of Ce-glp-1 and Cr-glp-1

143 Development of the vulva in C. elegans is mediated by the combinatorial act

144 k-1 MAP kinase signaling pathway induces the vulva in C. elegans.

145 h sensory functions and the uv1 cells of the vulva in hermaphrodites.

146 l precursor cells (VPCs), which generate the vulva in the hermaphrodite.

147 t of a connection between the uterus and the vulva in the nematode Caenorhabditis elegans requires sp

148 s by the LIN-3/EGF morphogen gradient during vulva induction in Caenorhabditis elegans.

149 negative regulator of EGFR signaling during vulva induction.

150 males inject sperm through the hermaphrodite vulva into the uterus.

151 ple, mirror-image symmetry of the C. elegans vulva is achieved by the opposite division orientation o

152 The Caenorhabditis elegans vulva is an elegant model for dissecting a gene regulato

153 The Caenorhabditis elegans vulva is an important paradigm for cell-cell interaction

154 6 reporter gene expression in the developing vulva is attenuated in lin-39(rf) mutants, and overexpre

155 The Caenorhabditis elegans vulva is comprised of highly similar anterior and poster

156 The pathogenesis of carcinoma of the vulva is diverse and includes both human papilloma virus

157 inement of spicule insertion attempts to the vulva is facilitated by D2-like receptor modulation of g

158 A precocious vulva is formed by essentially normal cell lineage patte

159 ke Caenorhabditis elegans and relatives, the vulva is formed from the four precursor cells P(5-8).p o

160 o maximize the probability that a functional vulva is formed.

161 vior reveal that anchor cell invasion of the vulva is important for forming the toroidal shape of the

162 fter vulval induction and that the 1 degrees vulva is necessary to induce the uv1 uterine cell fate.

163 The hermaphrodite vulva is not required for the cue.

164 The formation of the nematode vulva is one tractable system for such evolutionary deve

165 The C. elegans vulva is patterned by epidermal growth factor (EGF) acti

166 After the anchor cell has induced the vulva, it stretches toward the induced vulval cells.

167 causes these cells to form ectopic, anterior vulva-like invaginations.

168 We demonstrate that male vulva location behavior and expression of lov-1 and pkd-

169 rays, hook and head, which mediate response, vulva location, and potentially chemotaxis to hermaphrod

170 luding response to hermaphrodite contact and vulva location, but they do not perform the subsequent s

171 everal substeps: response, backing, turning, vulva location, spicule insertion and sperm transfer.

172 esponse to hermaphrodites, backing, turning, vulva location, spicule insertion, and sperm transfer, c

173 ves the steps of response, backing, turning, vulva location, spicule insertion, and sperm transfer.

174 ns HOA and HOB are specifically required for vulva location.

175 or two male sensory behaviours: response and vulva location.

176 ific sensory cilia required for response and vulva-location mating behaviors.

177 pithelial attachments, including the rectum, vulva, mechanosensory neurons, and excretory duct/pore.

178 mal cell terminal differentiation and proper vulva morphogenesis.

179 n anogenital malignancies (1.6%) were found: vulva (n=6), cervix (n=5), and anus (n=5).

180 The small-cell carcinomas of the vagina and vulva need to be distinguished from Merkel cell cancers.

181 are involved in gene regulation outside the vulva, negatively regulating the expression of the Delta

182 sion patterns of the cells in the developing vulva of nT1 mutants, we demonstrate that egl-18/elt-6 p

183 tations that perturb the invagination of the vulva of the Caenorhabditis elegans hermaphrodite, we ha

184 ments continue until the male shifts off the vulva or genital penetration is accomplished.

185 lopment of various cancers including penile, vulva, oropharyngeal and cervical cancers.

186 rminal bulb, the rectal epithelial cells and vulva; pB directs expression in the motor neurone PDA, t

187 ted with ulcers, plaques, and nodules in the vulva, perineum, inguinal creases, and left axilla.

188 NA interference of PAR-1 causes a protruding vulva phenotype.

189 ve activity upon lin-45 Raf and induce multi-vulva phenotypes in C.elegans.

190 for patterns of nucleotide polymorphism and vulva precursor cell lineage, and conduct a series of hy

191 frequency in African C. elegans for the P3.p vulva precursor cell, and in African C. briggsae for P4.

192 is elegans, the fates of the six multipotent vulva precursor cells (VPCs) are specified by extracellu

193 In vulva precursor cells (VPCs), a pathway of heterochronic

194 nchor cell and lateral signaling between the vulva precursor cells.

195 The Caenorhabditis elegans vulva provides a simple model for the genetic analysis o

196 equent grade 3 and 4 events were pain in the vulva, pruritus, fatigue, and headache.

197 netic screen for mutants having a protruding-vulva (Pvl) mutant phenotype.

198 he development of the Caenorhabditis elegans vulva requires the involution of epithelial cells and pr

199 , from the Caenorhabditis elegans developing vulva requires the lipoprotein receptor-related proteins

200 e hermaphrodite's surface for the vulva (the vulva search).

201 Development of the Caenorhabditis elegans vulva serves as a paradigm for intercellular signaling d

202 In the vulva, sex myoblasts, and hypodermis, lin-42 activity pr

203 METT-10 also promotes vulva, somatic gonad, and embryo development and ensures

204 tion together in a single complex to repress vulva-specific gene transcription.

205 e of Ras signaling by selectively activating vulva-specific genes.

206 Mutations in eight squashed vulva (sqv) genes in Caenorhabditis elegans cause defect

207 l neoplasia is a skin disorder affecting the vulva that, if left untreated, can become cancerous.

208 e we identify a gene, lov-1 (for location of vulva), that is required for two male sensory behaviours

209 earch of the hermaphrodite's surface for the vulva (the vulva search).

210 When the spicule tips penetrate the vulva, the protractors undergo prolonged contraction to

211 oductive system, cells that give rise to the vulva, the vulval precursor cells (VPCs), remain quiesce

212 rine pi cells whose daughters connect to the vulva, thereby organizing the uterine-vulval connection.

213 The uterine anchor cell (AC) induces the vulva through LIN-3/epidermal growth factor (EGF) signal

214 es over the past twenty years have shown the vulva to be a microcosm for organogenesis and a model fo

215 re of the two mirror-symmetric halves of the vulva to join into a single, coherent organ.

216 ing in vulval lineages, establishment of the vulva-uterine connection, development and function of th

217 ed for carcinomas and premalignancies of the vulva, vagina, anus, and oropharynx.

218 lly type 16) can cause cancer of the cervix, vulva, vagina, anus, penis, and oropharynx.

219 , site-by-site, for primary melanomas of the vulva, vagina, urethra, ovary, and the uterine cervix.

220 high-risk types to be first detected in the vulva/vagina (P = .03).

221 tions were more likely to be detected in the vulva/vagina than in the cervix (odds ratio, 4.38 [95% c

222 d, the AC induces patterned proliferation of vulva via expression of LIN-3 (EGF) and then invades int

223 ch the number of precursor cells forming the vulva was reduced from four to two.

224 s arising from genital skin (penis, scrotum, vulva) were higher in women (0.54) than in men (0.30).

225 precocious phenotypes in the hypodermis and vulva when expressed from multicopy arrays.

226 to allow the vaginal opening to form in the vulva, whereas in males and in females with CAH, androge

227 il, but typically HSNs were located near the vulva, which also varies in anterior-posterior position

228 gonadal cells organize the alignment of the vulva with the sex myoblasts, the progenitors of the egg

229 The Caenorhabditis elegans vulva, with its invariant cell lineage and interaction o

230 describe chronic burning and/or pain in the vulva without objective physical findings to explain the