ライフサイエンスコーパス: retinoblastoma

1 pathway in promoting invasion and growth of retinoblastoma.

2 treatment, and follow-up of eyes affected by retinoblastoma.

3 tcomes of secondary prevention screening for retinoblastoma.

4 play a role in the development of childhood retinoblastoma.

5 tecan-based therapy for advanced intraocular retinoblastoma.

6 classification scheme for vitreous seeds in retinoblastoma.

7 ines for children at risk for development of retinoblastoma.

8 , and 9 months of age, and all had bilateral retinoblastoma.

9 athologic characterization of PVR in treated retinoblastoma.

10 ions, and chromosomal copy number changes in retinoblastoma.

11 s seeding after intravenous chemotherapy for retinoblastoma.

12 aser combined with systemic chemotherapy for retinoblastoma.

13 nt modality for treating vitreous seeding in retinoblastoma.

14 ted in less than 0.5% of in eyes treated for retinoblastoma.

15 o met and discussed screening approaches for retinoblastoma.

16 ing recommendations for children at risk for retinoblastoma.

17 children at elevated risk for development of retinoblastoma.

18 e contributes to the development of sporadic retinoblastoma.

19 the national reference center for heritable retinoblastoma.

20 ecurrence after enucleation in children with retinoblastoma.

21 th bilateral disease had a family history of retinoblastoma.

22 , idarubicin, and vincristine, for stage III retinoblastoma.

23 nths after complete and stable regression of retinoblastoma.

24 ete German cohort of patients with heritable retinoblastoma.

25 part, by inactivating the tumor suppressor, retinoblastoma.

26 is superior to blood as a liquid biopsy for retinoblastoma.

27 us RD 21 months after the last treatment for retinoblastoma.

28 f which have not been reported previously in retinoblastoma.

29 Rb is independent of the age at diagnosis of retinoblastoma.

30 y suppressing MYCN expression in MYCN-driven retinoblastomas.

31 subset of cell cycle-related genes including retinoblastoma 1 is the target of Rbfox2 in cytoplasmic

32 ic stress granules, and Rbfox2 regulates the retinoblastoma 1 mRNA and protein expression levels duri

33 D1 (cyclin D1) or knockdown of its inhibitor retinoblastoma 1, partially rescued miR-184 levels.

34 signaling by binding E2F negative regulator Retinoblastoma-1 (RB).

35 ation included 370 consecutive patients with retinoblastoma (375 eyes) who underwent baseline MR imag

36 Finally, in an orthotopic zebrafish model of retinoblastoma, a 55% decrease in tumor spread was noted

37 is recommended for all children at risk for retinoblastoma above the population risk.

38 has been reported to more effectively treat retinoblastoma, allowing many previously unsalvageable e

39 tracellular pathways (ERK/JNK, MYC/MAX, WNT, retinoblastoma), altered oncogenes and tumor suppressor

40 analysis is important to identify heritable retinoblastoma among unilateral retinoblastoma cases.

41 ed by HSUR2, which include mRNAs that encode retinoblastoma and factors involved in p53 signalling an

42 ocular Retinoblastoma Classification group E retinoblastoma and glaucoma have a higher risk of MD at

43 y has emerged as a treatment for intraocular retinoblastoma and has been quickly adopted by centers w

44 etastatic relapse may occur in children with retinoblastoma and high-risk pathologic features (HRPFs)

45 7.9%]; 50 female [52.1%]) with nonmetastatic retinoblastoma and HRPFs (isolated massive choroidal inv

46 cohort study of patients with nonmetastatic retinoblastoma and HRPFs used prospectively defined incl

47 fied a high-risk population of children with retinoblastoma and HRPFs with MD.

48 The laterality of intraocular retinoblastoma and its treatment were not associated wit

49 monly develops after successful treatment of retinoblastoma and may result in traction or rhegmatogen

50 between the ages at diagnosis of intraocular retinoblastoma and pineal TRb.

51 ective regimen for the treatment of advanced retinoblastoma and results in globe salvage with vision.

52 key genetic driver alterations seen in human retinoblastoma and reveals the emergence of MYCN indepen

53 nctional improvement in eyes with history of retinoblastoma and scleral buckling developing tractiona

54 is detectable in patients with nonmetastatic retinoblastoma and to assess its prognostic effect on di

55 ated epigenetic analysis of murine and human retinoblastomas and induced pluripotent stem cells (iPSC

56 The tumor suppressor genes RB1 (retinoblastoma) and CDKN2a (cyclin-dependent kinase inhi

57 reatments on long-term survival in heritable retinoblastoma, and the genetic background of the patien

58 in almost all familial and sporadic forms of retinoblastoma, and this gene is mutated at variable fre

59 Patients with retinoblastoma are at risk of pineal TRb developing for

60 The most frequent focal alterations in human retinoblastoma are mutations in the tumor-suppressor gen

61 of intravitreous melphalan for treatment of retinoblastoma, as a single agent or with concomitant to

62 monstrated interaction between S18-2 and the retinoblastoma-associated protein (RB) and hypothesized

63 tors such as BCl-xL and the tumor suppressor retinoblastoma-associated protein 1 (RB1).

64 s, including a reduction in the abundance of retinoblastoma-associated protein and increases in the R

65 sis of pineal TRb in patients diagnosed with retinoblastoma at 6 months or younger versus older than

66 gical assessment of parents of patients with retinoblastoma at a tertiary care ocular oncology center

67 nivariate analysis, presentation age, foveal retinoblastoma (at initial examination), use of TTT, and

68 pression of the AMP-regulated protein kinase-retinoblastoma axis with miR-210 inhibition.

69 children diagnosed in Germany with heritable retinoblastoma between 1940 and 2008 was 93.2% (95% CI,

70 ren aged 18 years and younger diagnosed with retinoblastoma between 2000 and 2014.

71 ies of all patients presenting with cavitary retinoblastoma between August 2014 and January 2019 who

72 naling suppresses CSC properties by reducing retinoblastoma binding protein 5 (RBBP5), which is eleva

73 ynthesis, Sqle, carries a second mutation in retinoblastoma binding protein 8, endonuclease (Rbbp8, a

74 The rare diffuse anterior form of retinoblastoma can be managed with globe-salvaging alter

75 Retinoblastomas can arise from cone photoreceptor precur

76 s, suggesting larger systemic disparities in retinoblastoma care.

77 Approximately 40% of retinoblastoma cases are heritable, resulting from a ger

78 fy heritable retinoblastoma among unilateral retinoblastoma cases.

79 kdown decreased SKP2 expression and impaired retinoblastoma cell cycle progression, re-expression of

80 Significantly, expression of the Gonium retinoblastoma cell cycle regulator in unicellular Chlam

81 group formation evolved by co-option of the retinoblastoma cell cycle regulatory pathway.

82 Moreover, MYCN was essential to retinoblastoma cell growth and tumor formation, and ecto

83 ated p53 and induced p21(Cip1) expression in retinoblastoma cell lines that overexpress MdmX, suggest

84 t not MDM4 has a consistent critical role in retinoblastoma cell proliferation in vitro, as well as i

85 promotes SKP2 expression and SKP2-dependent retinoblastoma cell proliferation.

86 Y79 retinoblastoma cells and CD44-negative SK-N-DZ neuroblas

87 Here, we show that in human retinoblastoma cells TRbeta2 mRNA encodes two TRbeta2 pr

88 illance in the absence of detectable MDM2 in retinoblastoma cells, bringing into question the importa

89 Synaptophysin was used to stain retinoblastoma cells.

90 retinal iPSC cells, as well as the origin of retinoblastoma cells.

91 er component of the cone circuitry, MYCN, in retinoblastoma cells.

92 received at the pathology department of the Retinoblastoma Center of Houston from 2010 to 2015.

93 cancer staging and International Intraocular Retinoblastoma Classification (IIRC), and number of OCT

94 red in 8 of the 43 International Intraocular Retinoblastoma Classification group E eyes with glaucoma

95 that children with International Intraocular Retinoblastoma Classification group E retinoblastoma and

96 stage according to International Intraocular Retinoblastoma Classification.

97 , abandonment for patients with IRSS stage I retinoblastoma decreased from 16% to 4%.

98 et is linked to the age at which intraocular retinoblastomas develop, and the lead time from a detect

99 The retinoblastoma epigenome mapped to the developmental sta

100 Retinoblastoma eyes characterized by thinning of central

101 igh-risk histopathologic features in group D retinoblastoma eyes enucleated as primary or secondary t

102 initiated with IVC, 50% of salvaged Group D retinoblastoma eyes had <20/200 vision, with TTT being a

103 Whereas control of E2Fs by the retinoblastoma family of proteins is well established, m

104 trabismus, and nystagmus outcomes in Group D retinoblastoma following multimodality treatments in a n

105 that developed after successful treatment of retinoblastoma from 2003 to 2015.

106 All children newly diagnosed with retinoblastoma from January 2011 to December 2015 who ha

107 the HLH regulatory protein, Id2a, and of the retinoblastoma gene, p130, which regulates progression t

108 and 37 were International Classification of Retinoblastoma group C to E.

109 pRNFL thicknesses were detected compared to retinoblastoma group.

110 7-year-old boy with a history of unilateral retinoblastoma (group D) in his left eye presented with

111 7-year-old girl with a history of bilateral retinoblastoma (group D) presented with light perception

112 ana vitrectomy (PPV) in eyes with history of retinoblastoma has been associated with a significant ri

113 The "cavitary" form of retinoblastoma has historically demonstrated minimal tre

114 Whether MYCN overexpression drives retinoblastoma has not been assessed in model systems.

115 However, survivors of heritable retinoblastoma have a significantly increased risk of su

116 Survivors of hereditary retinoblastoma have excellent survival but substantially

117 Five European experts in retinoblastoma imaging evaluated the MRI examinations re

118 ct orbital tumor recurrence in children with retinoblastoma in a large study cohort.

119 defined as a person with a family history of retinoblastoma in a parent, sibling, or first- or second

120 counseling and testing clarify the risk for retinoblastoma in children with a family history of the

121 tion of improving outcomes for children with retinoblastoma in countries with limited resources.

122 aspiration biopsy confirmed the diagnosis as retinoblastoma in each case.

123 noblastoma presented with unilateral group C retinoblastoma in her right eye.

124 rongly with MYCN overexpression and leads to retinoblastoma in mice.

125 ted by a large multicenter study of sporadic retinoblastoma in which parents of 99 unilateral and 56

126 noblastoma is an exquisitely rare variant of retinoblastoma in which the tumor resides in the anterio

127 Retinoblastoma is a childhood retinal tumor that develop

128 Retinoblastoma is a rare childhood cancer of the retina.

129 Diffuse anterior retinoblastoma is an exquisitely rare variant of retinob

130 Intraocular retinoblastoma is curable, but survivors with a heritabl

131 nterpretation of histopathology of eyes with retinoblastoma is necessary to assign metastatic risk.

132 Retinoblastoma is the most common intraocular cancer in

133 he Parental Stress Index 4-Short Form, and a retinoblastoma Knowledge Assessment questionnaire were a

134 re but serious complication in children with retinoblastoma, leading to a high risk of metastasis and

135 Activin A/B, and GDF3) were expressed in six retinoblastoma lines, and evidence of downstream SMAD2 s

136 Methods Twenty-seven patients with bilateral retinoblastoma (male patients, n = 14; median age, 8.4 m

137 roves the accuracy of clinical evaluation in retinoblastoma management.

138 ed eye salvage for unilateral (cT2b/group D) retinoblastoma may risk tumor spread compared with prima

139 ry 6 months after the diagnosis of heritable retinoblastoma (median age, 6 months) until 36 months of

140 as identified in all children with bilateral retinoblastoma (n = 12), and these NGS results were 100%

141 t with IAC results in regression of cavitary retinoblastoma, often with greater reduction in tumor si

142 None of the patients developed recurrence of retinoblastoma or systemic metastasis.

143 of the study and 128 patients treated for a retinoblastoma or who underwent enucleation were exclude

144 pear to modify risk estimates for unilateral retinoblastoma (OR, 2.5; CI, 0.9-7.0 vs OR, 2.5; CI, 1.0

145 in the presence of brain tissue and that the retinoblastoma pathway enables overproliferation of cell

146 aining clouds (class 3 vitreous seeds) of 40 retinoblastoma patients (19 treated with OAC alone and 2

147 ve head in the free eyes of unilateral cured retinoblastoma patients and, also after enucleation usin

148 In this study, a cohort of hereditary retinoblastoma patients at increased risk for TRB was id

149 Analysis of 959 retinoblastoma patients revealed that 70.8% were enuclea

150 Retinoblastoma patients treated at a single center with

151 We reviewed the outcomes of retinoblastoma patients who were treated at KHCC after i

152 ital, and we compared that with outcomes for retinoblastoma patients who were treated before implemen

153 clin E1, inducing proliferation by promoting retinoblastoma phosphorylation and allowing for E2F tran

154 ates cyclin E abundance resulting in reduced retinoblastoma phosphorylation, decreased E2F activity,

155 uce reversible G1-phase cell-cycle arrest in retinoblastoma-positive tumor models.

156 When a parent had retinoblastoma, prenatal molecular diagnosis with early-

157 old female child without a family history of retinoblastoma presented with unilateral group C retinob

158 rs are deficient in cyclin D1 yet retain the retinoblastoma-proficient/p16(INK4a)-deficient profile a

159 ein 7 (MCM7) knockdown in phospho Ser807/811-retinoblastoma protein (p-Rb) defect cells.

160 The Retinoblastoma protein (RB) and DREAM complex (DP, RB-li

161 The retinoblastoma protein (Rb) and the homologous pocket pr

162 cally infected culture induces Mdm2-mediated retinoblastoma protein (Rb) degradation.

163 Retinoblastoma protein (Rb) is a tumor suppressor that b

164 is frequently disrupted by mutations in the retinoblastoma protein (RB) pathway.

165 ssion of several direct p53 targets, reduced retinoblastoma protein (Rb) phosphorylation, and defects

166 The tumor suppressor retinoblastoma protein (RB) regulates S-phase cell cycle

167 The retinoblastoma protein (RB) restricts cell cycle gene ex

168 ision cycle dilutes the cell cycle inhibitor Retinoblastoma protein (Rb) to trigger division in human

169 AR recruitment of the retinoblastoma protein (Rb) was required to strengthen t

170 this study, we show that HBZ protein targets retinoblastoma protein (Rb), which is a critical tumor s

171 lysine-9 (H3K9) methylation is essential for retinoblastoma protein (RB)-mediated heterochromatin for

172 Intriguingly, we also find that the retinoblastoma protein (RB1) is a direct target of JARID

173 le markers, including phosphorylation of the retinoblastoma protein and lamins, nuclear envelope brea

174 ited E2F2 expression and was associated with retinoblastoma protein phosphorylation attenuation, whic

175 The retinoblastoma protein RB is a tumor suppressor known to

176 well-known target of cyclin D-Cdk4,6 is the retinoblastoma protein Rb, which inhibits cell-cycle pro

177 which leads to eventual inactivation of the retinoblastoma protein Rb.

178 e, such as cyclin-dependent kinases and pRb (retinoblastoma protein), are necessary for efficient mes

179 and interference with the downstream CDK-Rb (retinoblastoma protein)-E2F signaling pathway.

180 sion by phosphorylating and inactivating the retinoblastoma protein, a tumor suppressor that restrain

181 of the central cell-cycle regulators CDKN1A, retinoblastoma protein, and cyclin D1 (CCND1), but did n

182 We found that YM155 rapidly activates the retinoblastoma protein, correlating with the loss of exp

183 pregulation of p27 and hypophoshorylation of retinoblastoma protein, leading to senescence.

184 reduced Ki67, c-Myc, and phosphorylation of retinoblastoma protein, suggesting inhibition of the G1-

185 preclinical data to support its activity in retinoblastoma protein-expressing tumors.

186 MCV large T up-regulated Sox2 through its retinoblastoma protein-inhibition domain, which in turn

187 nduction of cyclin D1 and phosphorylation of retinoblastoma protein.

188 vely phosphorylates the checkpoint regulator retinoblastoma protein.

189 The retinoblastoma Rb protein is an important factor control

190 a are mutations in the tumor-suppressor gene retinoblastoma (RB) and amplification of the oncogene MY

191 cyclin D1-CDK4 activity by p21 controls the retinoblastoma (Rb) and E2F transcription program in an

192 Most cancers preserve functional retinoblastoma (Rb) and may, therefore, respond to inhib

193 s 4 and 6 (CDK4/6) phosphorylate and inhibit retinoblastoma (RB) family proteins.

194 Sirt1 deacetylates retinoblastoma (Rb) in the Rb/E2F1 complex, leading to d

195 The tumor suppressor protein retinoblastoma (RB) is mechanistically linked to suppres

196 Retinoblastoma (Rb) is one of the first tumors to have a

197 eas tumor cells with PTEN, PIK3CA, PIK3R1 or retinoblastoma (Rb) mutation are more resistant to this

198 mitant with increased phosphorylation of the retinoblastoma (RB) protein by cyclin-dependent kinase (

199 The retinoblastoma (Rb) protein exerts its tumor suppressor

200 Retinoblastoma (RB) protein inactivation during tumor pr

201 lbociclib reduces tumor growth by decreasing retinoblastoma (RB) protein phosphorylation and inducing

202 ress PDAC proliferation through induction of retinoblastoma (RB) protein-mediated senescence.

203 activated gene that is also repressed by the Retinoblastoma (RB) protein.

204 ond major prosenescent tumor suppressor, the retinoblastoma (Rb) protein.

205 roposed to be mediated by phosphorylation of retinoblastoma (Rb) protein.

206 we can increase PNECs by reducing levels of retinoblastoma (RB) proteins with inhibitory RNA.

207 The retinoblastoma (RB) tumor suppressor is recognized as a

208 sizer protein, CDKG1, that acts through the retinoblastoma (RB) tumor suppressor pathway as a D-cycl

209 Disruption of the retinoblastoma (RB) tumor suppressor pathway, either thr

210 ndent kinase (v-CDK) UL97 phosphorylates the retinoblastoma (Rb) tumor suppressor.

211 etween the E2F transcription factors and the retinoblastoma (Rb) tumor suppressor.

212 E2F1 and retinoblastoma (RB) tumor-suppressor protein not only re

213 Mutations in the retinoblastoma (RB) tumour suppressor pathway are a hall

214 The human pocket proteins retinoblastoma (Rb), p107, and p130 are critical negativ

215 ter inactivates the tumor suppressor protein retinoblastoma (Rb), which leads to the overexpression o

216 or complex called dimerization partner (DP), retinoblastoma (RB)-like, E2F and MuvB (DREAM).

217 E2F-2 is a retinoblastoma (Rb)-regulated transcription factor induc

218 y of enucleated globes with the diagnosis of retinoblastoma received in the histopathology department

219 A total of 130 eyes of 120 patients with retinoblastoma receiving 630 intravitreous (melphalan, t

220 coding the miR cluster miR-17-92, while most retinoblastomas reemerged without clear genetic alterati

221 However, over time, retinoblastomas reemerged, typically without reactivatio

222 owing multimodality treatments in a national retinoblastoma referral center.

223 ologists, pathologists, and geneticists from retinoblastoma referral centers located in various geogr

224 that the regulatory role of the Arabidopsis RETINOBLASTOMA RELATED (RBR) in cell proliferation can b

225 Inducible overexpression of RETINOBLASTOMA RELATED (RBR), a sugar-dependent transcri

226 the cell cycle and differentiation regulator RETINOBLASTOMA-RELATED (RBR).

227 2F transcription factors in association with RETINOBLASTOMA-RELATED (RBR).

228 mimicking phenotypes of plants with reduced RETINOBLASTOMA-RELATED PROTEIN1 (RBR1) activity.

229 The E2F transcription factors and the RETINOBLASTOMA-RELATED repressor protein are principal r

230 with gammaH2AX, but only in the presence of RETINOBLASTOMA RELATED1.

231 (5) Children at high risk for retinoblastoma require more frequent screening, which ma

232 s in adults and children (uveal melanoma and retinoblastoma, respectively).

233 effective treatment for vitreous seeding in retinoblastoma, resulting in high rates of ocular surviv

234 th, cryopexy scars (retinal tear and treated retinoblastoma scar), bone spicules, white without press

235 Among our hereditary retinoblastoma screening cohort (n=215) 4 patients with

236 multiple injections are required to control retinoblastoma seeds.

237 ted before implementing a telemedicine-based retinoblastoma service at KHCC.

238 The choice of primary treatment for group D retinoblastoma should be carefully weighed, because acco

239 A subset of returning retinoblastomas showed genomic amplification of a Mycn t

240 Activation of AMP-regulated protein kinase-retinoblastoma signaling is important in NSC proliferati

241 nilateral intraocular disease (International Retinoblastoma Staging System [IRSS] stage I) were consi

242 2aN0M0H1, according to the 8th edition cTNMH Retinoblastoma Staging.

243 nfirmed some of the common second cancers in retinoblastoma survivors but found little evidence for a

244 -long oncologic follow-up is crucial for all retinoblastoma survivors, and less detrimental eye-prese

245 The retinoblastoma susceptibility gene (RB1) was the first t

246 ing with tractional retinal detachment after retinoblastoma therapy and scleral buckle surgery.

247 Approximately 45% of patients with retinoblastoma-those with a germline RB1 pathogenic vari

248 ncluding ovarian cancer, hepatocarcinoma and retinoblastoma, through the inhibition of the YAP-TEAD c

249 creening tool for the orbit in children with retinoblastoma to exclude tumor recurrence, especially i

250 to which children are at risk of trilateral retinoblastoma (TRb) developing, whether its onset is li

251 afterward as a screening tool for trilateral retinoblastoma (TRB), but there is no consensus on timin

252 of this study is to evaluate the outcomes of retinoblastoma treated with intravenous chemotherapy and

253 eview of patients with vitreous seeding from retinoblastoma treated with intravenous chemotherapy and

254 escribes the results of advanced intraocular retinoblastoma treated with neoadjuvant chemotherapy.

255 evelop proliferative vitreoretinopathy after retinoblastoma treatment.

256 ose To assess the correlation of intraocular retinoblastoma tumor size measured with magnetic resonan

257 eraction between CHT7 and the C. reinhardtii retinoblastoma tumor suppressor (RB) protein homolog MAT

258 sing an HPV16 E7 variant that can inactivate retinoblastoma tumor suppressor (RB1) but cannot degrade

259 risk HPV E7 proteins to bind and degrade the retinoblastoma tumor suppressor or activate E2F target g

260 Downregulation of Cdc25A led to reduction in retinoblastoma tumor suppressor protein (pRb) phosphoryl

261 phate site to promote phosphorylation of the retinoblastoma tumor suppressor protein (Rb) and other s

262 The retinoblastoma tumor suppressor protein (RB) plays a cri

263 The retinoblastoma tumor suppressor protein (RB) plays an im

264 radigm for G1/S control, Cdks inactivate the retinoblastoma tumor suppressor protein (Rb) through pho

265 functional role for the cyclin D1/Cdk4/pRb (retinoblastoma tumor suppressor protein) pathway in dela

266 nd maturation by TGFbeta is dependent on the retinoblastoma tumor suppressor protein/E2 promoter bind

267 cus 3-4 (mat3-4), which contains a defective retinoblastoma tumor suppressor-related protein of Chlam

268 Children with any clinically invisible retinoblastoma tumor that was detected on OCT posterior

269 Histopathologic evaluation revealed treated retinoblastoma tumor with a Type 3 regression pattern, p

270 Although the retinoblastoma tumor-suppressor gene (RB1) is frequently

271 Mutations of the retinoblastoma tumor-suppressor gene (RB1) or components

272 enomic alterations to the p53 pathway during retinoblastoma tumorigenesis.

273 Invisible retinoblastoma tumors are now detected with screening fo

274 Eight cavitary retinoblastoma tumors in 6 eyes of 4 patients were treat

275 was to report treatment response of cavitary retinoblastoma tumors to IAC.

276 precision results in managing invisible new retinoblastoma tumors.

277 atectomy by promoting the phosphorylation of retinoblastoma tumour suppressor protein at known CDK ta

278 be the inhibition of phosphorylation of the retinoblastoma tumour suppressor, inducing G1 cell cycle

279 There were 138 parents of children with retinoblastoma (unifocal: n = 77, multifocal: n = 61).

280 a were analyzed between 1992 and 2018 at the Retinoblastoma Unit, Royal London Hospital, London, Unit

281 A recent classification scheme for retinoblastoma vitreous seeds has shown promise in predi

282 he efficacy and toxicity of treating class 3 retinoblastoma vitreous seeds with ophthalmic artery che

283 The salvage rate secondary to active retinoblastoma was 79%.

284 Unilateral retinoblastoma was associated with parental insecticide

285 Treatment for retinoblastoma was performed at the Hospital for Sick Ch

286 essenger RNA for MD evaluation in metastatic retinoblastoma was previously reported, but no data in n

287 The epigenome of retinoblastomas was more similar to that of the normal r

288 aphs of the enucleated eyes of patients with retinoblastoma were analyzed to select those with vitreo

289 n newly diagnosed with enucleated unilateral retinoblastoma were enrolled prospectively.

290 er 17 years, 813 eyes from 478 children with retinoblastoma were treated at KHCC.

291 equenced RNA transcripts in five snap frozen retinoblastomas which invaded the optic nerve and five w

292 receptor of the TGF-beta family, in invasive retinoblastomas, while downregulation of DACT2 and LEFTY

293 Three patients with treated retinoblastoma who developed severe PVR and required enu

294 controlled study population of patients with retinoblastoma who had central pathologic review, our fi

295 rt of 952 irradiated survivors of hereditary retinoblastoma who were originally diagnosed during 1914

296 Patients presenting with cavitary retinoblastoma who were treated with IAC.

297 promoted excessive proliferation, and led to retinoblastoma with anaplastic changes.

298 Controlling retinoblastoma with seeding is challenging despite advan

299 revealed parents of children with multifocal retinoblastoma with severe depression (1.4% vs 10.2%, P

300 e OCT sessions for fellow eyes of unilateral retinoblastoma without any suspicious lesion and those p