ライフサイエンスコーパス: retinoblastoma

1 e contributes to the development of sporadic retinoblastoma.

2 the national reference center for heritable retinoblastoma.

3 ecurrence after enucleation in children with retinoblastoma.

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

5 nths after complete and stable regression of retinoblastoma.

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

7 ete German cohort of patients with heritable retinoblastoma.

8 part, by inactivating the tumor suppressor, retinoblastoma.

9 ed as a primary treatment for advanced-stage retinoblastoma.

10 ic artery chemotherapy can fail in eyes with retinoblastoma.

11 st in the care and outcomes of children with retinoblastoma.

12 used in the treatment of vitreous seeding of retinoblastoma.

13 ent retinae, making them more susceptible to retinoblastoma.

14 play a role in the development of childhood retinoblastoma.

15 respectively, among patients with bilateral retinoblastoma.

16 tecan-based therapy for advanced intraocular retinoblastoma.

17 classification scheme for vitreous seeds in retinoblastoma.

18 ines for children at risk for development of retinoblastoma.

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

20 athologic characterization of PVR in treated retinoblastoma.

21 s seeding after intravenous chemotherapy for retinoblastoma.

22 aser combined with systemic chemotherapy for retinoblastoma.

23 nt modality for treating vitreous seeding in retinoblastoma.

24 o met and discussed screening approaches for retinoblastoma.

25 ing recommendations for children at risk for retinoblastoma.

26 children at elevated risk for development of retinoblastoma.

27 ibute to the etiology of partially penetrant retinoblastomas.

28 y suppressing MYCN expression in MYCN-driven retinoblastomas.

29 inding partners for E2F1, we queried whether retinoblastoma 1 (Rb1) might be involved.

30 estoration of host tumor suppressors p53 and retinoblastoma 1 (RB1), which are targeted by E6 and E7,

31 2F transcription factor 1 (E2F1) and loss of retinoblastoma 1 (RB1).

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

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

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

35 ent primary enucleation for the treatment of retinoblastoma, 145 (36%) had high-risk features on hist

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

37 Seventeen patients with metastatic retinoblastoma (9 at diagnosis, 8 at relapse; age range:

38 When this process is disrupted, retinoblastoma, a developmental tumor of the retina, can

39 have critical tumor suppressive functions in retinoblastoma, a tumor of neural origin, and neuroendoc

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

41 e unadjusted chance of developing trilateral retinoblastoma across all cohorts was 5.3% (95% confiden

42 In patients with hereditary retinoblastoma (all bilateral cases, and the unilateral

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

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

45 Rb inactivation is the initiating lesion in retinoblastoma and current models propose that induction

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

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

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

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

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

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

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

53 the predominant initiating genetic lesion in retinoblastoma and is rate limiting for tumorigenesis.

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

55 ction of CRX mRNA as a marker for metastatic retinoblastoma and MD in bone marrow and CSF and its cor

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

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

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

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

60 deletions in partially penetrant hereditary retinoblastomas and is known to impair cell growth and t

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

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

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

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

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

66 suggest that CRX mRNA is a novel marker for retinoblastoma at extraocular sites.

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

71 The retinoblastoma binding protein KDM5A removes methyl mark

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

73 Invasiveness and metastasis of retinoblastoma can occur at the early stage of tumor dev

74 Retinoblastomas can arise from cone photoreceptor precur

75 fy heritable retinoblastoma among unilateral retinoblastoma cases.

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

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

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

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

80 Seventeen retinoblastoma primary tumors, 2 retinoblastoma cell lines, and 47 samples of bone marrow

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

82 Intravitreal implantation of color-coded retinoblastoma cells allowed us to kinetically monitor t

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

84 Further, interactions between retinoblastoma cells and surrounding microvasculatures w

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

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

87 Synaptophysin was used to stain retinoblastoma cells.

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

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

90 h group 5 or International Classification of Retinoblastoma (Children's Oncology Group) group D or E

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

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

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

94 We included 23 retinoblastoma cohorts from 26 studies.

95 verestimation bias we restricted analysis to retinoblastoma cohorts with a minimum size of 100 patien

96 ly significant higher incidence of high-risk retinoblastoma compared with controls (39% vs. 16%; P =

97 3-kinase/phosphatase and tensin homolog/AKT, retinoblastoma/cyclin-dependent kinase (CDK) N2A-p16(INK

98 the tightly coordinated Ubiquitin- Cyclin E- Retinoblastoma- E2F bistable-signalling pathway controll

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 Retinoblastoma eyes requiring second-course OAC after in

104 of the cell cycle, activates proteins in the retinoblastoma family, and subsequently increases the di

105 Additionally, we documented that the Retinoblastoma-family protein (Rbf), a proven regulator

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

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

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

109 The retinoblastoma gene (Rb) is mutated at significant frequ

110 The retinoblastoma genome can be very stable; therefore, epi

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

112 pRNFL thicknesses were detected compared to retinoblastoma group.

113 International Classification of Intraocular Retinoblastoma, group E tumor had a statistically signif

114 The International Classification of Retinoblastoma groups were B in 1 eye (8%), C in 4 eyes

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

116 than Mexico had a higher risk for unilateral retinoblastoma (HR, 2.03; 95% CI, 1.33-3.11).

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 aspiration biopsy confirmed the diagnosis as retinoblastoma in each case.

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

123 of Brg1 (Smarca4) in retinal development and retinoblastoma in mice using molecular and cellular appr

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

125 OAC group (5.2%) and more eyes with group E retinoblastoma in the enucleation group (87.3%) than in

126 Most children with retinoblastoma in the United States are diagnosed as hav

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

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

129 (95% CI: 1.2%-6.7%) and a pineal trilateral retinoblastoma incidence of 3.2% (95% CI: 1.4%-5.6%).

130 tinoblastoma we found an adjusted trilateral retinoblastoma incidence of 3.5% (95% CI: 1.2%-6.7%) and

131 (95% CI: 1.9%-7.1%) and a pineal trilateral retinoblastoma incidence of 3.7% (95% CI: 1.8%-6.2%).

132 germline RB1 mutation) we found a trilateral retinoblastoma incidence of 4.1% (95% CI: 1.9%-7.1%) and

133 1966 and July 2015 that assessed trilateral retinoblastoma incidence.

134 loped an orthotopic zebrafish model in which retinoblastoma invasion and metastasis can be monitored

135 wever, an optimal preclinical model to study retinoblastoma invasiveness and metastasis in relation t

136 Retinoblastoma is a highly invasive malignant tumor that

137 Retinoblastoma is a pediatric tumor of the developing re

138 Diffuse anterior retinoblastoma is an exquisitely rare variant of retinob

139 Intraocular retinoblastoma is curable, but survivors with a heritabl

140 The estimated incidence of trilateral retinoblastoma is lower than what is reported in previou

141 The management of intraocular retinoblastoma is rapidly changing, and even recent revi

142 Disseminated retinoblastoma is usually fatal.

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

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

145 roves the accuracy of clinical evaluation in retinoblastoma management.

146 for malignancy and included B-cell lymphoma, retinoblastoma, melanoma, and metastatic adenocarcinoma.

147 These findings demonstrate that retinoblastoma metastasis occurs at the early stage and

148 Thus, this orthotopic retinoblastoma model offers a new and unique opportunity

149 High-risk retinoblastoma occurred in 16% of (8/50) group D eyes an

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

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

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

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

154 ion capacity, possibly linked to a perturbed retinoblastoma pathway.

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

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

157 Retinoblastoma patients treated at a single center with

158 dard histopathologic criteria in identifying retinoblastoma patients who do not have high-risk histol

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

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

161 his directly promotes invasion by increasing retinoblastoma phosphorylation, E2F-dependent Cdc2 expre

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

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

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

165 Seventeen retinoblastoma primary tumors, 2 retinoblastoma cell lin

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

167 on through the cell cycle is associated with retinoblastoma protein (pRb) inactivation via sequential

168 Here, we present evidence that the retinoblastoma protein (pRB) utilizes a cell-cycle-indep

169 The retinoblastoma protein (pRb/p105) tumor suppressor plays

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

171 a significant decrease in phosphorylation of retinoblastoma protein (RB) at specific sites including

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

173 Inactivation of the retinoblastoma protein (RB) has a major role in the deve

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

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

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

177 ression of Src regulates the activity of the retinoblastoma protein and enhances the differentiation

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

179 and p21 resulted in hyperphosphorylation of retinoblastoma protein at serine 780 (p-RB(Ser-780)) fol

180 endent upon the interaction of HPV16 E7 with retinoblastoma protein family members.

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

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

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 and CDK4, and reduced phosphorylation of the retinoblastoma protein.

187 nduction of cyclin D1 and phosphorylation of retinoblastoma protein.

188 AECs promotes proliferation by inhibiting a retinoblastoma protein/c-Abl interaction leading to grea

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 uman cancers and murine models indicate that retinoblastoma (Rb) and p53 have critical tumor suppress

194 urvival rates for individuals diagnosed with retinoblastoma (RB) exceed 95% in the United States; how

195 E2Fs are negatively regulated by the retinoblastoma (RB) family of tumor suppressor proteins,

196 alyse the association between these SNPs and retinoblastoma (RB) in a Chinese Han population.

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

198 resistant EGFR mutant patients revealed that Retinoblastoma (RB) is lost in 100% of these SCLC transf

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

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

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

202 The retinoblastoma (Rb) protein exerts its tumor suppressor

203 ng multiple viral proteins that modulate the retinoblastoma (Rb) protein in a manner classically defi

204 Retinoblastoma (RB) protein inactivation during tumor pr

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

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

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

208 The retinoblastoma (RB) tumor suppressor and related family

209 The retinoblastoma (Rb) tumor suppressor controls cell cycle

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

211 The retinoblastoma (Rb) tumor suppressor is well established

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

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

214 The N-terminal domain of the retinoblastoma (Rb) tumor suppressor protein (RbN) harbo

215 The retinoblastoma (Rb) tumor suppressor restricts cell cycl

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

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

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

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

220 cant association between deregulation of the retinoblastoma (RB)-E2F pathway and the molecular subtyp

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

222 ound that simultaneous mutation of lin-35, a retinoblastoma (Rb)-related gene, and fzr-1, an ortholog

223 The DREAM (DP, Retinoblastoma [Rb]-like, E2F, and MuvB) complex control

224 ested that human papillomaviruses target the retinoblastoma (RB1) and TP53 tumor suppressor networks

225 via inhibition of tumor suppressors such as retinoblastoma (RB1) by mutated viral T antigens, but th

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

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

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

229 owing multimodality treatments in a national retinoblastoma referral center.

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

231 ies of 12 enucleated eyes (11 patients) with retinoblastoma refractory to intraophthalmic artery chem

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

233 s with the repressor-type E2F, E2FC, and the RETINOBLASTOMA RELATED proteins.

234 NT SEED (fis) mutants, but similar to lethal RETINOBLASTOMA-RELATED (rbr) mutants, no seed coat devel

235 The phosphorylation of plant retinoblastoma-related (RBR) proteins by cyclin-dependen

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

237 , and minichromosome maintenance) and of the retinoblastoma-related protein gene P. patens retinoblas

238 We report here that rice retinoblastoma-related protein-1 (OsRBR1) interacted wit

239 etinoblastoma-related protein gene P. patens retinoblastoma-related protein1.

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

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

242 %) for any, pineal, and nonpineal trilateral retinoblastoma, respectively, among patients with bilate

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

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

245 multiple injections are required to control retinoblastoma seeds.

246 Ten retinoblastomas served as controls and to determine the

247 ge London Institute of Ophthalmology and the Retinoblastoma Service, Royal London Hospital.

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

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

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

251 with a favorable tumor stage (International Retinoblastoma Staging System stage 0 or I).

252 2aN0M0H1, according to the 8th edition cTNMH Retinoblastoma Staging.

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

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

255 lights the genetic and epigenetic changes in retinoblastoma that have been reported, with special emp

256 osurgery (OAC) for patients with intraocular retinoblastoma that recurred after prior OAC.

257 For patients with bilateral retinoblastoma the unadjusted chance of developing trila

258 retrospective study of advanced intraocular retinoblastoma, there were more orbital recurrences in t

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

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

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

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

263 evelop proliferative vitreoretinopathy after retinoblastoma treatment.

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

265 The retinoblastoma tumor suppressor (pRb) protein associates

266 Mutations in the retinoblastoma tumor suppressor gene Rb are involved in

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

268 factors is the key downstream target of the retinoblastoma tumor suppressor protein (pRB), which is

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

270 The retinoblastoma tumor suppressor protein pRb restricts ce

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

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

273 eins, which is essential for blockade of the retinoblastoma tumor suppressor, is also important for a

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

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

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

277 enomic alterations to the p53 pathway during retinoblastoma tumorigenesis.

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

279 Recent whole-genome sequencing of retinoblastoma uncovered a tumor that had no coding-regi

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

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

282 6.2%) and the chance of nonpineal trilateral retinoblastoma was 0.8% (95% CI: 0.4%-1.3%).

283 3.3%-7.7%); the chance of pineal trilateral retinoblastoma was 4.2% (95% CI: 2.6%-6.2%) and the chan

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

285 Unilateral retinoblastoma was associated with parental insecticide

286 artery chemosurgery for advanced intraocular retinoblastoma was not found to increase the chance of o

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

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

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

290 Among hereditary retinoblastoma we found an adjusted trilateral retinobla

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

292 oma (Children's Oncology Group) group D or E retinoblastoma were included; 63 patients (63 eyes) were

293 000, through December 31, 2010, 830 cases of retinoblastoma were recorded for children aged 0 to 9 ye

294 tients who underwent primary enucleation for retinoblastoma were reviewed.

295 The 10 retinoblastomas were LIN28A and C19MC negative.

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

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

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

299 Controlling retinoblastoma with seeding is challenging despite advan

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