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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

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