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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.
30 estoration of host tumor suppressors p53 and retinoblastoma 1 (RB1), which are targeted by E6 and E7,
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
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
39 have critical tumor suppressive functions in retinoblastoma, a tumor of neural origin, and neuroendoc
41 e unadjusted chance of developing trilateral retinoblastoma across all cohorts was 5.3% (95% confiden
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
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
67 nivariate analysis, presentation age, foveal retinoblastoma (at initial examination), use of TTT, and
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
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
85 illance in the absence of detectable MDM2 in retinoblastoma cells, bringing into question the importa
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
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
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
104 of the cell cycle, activates proteins in the retinoblastoma family, and subsequently increases the di
106 trabismus, and nystagmus outcomes in Group D retinoblastoma following multimodality treatments in a n
113 International Classification of Intraocular Retinoblastoma, group E tumor had a statistically signif
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
123 of Brg1 (Smarca4) in retinal development and retinoblastoma in mice using molecular and cellular appr
125 OAC group (5.2%) and more eyes with group E retinoblastoma in the enucleation group (87.3%) than in
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
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
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
146 for malignancy and included B-cell lymphoma, retinoblastoma, melanoma, and metastatic adenocarcinoma.
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
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
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
164 old female child without a family history of retinoblastoma presented with unilateral group C retinob
167 on through the cell cycle is associated with retinoblastoma protein (pRb) inactivation via sequential
171 a significant decrease in phosphorylation of retinoblastoma protein (RB) at specific sites including
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
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
184 reduced Ki67, c-Myc, and phosphorylation of retinoblastoma protein, suggesting inhibition of the G1-
188 AECs promotes proliferation by inhibiting a retinoblastoma protein/c-Abl interaction leading to grea
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
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
198 resistant EGFR mutant patients revealed that Retinoblastoma (RB) is lost in 100% of these SCLC transf
201 eas tumor cells with PTEN, PIK3CA, PIK3R1 or retinoblastoma (Rb) mutation are more resistant to this
203 ng multiple viral proteins that modulate the retinoblastoma (Rb) protein in a manner classically defi
212 sizer protein, CDKG1, that acts through the retinoblastoma (RB) tumor suppressor pathway as a D-cycl
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
222 ound that simultaneous mutation of lin-35, a retinoblastoma (Rb)-related gene, and fzr-1, an ortholog
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
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
234 NT SEED (fis) mutants, but similar to lethal RETINOBLASTOMA-RELATED (rbr) mutants, no seed coat devel
237 , and minichromosome maintenance) and of the retinoblastoma-related protein gene P. patens retinoblas
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
248 The choice of primary treatment for group D retinoblastoma should be carefully weighed, because acco
250 Activation of AMP-regulated protein kinase-retinoblastoma signaling is important in NSC proliferati
253 -long oncologic follow-up is crucial for all retinoblastoma survivors, and less detrimental eye-prese
255 lights the genetic and epigenetic changes in retinoblastoma that have been reported, with special emp
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
264 ose To assess the correlation of intraocular retinoblastoma tumor size measured with magnetic resonan
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
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
278 be the inhibition of phosphorylation of the retinoblastoma tumour suppressor, inducing G1 cell cycle
281 he efficacy and toxicity of treating class 3 retinoblastoma vitreous seeds with ophthalmic artery che
283 3.3%-7.7%); the chance of pineal trilateral retinoblastoma was 4.2% (95% CI: 2.6%-6.2%) and the chan
286 artery chemosurgery for advanced intraocular retinoblastoma was not found to increase the chance of o
288 essenger RNA for MD evaluation in metastatic retinoblastoma was previously reported, but no data in n
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
297 controlled study population of patients with retinoblastoma who had central pathologic review, our fi
300 e OCT sessions for fellow eyes of unilateral retinoblastoma without any suspicious lesion and those p
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