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NCI CANCERLIT® Search: Retinoblastoma - August 2002
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Ultima Vez Modificado: 1 de agosto del 2002
- Tumor suppressor gene p16 and Rb expression in gastric cardia precancerous lesions from subjects at a high incidence area in northern
- A prospective study of children treated for retinoblastoma: cognitive and visual outcomes in relation to treatment.
- Downregulation of the retinoblastoma gene expression in the progression of malignant melanoma.
- Proliferation-dependent expression and phosphorylation of pRB in B cell non-Hodgkin's lymphomas: dependence on RB1 copy number.
- Second nonocular tumors in survivors of heritable retinoblastoma and prior radiation therapy.
- The triad of bilateral retinoblastoma, dysplastic naevus syndrome and multiple cutaneous malignant melanomas: a case report and review of the
- [Molecular diagnosis of retinoblastoma. First experience in Russia]
- p130 mediates TGF-beta-induced cell-cycle arrest in Rb mutant HT-3 cells.
- Re-expression of hSNF5/INI1/BAF47 in pediatric tumor cells leads to G1 arrest associated with induction of p16ink4a and activation of RB.
Table of Contents
1
UI - 12046062
AU - Zhou Y; Gao SS; Li YX; Fan ZM; Zhao X; Qi YJ; Wei JP; Zou JX; Liu G;
TI -
Jiao LH; Bai YM; Wang LD
Tumor suppressor gene p16 and Rb expression in gastric cardia
precancerous lesions from subjects at a high incidence area in northern
China.
SO - World J Gastroenterol 2002 Jun;8(3):423-5
AD - Department of Oncology, the First Affiliated Hospital, Zhengzhou
University, Zhengzhou 450052, Henan Province China.
AIM:To further understand the molecular basis for gastric cardia
carcinogenesis and to provide etiological clues. METHODS: Endoscopic
mucosa biopsy and histopathological examinations were made on 37
subjects from a high incidence area for both esophageal and gastric
cardia carcinomas in northern China. All the biopsy samples were fixed
in 850 ml. (-1)L alcohol and embedded in paraffin. Each block contained
one piece of tissue and was serially section at 5 microm.
Immunohistochemistry (ABC) was carried out on these gastric cardia
samples to determine the alterations of p16 and Rb. RESULTS: Based on
the histopathlogical examination there were 11 cases of chronic
superficial gastritis, 12 cases of chronic atrophic gastritis and 14
cases of dysplasia. The immunostaining demonstrated different levels of
unclear immunostaining of p16 and Rb in normal gastric cardia tissue and
the tissues with different severity of lesions. With the lesions
progressing, the positive immunostaining rates for p16 protein had a
decreasing tendency. In contrast, the positive immunostaining rate for
Rb protein had an increasing tendency. There was a significant negative
relationship between the two parameters. Changes of p16 was CSG
11(100%), CAG 7(58%), DYS 4(29%) and changes of Rb was CSG 2(18%), CAG
8(67%) and DYS 12(86%), (P<0.05). CONCLUSION: The alterations of p16 and
Rb protein may play a role in the early stages of gastric cardia
carcinogenesis.
2
UI - 12059869
AU - Ek U; Seregard S; Jacobson L; Oskar K; Af Trampe E; Kock E
TI -
A prospective study of children treated for retinoblastoma: cognitive
and visual outcomes in relation to treatment.
SO - Acta Ophthalmol Scand 2002 Jun;80(3):294-9
AD - University of Stockholm, Stockholm, Sweden. ulla.ek@sit.se
PURPOSE: : To assess cognitive and visual outcomes in children treated
for retinoblastoma. PATIENTS AND METHODS: A population-based group of 22
children treated for retinoblastoma were followed in a longitudinal,
prospective study. Eleven children had unilateral tumours, all of which
had been enucleated. The remaining 11 had bilateral tumours. Seven of
these had undergone unilateral enucleation and local or external beam
radiation to the other eye. Four children had been treated with local or
external beam radiation only. Cognitive outcome and visual function was
assessed at 4 and 6 years of age. RESULTS: We found no general delay in
cognitive or motor development at 4 or 6 years of age. Better cognitive
capacities were found in the bilateral/irradiated retinoblastoma
patients than in unilateral/non-irradiated patients. However, two of the
irradiated children, both of whom had been treated at 1 month of age,
performed below group mean. None of the children was totally blind.
Three children were visually impaired due to tumours affecting the
macular area in the remaining eye; another three had subnormal visual
acuity but no macular pathology. A total of 14 children had been
enucleated and had normal vision in the remaining eye. Visual fields and
dark adaptation were adversely affected in a few cases, but colour
vision was normal in all. CONCLUSION: Bilateral retinoblastoma seems to
be associated with superior cognitive capacities. Few children were
visually impaired according to WHO criteria. We speculate that children
treated during the first months of life may be at risk of adverse
cognitive and visual outcomes. The immature brain may be affected by
radiation treatment, causing both cognitive and visual deviations.
3
UI - 12107345
AU - Korabiowska M; Ruschenburg I; Betke H; Stachura J; Schlott T; Cardo CC;
TI -
Brinck U
Downregulation of the retinoblastoma gene expression in the progression
of malignant melanoma.
SO - Pathobiology 2001;69(5):274-80
AD - Department of Cytopathology, Georg August University, Gottingen,
Germany.
The retinoblastoma gene is a cell cycle regulator preventing cells from
entering into S-phase. An altered expression of the retinoblastoma gene
has been reported in the majority of human malignancies. The main aim of
this study was to investigate retinoblastoma gene expression in the full
spectrum of melanoma progression from naevus to melanoma metastases by
applying immunohistochemistry and RT-PCR. All naevi with and without
dysplasia showed high expression of the retinoblastoma gene. In primary
melanomas, Rb-positive cells were found in 82 out of 106. Loss of
expression correlated with an increase in Clark level and shorter
survival rates. An independent prognostic role of the retinoblastoma
gene was confirmed by Cox multivariate analyses (p < 0.01). In melanoma
metastases, retinoblastoma gene expression (at the RNA level) was found
in 18 out of 26 melanoma lymphatic metastases, and in 2 out of 5 liver
metastases. Our results indicate a downregulation of the retinoblastoma
gene in the progression of melanocytic tumours. Copyright 2002 S. Karger
AG, Basel
4
UI - 12145697
AU - Galteland E; Smedshammer L; Suo Z; DeAngelis P; Stokke T
TI -
Proliferation-dependent expression and phosphorylation of pRB in B cell
non-Hodgkin's lymphomas: dependence on RB1 copy number.
SO - Leukemia 2002 Aug;16(8):1549-55
AD - Department of Biophysics, The Norwegian Radium Hospital, Oslo, Norway.
Some studies have suggested that a significant fraction of non-Hodgkin's
lymphomas (NHL) do not express pRB protein, possibly due to deletions of
RB1. We examined RB1/centromere 17 copy number by fluorescent in situ
hybridisation, and pRB expression/phosphorylation by
immunohistochemistry (IHC) and immunoblotting (IB) in 66 cases of B cell
NHL. Thirteen cases had lost one RB1 copy relative to centromere 17 copy
number and total DNA content. Case 458/88 had no RB1 copies. pRB levels
were heterogeneous as assessed by IB (0.04-1.12 relative units), but all
tumours, except for case 458/88, expressed pRB localised to the nucleus
in >75% of the tumour cells by IHC. The fraction of phosphorylated pRB
was correlated with pRB expression (r(2)= 0.56, P < 0.001). The 14 cases
with loss of RB1 had lower pRB expression (median 0.25) than those
without (median 0.48, P < 0.001), but a correlation with S phase
fraction (r(2) = 0.43, P < 0.001; previously published data for
tumour-specific S phase and apoptotic fractions) indicated that the
variation in pRB expression was due to differences in proliferative
activity. Furthermore, the regression lines for pRB expression vs S
phase fraction were not different for the cases with or without loss of
one RB1 copy (P = 0.5). Cases 154/88 (one RB1 copy) and 258/88 (two RB1
copies), in addition to case 458/88, had low expression of
(hypophosphorylated) pRB (0.04, 0.08 and 0.04), despite their high S
phase fractions (21%, 17% and 21%). There was no association between pRB
expression/RB1 copy number and apoptotic fraction. Neither pRB
expression nor loss of RB1 had prognostic value, but cases 154/88,
258/88, and 458/88 had short survival times (5, 3 and 46 months,
respectively) compared to the others (median survival: 44 months, P =
0.03). It is suggested that pRB expression and function are normal in 63
of 66 NHL cases, including 12 of 13 lymphomas with loss of one RB1
allele.
5
UI - 9727521
AU - Mohney BG; Robertson DM; Schomberg PJ; Hodge DO
TI -
Second nonocular tumors in survivors of heritable retinoblastoma and
prior radiation therapy.
SO - Am J Ophthalmol 1998 Aug;126(2):269-77
AD - Department of Surgery, East Tennessee State University, Johnson City
37614, USA.
PURPOSE: The principal objectives of this study were to estimate the
incidence of second tumors among children treated for heritable
retinoblastoma during a 50-year period and to investigate the
relationship between these tumors and previous radiation therapy.
METHODS: The records of all retinoblastoma patients examined at the Mayo
Clinic from 1941 through 1990 were retrospectively reviewed. The
therapeutic modality used to manage the tumor, the occurrence of any
second malignancy, and current follow-up on all patients were evaluated.
RESULTS: Eighty-two (46%) of 180 children with retinoblastoma had
bilateral tumors (76 patients) or unilateral disease and a positive
family history (six patients) and were followed for an average of 21.8
years (range, 1 month to 53 years). The Kaplan-Meier estimates of second
nonocular tumors among the 82 patients with heritable retinoblastoma
were 12% at 10 years, 16% at 25 years, and 30% at 40 years. Although 14
of the 15 patients who developed second malignancies had received
radiation therapy, only four of the malignancies occurred within the
field of irradiation. CONCLUSIONS: The relatively low incidence of
second tumors among long-term survivors of heritable retinoblastoma in
this series of patients occurred predominantly outside the field of
irradiation. The variable incidence of second nonocular malignancies in
previous reports may reflect variations in radiation technique and
dosage.
6
UI - 11930116
AU - Belt PJ; Smithers M; Elston T
TI -
The triad of bilateral retinoblastoma, dysplastic naevus syndrome and
multiple cutaneous malignant melanomas: a case report and review of the
literature.
SO - Melanoma Res 2002 Apr;12(2):179-82
AD - Department of Plastic and Reconstructive Surgery, University of
Queensland, Princess Alexandra Hospital, Brisbane, Queensland,
Australia. pbelt@plasticsurgery.org.au
We report a case of a patient with the triad of retinoblastoma,
dysplastic naevus syndrome (DNS) and multiple cutaneous melanomas. The
combination of retinoblastoma and DNS is a significant risk factor for
the development of cutaneous melanoma. This risk extends to family
members. We recommend that survivors of (inherited) retinoblastoma and
their relatives are closely screened for the presence of dysplastic
naevi.
7
UI - 11898356
AU - Babenko OV; Brovkina AF; Zaletaev DV; Kozlova VM; Saakian SV; Nemtsova
TI -
MV
[Molecular diagnosis of retinoblastoma. First experience in Russia]
SO - Vestn Oftalmol 2002 Jan-Feb;118(1):28-31
The first experience with molecular diagnosis of retinoblastoma (RB) in
Russia is presented. A protocol based on the use of up-to-date molecular
diagnostic methods helps detect structural and functional abnormalities
in RB1 gene, diagnose RB in disputable cases and at early stages of the
disease. Forty-five families with various forms of RB were examined.
Twenty-three mutations in various sites of RB1 gene were characterized.
Abnormal methylation in the promotor area of RB1 gene was detected in
20% cases and loss of heterozysity by intragene microsatellite markers
was detected in 70% cases. Hence, the causes of RB were detected in 80%
families, which led to early diagnosis in close relatives of patients
and helped evaluate the repeated risk of the tumor in families of
patients with RB.
8
UI - 12144826
AU - Ho Choi H; Jong HS; Hyun Song S; You Kim T; Kyeong Kim N; Bang YJ
TI -
p130 mediates TGF-beta-induced cell-cycle arrest in Rb mutant HT-3
cells.
SO - Gynecol Oncol 2002 Aug;86(2):184-9
AD - Cancer Research Center, Seoul National University College of Medicine,
Seoul, Republic of Korea.
OBJECTIVE: The retinoblastoma proteins include Rb and the functionally
and structurally related proteins p107 and p130. It has been reported
that HT-3 cells are sensitive to TGF-beta growth inhibition, despite the
Rb mutation. The purpose of this study was to elucidate the
growth-inhibitory mechanism of TGF-beta in Rb mutant HT-3 cells.
METHODS: Growth inhibition by TGF-beta in cervical carcinoma cell lines
was evaluated by counting cell numbers. Cell-cycle distribution was
determined by staining DNA with propidium iodide (PI) and measured using
a flow cytometer. The level of each protein expression was determined by
Western blot analysis. To evaluate the assembly of cdk2/p21, cdk2/cyclin
E, and E2F-4/p130 complexes by TGF-beta, immunoprecipitation was
performed. RESULTS: TGF-beta inhibited the proliferation of HT-3 cells
expressing mutant Rb protein and efficiently induced cell-cycle arrest
at G(1) phase. p21 protein level was elevated in TGF-beta-treated HT-3
cells, while other G(1) regulatory protein levels were unaltered.
TGF-beta markedly enhanced the binding of p21 with cdk2 but decreased
that of cdk2 with cyclin E and inhibited the phosphorylation of p130 but
did not change Rb and p107 protein status. We also found that E2F-1
protein level was lower in TGF-beta-treated cells and suggest that this
might be the result of enhanced binding between E2F-4 and p130.
CONCLUSIONS: Our results demonstrate that p130, instead of Rb, can
mediate growth inhibition by TGF-beta in Rb mutant HT-3 cells.
9
UI - 12149641
AU - Betz BL; Strobeck MW; Reisman DN; Knudsen ES; Weissman BE
TI -
Re-expression of hSNF5/INI1/BAF47 in pediatric tumor cells leads to G1
arrest associated with induction of p16ink4a and activation of RB.
SO - Oncogene 2002 Aug 8;21(34):5193-203
AD - Department of Pathology and Laboratory Medicine and The Lineberger
Comprehensive Cancer Center, University of North Carolina, Chapel Hill,
North Carolina, NC 27599, USA.
Truncating mutations and homozygous deletions in the hSNF5/INI1/BAF47
subunit of human SWI/SNF complexes occur in most malignant rhabdoid
tumors and some other malignancies. How loss of hSNF5 contributes to
tumorigenesis remains unknown. Because the SWI/SNF subunit BRG1 is
required for RB-mediated cell cycle arrest, we hypothesized that hSNF5
deficiency disrupts RB signaling. Here we demonstrate that unlike BRG1,
hSNF5 deficient cells retain functional RB since ectopic expression of
either p16ink4a or a constitutively active form of RB (PSM-RB) led to
cell cycle arrest. To determine how hSNF5 loss might contribute to
tumorigenesis, we used a retrovirus to introduce hSNF5 into multiple
deficient cell lines. In all cases, re-expression inhibited colony
formation and induced cell cycle arrest characterized by a flattened
morphology. Flow cytometry revealed that these cells accumulated in
G0/G1. Importantly, arrested cells exhibited strong induction of
p16ink4a, hypophosphorylated RB, and down-regulation of cyclin A,
suggesting that hSNF5 signals upstream of RB to induce growth arrest.
Co-expression of SV40 T/t abolished hSNF5-induced G1 arrest and
activation of RB. Likewise, HPV-16 E7 was sufficient to partially
overcome cell cycle arrest. These results suggest that hSNF5 loss is not
equivalent to BRG1/BRM loss in human tumor cell lines. Furthermore,
hSNF5-induced cell cycle arrest of deficient cells is mediated in part
through activation of p16ink4a expression. These findings provide
insight into mechanisms of hSNF5-mediated tumor suppression.
The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.
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