UI - 12187430
AU - Ata-ur-Rasheed M; Vemuganti G; Honavar S; Ahmed N; Hasnain S; Kannabiran
Mutational analysis of the RB1 gene in Indian patients with
SO - Ophthalmic Genet 2002 Jun;23(2):121-8
AD - L.V. Prasad Eye Institute, L.V. Prasad Marg, Banjara Hills, Hyderabad,
Andhra Pradesh, India.
Twenty-one probands, twelve with bilateral and nine with unilateral
retinoblastoma, were screened for mutations in the RB1 gene using
genomic DNA from peripheral blood leukocytes as well as tumors.
Amplification of individual exons and flanking regions of the RB1 gene
were carried out, followed by direct sequencing of the amplified
products. Sequences of affected individuals were compared with those of
controls. Mutations were identified in seven patients, five with
bilateral and two with unilateral retinoblastoma. Six out of seven
mutations involved the formation of premature termination codons by
means of single base substitutions (2), frameshifts due to splice-site
mutations (2), or deletion and duplication (2). One missense mutation
was identified. Of the remaining fourteen patients, seven with bilateral
disease had no mutations in peripheral blood (7 cases) or tumors (3/7
cases). Analysis of the peripheral blood of seven patients with
unilateral disease also showed no mutations. Mutations were detected in
about one-third of the cases, suggesting that hemizygous deletions at
the RB1 locus or mutations outside the coding regions of RB1 may be
responsible for the disease in the remaining patients.
UI - 12215105
AU - Abramson DH; Schefler AC; Beaverson KL; Rollins IS; Ruddat MS; Kelly CJ
Rapid growth of retinoblastoma in a premature twin.
SO - Arch Ophthalmol 2002 Sep;120(9):1232-3
AD - DHAMD@aol.com
UI - 12177314
AU - Dai H; Meyer M; Stepaniants S; Ziman M; Stoughton R
Use of hybridization kinetics for differentiating specific from
non-specific binding to oligonucleotide microarrays.
SO - Nucleic Acids Res 2002 Aug 15;30(16):e86
AD - Rosetta Inpharmatics, 12040 115th Avenue NE, Kirkland, WA 98034, USA.
Hybridization kinetics were found to be significantly different for
specific and non-specific binding of labeled cRNA to surface-bound
oligonucleotides on microarrays. We show direct evidence that in a
complex sample specific binding takes longer to reach hybridization
equilibrium than the non- specific binding. We find that this property
can be used to estimate and to correct for the hybridization contributed
by non-specific binding. Useful applications are illustrated including
the selection of superior oligonucleotides, and the reduction of false
positives in exon identification.
UI - 12144826
AU - Choi HH; Jong HS; Hyun Song S; You Kim T; Kyeong Kim N; Bang YJ
p130 mediates TGF-beta-induced cell-cycle arrest in Rb mutant HT-3
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.
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