Donate

Oncolink Features

Find My Cancer Drug

Cancer Types / Pediatric Cancers / Retinoblastoma / NCI Resources

NCI CANCERLIT^® Search: Retinoblastoma, Hereditary - September 2002

National Cancer Institute^®
Last Modified: September 1, 2002

Mutational analysis of the RB1 gene in Indian patients with retinoblastoma.
Rapid growth of retinoblastoma in a premature twin.
Use of hybridization kinetics for differentiating specific from non-specific binding to oligonucleotide microarrays.
p130 mediates TGF-beta-induced cell-cycle arrest in Rb mutant HT-3 cells.

Table of Contents

1
UI - 12187430
AU - Ata-ur-Rasheed M; Vemuganti G; Honavar S; Ahmed N; Hasnain S; Kannabiran
TI - C Mutational analysis of the RB1 gene in Indian patients with retinoblastoma.
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.

2
UI - 12215105
AU - Abramson DH; Schefler AC; Beaverson KL; Rollins IS; Ruddat MS; Kelly CJ
TI - Rapid growth of retinoblastoma in a premature twin.
SO - Arch Ophthalmol 2002 Sep;120(9):1232-3
AD - DHAMD@aol.com

3
UI - 12177314
AU - Dai H; Meyer M; Stepaniants S; Ziman M; Stoughton R
TI - 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.

4
UI - 12144826
AU - Choi HH; 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.

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.

OncoLink I wish u knew...

Marianna provides tips for people starting cancer treatments and talks about the cancer experience. Read more.

Cancer Types
Bone Cancer
Brain Tumors
Breast Cancer
Carcinoid Tumors
Endocrine System Cancers
Gastrointestinal Cancers
Gynecologic Cancers
Head and Neck Cancers
Leukemia
Lung Cancers
Lymphomas
Myelomas
Pediatric Cancers
Penile Cancer
Prostate Cancer
Sarcomas
Skin Cancers
Testicular Cancer
Thyroid Cancer
Urinary Tract Cancers
OncoLink Vet

Cancer Treatment
Biologic Therapy
Bone Marrow Transplants
Chemotherapy
Clinical Trials
Complementary Medicine
Gene Therapy
General Treatment Concerns
Hormone Therapy
PDT Center
Proton Therapy
Radiation Oncology
Surgical Oncology
Targeted Therapies
Vaccine Therapies

Cancer Support
Caregivers
Hospice Care and Bereavement
Nutrition and Cancer
Sexuality & Fertility
Side Effects
Support
Survivorship
Exercise and Cancer

Cancer Resources
Cancer News
OncoLink University
Nurses' Notes
Conferences
Newly Diagnosed Patients
Causes and Prevention
Legal and Financial Information for Patients
LGBT Resources
NCI Resources
Global Resources
Cancer Resource List
Resources for Young Adults

OncoLink Media Library
OncoLink TV
Book, Music and Video Reviews

Ask the Experts
Brown Bag Chat
Tracy's Corner

About OncoLink
About OncoLink
Giving to OncoLink
Contact Information
Usage Policy
Editorial Board
How to Partner with OncoLink
Link to OncoLink
Mission Statement