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Cancer Types / Pediatric Cancers / Retinoblastoma / NCI Resources

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

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

Expression of the retinoblastoma-related p107 and Rb2/p130 genes in human placenta: an immunohistochemical study.

Risk factors for metastasis in retinoblastoma.

Genomic amplification in retinoblastoma narrowed to 0.6 megabase on chromosome 6p containing a kinesin-like gene, RBKIN.

Table of Contents

1
UI - 11642725
AU - Cavallotti I; De Luca L; D'Aponte A; De Falco M; Acanfora F; Visciano
TI - ML; Gualdiero L; De Luca B; Baldi A; De Luca A Expression of the retinoblastoma-related p107 and Rb2/p130 genes in human placenta: an immunohistochemical study.
SO - Histol Histopathol 2001 Oct;16(4):1057-60
AD - Institute of Topographical Anatomy, School of Medicine, Second University of Naples, Italy.
It has been proposed that tumor suppressor genes may have a role in the mechanisms of proliferation and differentiation during human placental development. The Retinoblastoma gene family is a well known family of tumor suppressor genes. Many studies have pointed out a role of this family not only in cell cycle progression, but also during development and differentiation. On the light of these observations we have investigated the immunohistochemical expression pattern of the Retinoblastoma family members, p107 and Rb2/p130 in human placenta samples in first trimester and full-term placental sections. p107 and pRb2/p130 showed the most abundant expression levels during the first trimester of gestation and progressively declined to being barely detectable in the placenta by late gestation. These results indicate that the expression of the above genes is modulated during placental development and suggest a mechanism for controlling trophoblast proliferation.

2
UI - 11801265
AU - Finger PT; Harbour JW; Karcioglu ZA
TI - Risk factors for metastasis in retinoblastoma.
SO - Surv Ophthalmol 2002 Jan-Feb;47(1):1-16
AD - The New York Eye Cancer Center, New York, NY, USA.
Children with retinoblastoma typically survive their cancer due to advances in early diagnosis and treatment. Despite this success, risk factors persist for metastasis that are thought to be related to patient age, sex, laterality, treatment, genetics, histopathology, and extraocular extension. This review has found that invasion of the uvea, orbit, and optic nerve continue to be the most important predictors of metastatic retinoblastoma. Bilaterality and delays in diagnosis are also important factors. We examine molecular and genetic studies that offer the potential of predicting which tumors are likely to metastasize, which will recur within the eye, and which will undergo senescence. In this review, we describe which clinical evaluations, genetic studies, and histopathologic evaluations of retrieved specimens are currently used widely. This review has been performed to help those caring for patients with retinoblastoma and to aid informed consent.

3
UI - 11861365
AU - Chen D; Pajovic S; Duckett A; Brown VD; Squire JA; Gallie BL
TI - Genomic amplification in retinoblastoma narrowed to 0.6 megabase on chromosome 6p containing a kinesin-like gene, RBKIN.
SO - Cancer Res 2002 Feb 15;62(4):967-71
AD - Division of Cancer Informatics, Ontario Cancer Institute/Princess Margaret Hospital, University Health Network, Toronto, M5G 2M9 Canada.
All retinoblastomas (RBs) show genomic changes in addition to loss of both RB1 alleles. Quantitative-multiplex PCR analysis identified in 41 of 70 (59%) RBs a 0.6-Mb minimal region of chromosome 6p22 gain from which we cloned the human kinesin gene, RBKIN/KIF13A, by rapid amplification of retinal cDNA. RBKIN is expressed ubiquitously in adult tissues, at low levels in fetal tissues, and at high levels in RB. Antisense RBKIN oligonucleotide reduced the growth rate of RB cell lines. RBKIN and/or another closely linked gene are candidate oncogenes contributing to malignant progression of RB.

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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