The retinoblastoma sensitivity protein (Rb) and the p53 gene product both appear to function as negative regulators of cell division or abnormal cellular growth in some differentiated cell types.
Two prostate carcinoma cell lines, DU-145 and PC-3, were examined for abnormalities in the retinoblastoma (Rb) and the p53 putative tumor suppressor genes.
Data concerning mutations of protooncogenes (H-, K-, and N-RAS) and tumor suppressor genes (retinoblastoma and p53 genes) in various common cancers are providing evidence of multiple genetic lesions that occur during the multistage process of carcinogenesis.
If both RB1 and TP53 are involved in the initiation of osteosarcoma, the mechanisms for development of the retinoblastoma and osteosarcoma tumors are different.
Classical examples are the Rb-1 gene associated with the development of retinoblastoma and the p53 gene, which is associated with a wider range of neoplasms, including breast cancer.
This element overlaps the basal transcription unit of the Rb promoter, suggesting that p53 suppresses Rb transcription through inhibition of the basal promoter activity.
LOH affecting p53 was observed in 8 of 17 (47%) of heterozygous patients, while LOH of Rb and the mcc/apc locus was observed in 9 of 27 (33%) and 13 of 39 (33%) of heterozygotes, respectively.
In addition, we studied the c-myc gene for rearrangements by Southern blotting and assessed expression of the retinoblastoma (Rb) and p53 genes by immunostaining.
Human malignant gliomas (glioblastomas and anaplastic astrocytomas) are the most frequent brain tumors and are associated with a variety of genetic alterations including retinoblastoma (RB) and p53 gene mutations, loss of interferon alpha and beta (IFNA, IFNB) genes and lack of O6-methylguanine-DNA methyltransferase (MGMT) expression.
The discovery of the tumor suppressor genes, for which loss of function mutations are oncogenic as in the RB gene of the retinoblastoma and p53 gene, has introduced a new concept of oncogenesis which could be useful even in the cure of the neoplasms.
The HPV oncoproteins E6 and E7 are though to play a crucial role in this process by their interactions with the p53 protein and the retinoblastoma susceptibility gene product, respectively.
Two tumor suppressor genes, the retinoblastoma susceptibility gene (RB) and the gene encoding the p53 protein, are frequently found to be deleted or mutated in breast cancer cell lines and primary tumor samples.
Molecular analysis of a metastatic lesion of an atypical carcinoid tumor of the lung obtained from a 77-year-old man at autopsy revealed a point mutation in the p53 gene and a deletion in the retinoblastoma (Rb) mRNA.
Effect of sodium butyrate on the expression of retinoblastoma (RB1) and P53 gene and phosphorylation of retinoblastoma protein in human colon tumor cell line HT29.
The current study on endometrioid carcinoma was undertaken to examine the status of two tumor suppressor genes that frequently have been found to be altered in human malignancies (the p53 gene and the retinoblastoma [Rb] gene) and to examine the status of the candidate metastatic suppressor gene, nm23-H1.
BON cells also exhibited increased expression of c-myc and cdc2 kinase mRNA and protein; TGF-beta 1, p53 and retinoblastoma (RB) mRNA and protein levels were decreased.
These data seem to suggest that whereas mutant type of p53 and retinoblastoma susceptibility genes may exhibit "oncogenic" function in many human tumors, mutational inactivation of these genes may not be an important feature in the carcinogenic development of human papillomavirus-negative small cell cervical carcinomas.