Alterations of the retinoblastoma gene in human prostate adenocarcinoma

Tricoli, James V.; Gumerlock, Paul H.; Yao, Joyce; Chi, Sung–Gil; D’Souza, Sharon; Nestok, Blake R.; White, Ralph W. deVere

doi:10.1002/(sici)1098-2264(199602)15:2<108::aid-gcc5>3.0.co;2-7

Cited by 58 publications

(28 citation statements)

References 18 publications

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“…The strategy for our semi-quantitative RT-PCR was previously described (Chi et al, 1994;Tricoli et al, 1996). Briefly, 1 mg of RNA was converted to cDNA by reverse transcription using random hexamer primers and MoMuLV reverse transcriptase (Life Technologies Inc., Gaithersburg, MD, USA).…”

Section: Semi-quantitative Rt-and Genomic Pcr Analysismentioning

confidence: 99%

Promoter CpG hypermethylation and downregulation of XAF1 expression in human urogenital malignancies: implication for attenuated p53 response to apoptotic stresses

Chung

et al. 2006

Oncogene

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Section: Semi-quantitative Rt-and Genomic Pcr Analysismentioning

confidence: 99%

Promoter CpG hypermethylation and downregulation of XAF1 expression in human urogenital malignancies: implication for attenuated p53 response to apoptotic stresses

Chung

et al. 2006

Oncogene

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“…Between 17% and 60% of prostate cancers demonstrate loss of heterozygosity of the Rb locus (15,(17)(18)(19), and both reduced expression of Rb mRNA (18) and pRB protein have been reported (15,17). Although there has been no clear correlation between pRB loss and tumor stage or grade, several studies suggest that mutations in Rb can be early events in prostate cancer (5,15,20).…”

Section: Introductionmentioning

confidence: 99%

Conditional Deletion of Rb Causes Early Stage Prostate Cancer

Maddison

Sutherland

Barrios³

et al. 2004

Cancer Research

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Prostate cancer remains the second leading cause of cancer-related death for men in the United States. Mutations in tumor suppressor genes including retinoblastoma (Rb), p53, and PTEN have been linked to the development of prostate cancer in man and mouse models, and loss of heterozygosity of the Rb locus has been observed in up to 60% of clinical cases. In this study we demonstrate that conditional somatic deletion of even a single Rb allele in the epithelial cells of the mouse prostate causes focal hyperplasia, thereby establishing a causal relationship between Rb loss and development of early stage prostate cancer. As a consequence of Rb ablation we observed increased expression of E2F target genes and a concomitant increase in proliferation in the epithelial compartment. However, by 52 weeks of age these lesions had not become malignant and represent an early stage of the disease. Nevertheless, the multifocal nature of the phenotype in the mice closely resembled multifocality of clinical disease. Taken together, our data demonstrated that loss of pRB-mediated cell cycle control directly caused the initiation of proliferative prostate disease but was insufficient to cause malignancy. Establishment of this early initiation model will aid efforts to thoroughly characterize early prostate disease as well as the elucidation of molecular mechanisms that cooperate with Rb loss to facilitate progression and metastasis.

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“…Furthermore, immunostaining studies have revealed that the Rb1 expression is frequently decreased or absent in a signi®cant proportion of sporadic prostate cancers (Phillips et al, 1994). However, screening for somatic mutations in Rb1 have given negative results also in the studies where larger series of tumors have been examined (Kubota et al, 1995;Sarkar et al, 1992;Tricoli et al, 1996). On the other hand, in one study on families with hereditary breast cancer attributable to BRCA2, the male carriers have a 3.3-fold increased risk of developing prostate cancer as compared to non carriers (Wooster et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Identification of two distinct deleted regions on chromosome 13 in prostate cancer

Larsson

Futreal

et al. 1998

Oncogene

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Aberrations of 13q occur frequently in prostate cancer and this chromosome contains two known tumor suppressor genes, BRCA2 and Rb1. This study analysed 13q LOH, DNA ploidy, BRCA2 mutation and pRb expression in prostate cancers. In total, 13q deletions were found in 18 of 36 tumors but did not correlate with histological grade, stage or DNA ploidy. Two smallest regions of overlapping deletions were de®ned: one¯anked by D13S218 and D13S153; the other¯anked by D13S31 and D13S137. BRCA2 was less frequently deleted whereas Rb1 did have a high frequency of deletion. None of the two genes was located in any of these two regions. Furthermore, BRCA2 mutation was not found in the ®ve tumors where deletions had involved the BRCA2 locus. Neither did the Rb1 deletion correlate with absent pRb expression. In addition, tetraploidy was found in 14 out of 25 tumors analysed and correlated with aberrant pRb expression. Our results indicate that 13q deletion is an early non-random event. Tumor suppressor genes other than BRCA2 or Rb1 may be the target of 13q deletions. Aberrant pRb expression may not re¯ect the two-hit Rb1 inactivation but may be involved in the tetraploidization of prostate cancer cells.

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Alterations of the retinoblastoma gene in human prostate adenocarcinoma

Cited by 58 publications

References 18 publications

Promoter CpG hypermethylation and downregulation of XAF1 expression in human urogenital malignancies: implication for attenuated p53 response to apoptotic stresses

Promoter CpG hypermethylation and downregulation of XAF1 expression in human urogenital malignancies: implication for attenuated p53 response to apoptotic stresses

Conditional Deletion of Rb Causes Early Stage Prostate Cancer

Identification of two distinct deleted regions on chromosome 13 in prostate cancer

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