Deleted in bladder cancer protein 1 is a protein that in humans is encoded by the DBC1gene.[5][6][7][8][9]
This gene is located within chromosome 9 (9q32-33), a chromosomal region that frequently shows loss of heterozygosity in transitional cell carcinoma of the bladder. It contains a 5' CpG island that may be a frequent target of hypermethylation, and it may undergo hypermethylation-based silencing in some bladder cancers.[7]
The functions of this gene are unknown, and it has not yet been placed in a protein family or functional pathway. Nonetheless, it is suspected to act as a tumor suppressor gene.
^Nishiyama H, Hornigold N, Davies AM, Knowles MA (Nov 1999). "A sequence-ready 840-kb PAC contig spanning the candidate tumor suppressor locus DBC1 on human chromosome 9q32-q33". Genomics. 59 (3): 335–8. doi:10.1006/geno.1999.5891. PMID10444335.
^Nishiyama H, Hornigold N, Davies AM, Knowles MA (August 1999). "A sequence-ready 840-kb PAC contig spanning the candidate tumor suppressor locus DBC1 on human chromosome 9q32-q33". Genomics. 59 (3): 335–8. doi:10.1006/geno.1999.5891. PMID10444335.
Auffray C, Behar G, Bois F, et al. (1995). "[IMAGE: molecular integration of the analysis of the human genome and its expression]". Comptes Rendus de l'Académie des Sciences, Série III. 318 (2): 263–72. PMID7757816.
Habuchi T, Luscombe M, Elder PA, Knowles MA (1998). "Structure and methylation-based silencing of a gene (DBCCR1) within a candidate bladder cancer tumor suppressor region at 9q32-q33". Genomics. 48 (3): 277–88. doi:10.1006/geno.1997.5165. PMID9545632.
Wright KO, Messing EM, Reeder JE (2002). "Increased expression of the acid sphingomyelinase-like protein ASML3a in bladder tumors". J. Urol. 168 (6): 2645–9. doi:10.1016/s0022-5347(05)64236-x. PMID12442002.
Beetz C, Brodoehl S, Patt S, et al. (2005). "Low expression but infrequent genomic loss of the putative tumour suppressor DBCCR1 in astrocytoma". Oncol. Rep. 13 (2): 335–40. doi:10.3892/or.13.2.335 (inactive 1 November 2024). PMID15643521.{{cite journal}}: CS1 maint: DOI inactive as of November 2024 (link)