Bladder Cancer

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WHO-ICD-10 version:2010

Neoplasms

Malignant neoplasms

OMIM Number

109800

Gene Map Locus

4p16.3,11p15.5,12p12.1,13q14.2

Description

Bladder cancer accounts for approximately 90% of cancers of the urinary tract and the incidence increases with age. People over the age of 70 develop the disease, two to three times more often than those aged 55-69. Male: female ratio of bladder cancer is 3:1. The highest frequency of bladder cancer in the world is in Egypt due to the endemic schistosomiasis. Tumors that develop in the bladder are classified into low-stage (superficial) or high-stage (muscle invasive). Superficial tumors can be "shaved off" or they can be treated by chemotherapy. On the other hand, cystectomy or a combination of radiation and chemotherapy must be used in muscle invasive tumors.

Bladder cancer usually result from somatic mutations that develops in certain bladder cells. Fibroblast growth factor receptor 3 (FGFR3), V-Ha-Ras Harvey rat sarcoma viral (HRAS) oncogene homolog, retinoblastoma 1 (RB1), and tumor protein p53 (TP53) are the genes associated with bladder cancer. These genes play an important role in regulating the cell division cycle and preventing cells from dividing too rapidly or in an uncontrolled manner. The most common risk factors for developing genetic mutations are smoking and exposure to industrial chemicals. Family history of bladder cancer is another known risk factor, although bladder cancer is not inherited.

Epidemiology in the Arab World

View Map
Subject IDCountrySexFamily HistoryParental ConsanguinityHPO TermsVariantZygosityMode of InheritanceReferenceRemarks
109800.G.1LebanonNo Bladder neoplasm... CYP2E1*5B Allele NM_000773.3:c.[-1295G>C;-1055C>T], NAT1*14A, NAT1*14B, NAT1*10, NAT1*15, NAT1*3, NM_000903.2:c.559C>TYassine et al. 2012 54 cases with bladde...

Other Reports

Egypt

El- Rifai et al (2000) examined the DNA copy number changes in 38 Egyptians suffering from schistosoma-associated bladder cancer (SA-BC) and 16 Egyptians with non-schistosoma-associated bladder cancer (NSA-BC). Comparative genomic hybridization (CGH) experiments were done by extracting the DNA from frozen tissue sections or paraffin-embedded tissue sections.A negative control and a positive control were involved in each CGH experiment. Light microscope examination was used for classification and grading the tumor depending on WHO classification criteria of urinary bladder carcinomas. Most tumors were staged as pT2-pT4. Of the 38 SA-BC, 28 were squamous cell carcinoma (SA-SCC) and 10 were transitional cell carcinoma (SA-TCC). There were 22 detected tumors in SA-SCC and four detected tumors in SA-TCC. SA-BC showed more gains and loses of DNA copies (1.7:1) than NAS-BC and that referred to the chronic inflammation and irritation in the bladder caused by schistosomiasis that resulted in producing reactive oxygen species or urinary nitrosamines which caused chromosome instability. Gains and high- level amplifications at 11q13 were seen in 65% of SA-BC which might be related to the schistosomal status irrespective of the histological subtype. Gains and high-level amplifications at 5p were observed only in SA-SCC (21%) which could indicate the higher stage of SCC compared to TCC. Changing in other chromosomal regions was almost equal between SA-BC and NSA-BC indicating that they might be related to bladder tumors rather than to schistosomal status. Some changes were more prevalent in TCC than in SCC such as; gains at 1q21-q24 and 17q11-q22 and loses in 4q24-qter and 6q11-q21. Gains at 11q13 and loses in 13q were equally occurred among SA-BC and NSA-BC. The minimal common overlapping region in the studied tumors was 13q21, which suggested a possibility of an unidentified tumor suppressor gene in that region.

Qatar

Bener et al. (2008) retrospectively studied the Qatar National Cancer Registry to assess the trend in various cancer incidences in Qatar. Bladder cancer was diagnosed in 26 Qatari patients between 1991 and 1996, 34 Qataris between 1997 and 2001, and in 31 Qataris between 2002 and 2006.

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