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==Overview==
==Overview==
==Pathophysiology==
Genes involved in the pathogenesis of bladder cancer include [[HRAS]] mutation
===Genetics===
* [[Retinoblastoma protein|Rb1]] mutation
Like virtually all cancers, bladder cancer development involves the acquisition of mutations in various [[oncogene]]s and [[tumor supressor gene]]s. Genes which may be altered in bladder cancer include [[H19 (gene)|H19]], [[FGFR3]], [[HRAS]], [[RB1]] and [[TP53]]. Several genes have been identified which play a role in regulating the cycle of cell division, preventing cells from dividing too rapidly or in an uncontrolled way. Alterations in these genes may help explain why some bladder cancers grow and spread more rapidly than others.
* [[PTEN]]/MMAC1 mutation
* NAT2 slow acetylator phenotype
* GSTM1 null phenotype
 
==Pathogenesis==
* Under normal conditions, the bladder, the lower part of the kidneys (the renal pelvises), the ureters, and the proximal urethra are lined with a specialized mucous membrane referred to as transitional epithelium (also called urothelium).
* Most cancers that form in the bladder, the renal pelvises, the ureters, and the proximal urethra are transitional cell carcinomas (also called urothelial carcinomas) that derive from transitional epithelium.
 
==Genetics==
Genetic mutations:
* [[HRAS]] mutation
* [[Retinoblastoma protein|Rb1]] mutation
* [[PTEN]]/MMAC1 mutation
* NAT2 slow acetylator phenotype
* GSTM1 null phenotype
 
==Gross Pathology==
Transitional cell carcinomas have 2 main growth patterns. Papillary urothelial carcinomas have slim finger-like projections that grow from the lining of the bladder into the bladder cavity. Flat urothelial carcinomas lay flat in the lining of the bladder. They grow deeper into the layers of the bladder wall rather than into the bladder cavity.
 
==Microscopic Pathology==


A family history of bladder cancer is also a risk factor for the disease. Many cancer experts assert that some people appear to inherit reduced ability to break down certain chemicals, which makes them more sensitive to the cancer-causing effects of tobacco smoke and certain industrial chemicals.


==References==
==References==

Revision as of 18:28, 1 October 2015

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Steven C. Campbell, M.D., Ph.D.

Overview

Genes involved in the pathogenesis of bladder cancer include HRAS mutation

  • Rb1 mutation
  • PTEN/MMAC1 mutation
  • NAT2 slow acetylator phenotype
  • GSTM1 null phenotype

Pathogenesis

  • Under normal conditions, the bladder, the lower part of the kidneys (the renal pelvises), the ureters, and the proximal urethra are lined with a specialized mucous membrane referred to as transitional epithelium (also called urothelium).
  • Most cancers that form in the bladder, the renal pelvises, the ureters, and the proximal urethra are transitional cell carcinomas (also called urothelial carcinomas) that derive from transitional epithelium.

Genetics

Genetic mutations:

  • HRAS mutation
  • Rb1 mutation
  • PTEN/MMAC1 mutation
  • NAT2 slow acetylator phenotype
  • GSTM1 null phenotype

Gross Pathology

Transitional cell carcinomas have 2 main growth patterns. Papillary urothelial carcinomas have slim finger-like projections that grow from the lining of the bladder into the bladder cavity. Flat urothelial carcinomas lay flat in the lining of the bladder. They grow deeper into the layers of the bladder wall rather than into the bladder cavity.

Microscopic Pathology

References

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