Renal cell carcinoma pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===Genetics=== | ===Genetics=== | ||
Recent genetic studies have altered the approaches | Recent genetic studies have altered the approaches of understanding renal cell carcinoma. <ref name="pmid10768592">{{cite journal |author=Reuter VE, Presti JC |title=Contemporary approach to the classification of renal epithelial tumors |journal=Semin. Oncol. |volume=27 |issue=2 |pages=124–37 |year=2000 |month=April |pmid=10768592 |doi= |url=}}</ref><ref name="pmid12351585">{{cite journal |author=Bodmer D, van den Hurk W, van Groningen JJ, ''et al'' |title=Understanding familial and non-familial renal cell cancer |journal=Hum. Mol. Genet. |volume=11 |issue=20 |pages=2489–98 |year=2002 |month=October |pmid=12351585 |doi= |url=http://hmg.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=12351585}}</ref><ref name="isbn0-7216-0187-1">{{cite book |author=Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. |title=Robbins and Cotran pathologic basis of disease |publisher=Elsevier Saunders |location=St. Louis, Mo |year=2005 |pages=1016 |isbn=0-7216-0187-1 |oclc= |doi= |accessdate=}}</ref> | ||
* | * [[Von Hippel-Lindau tumor suppressor|VHL]] and others on [[chromosome 3]] - [[Clear cell carcinoma]] | ||
* [[C-Met|MET]], [[PRCC (gene)|PRCC]] - [[Papillary]] carcinoma | |||
* Other associated genes include TRC8, OGG1, [[HNF1A]], [[HNF1B]], [[TFE3]], RCCP3, and RCC17. | |||
* | |||
Other associated genes include TRC8, OGG1, [[HNF1A]], [[HNF1B]], [[TFE3]], RCCP3, and RCC17. | |||
===Pathology=== | ===Pathology=== | ||
Revision as of 20:05, 27 August 2012
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
Renal cell carcinoma is the most common form of kidney cancer arising from the renal tubule. It is the most common type of kidney cancer in adults. Initial treatment is surgery. It is notoriously resistant to radiation therapy and chemotherapy, although some cases respond to immunotherapy. The advent of targeted cancer therapies such as sunitinib has vastly improved the outlook for treatment of RCC.
Pathophysiology
Genetics
Recent genetic studies have altered the approaches of understanding renal cell carcinoma. [1][2][3]
- VHL and others on chromosome 3 - Clear cell carcinoma
- MET, PRCC - Papillary carcinoma
- Other associated genes include TRC8, OGG1, HNF1A, HNF1B, TFE3, RCCP3, and RCC17.
Pathology
Gross examination shows a hypervascular lesion in the renal cortex, which is frequently multilobulated, yellow (because of the lipid accumulation) and calcified.
Light microscopy shows tumor cells forming cords, papillae, tubules or nests, and are atypical, polygonal and large. Because these cells accumulate glycogen and lipids, their cytoplasm appear "clear", lipid-laden, the nuclei remain in the middle of the cells, and the cellular membrane is evident. Some cells may be smaller, with eosinophilic cytoplasm, resembling normal tubular cells. The stroma is reduced, but well vascularized. The tumor grows in large front, compressing the surrounding parenchyma, producing a pseudocapsule.[4]
Secretion of vasoactive substances (e.g. renin) may cause arterial hypertension, and release of erythropoietin may cause polycythemia (increased production of red blood cells).
References
- ↑ Reuter VE, Presti JC (2000). "Contemporary approach to the classification of renal epithelial tumors". Semin. Oncol. 27 (2): 124–37. PMID 10768592. Unknown parameter
|month=ignored (help) - ↑ Bodmer D, van den Hurk W, van Groningen JJ; et al. (2002). "Understanding familial and non-familial renal cell cancer". Hum. Mol. Genet. 11 (20): 2489–98. PMID 12351585. Unknown parameter
|month=ignored (help) - ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease. St. Louis, Mo: Elsevier Saunders. p. 1016. ISBN 0-7216-0187-1.
- ↑ http://www.pathologyatlas.ro/Renal%20Clear%20Cell%20Carcinoma.html