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Renal Cell Carcinoma


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Renal Cell Carcinoma

Renal cell carcinoma (RCC) accounts for 2–3% of all malignant diseases in adults. It is the seventh most common cancer in men and the ninth most common in women. RCC originates from the tubular structures of the kidney and is classified into four major histological cell types. Clear cell (cc) is the most common type, accounting for around 75–80% of all cases of RCC. Other types are papillary (10–15%), chromophobe (5%) and collecting duct (1%) RCC. About 4% of RCCs are hereditary and 96% sporadic. In fact, all familial cases of ccRCC are due to inherited mutation in the von Hippel-Lindau (VHL) tumor suppressor gene. Moreover, in at least two-thirds of sporadic cases of ccRCC, the VHL gene is inactivated either by point mutation, deletion or promoter hypermethylation.

An activating point mutation in the tyrosine kinase domain of the c-MET proto-oncogene is responsible for one form of hereditary papillary RCC. Point mutation of MET is found in only 5–13% of sporadic papillary RCCs. A second and rare form of hereditary papillary RCC arises from inactivating mutations of the Krebs cycle enzyme fumarate hydratase (FH) tumor suppressor gene. There is no evidence of mutation of FH in sporadic papillary RCC. While chromophobe RCC is seen in patients with the hereditary Birt-Hogg-Dube (BHD) syndrome, the BHD tumor suppressor gene is rarely mutated in sporadic chromophobe RCC. The rare collecting duct RCC arises from the distal portion of the nephron and is usually of high grade and very aggressive. No genes have been shown to be mutated in collecting duct RCC but deletions of chromosomes 1q, 8p and 13q have been reported. Because the inherited RCC genes VHL, FH (fumarate hydratase), MET (met proto-oncogene), FLCN (folliculin), SDH (succinate dehydrogenase) and also the TSC1 and 2 (tuberous sclerosis complex) genes are all involved in metabolic pathways related to oxygen, iron, energy and nutrient sensing, Linehan et al. have described RCC as a metabolic disease.

Cancer is invariably accompanied by changes in signal transduction. Alterations in proto-oncogenes and tumor suppressor genes result in dysregulated signal transduction that underlies the abnormal growth and proliferation of cancer cells. In some cases, tumor-associated mutations specifically target genes coding for critical signaling proteins. Alternatively, signaling proteins that are centrally located in important cancer-associated signaling networks can serve as therapeutic targets, even though their function is not specifically altered as part of the disease etiology. An increased understanding of the underlying molecular biology of RCC has established the VEGF and mammalian target of rapamycin (mTOR) pathways as relevant therapeutic targets. These drugs act by blocking critical signaling pathways associated with RCC tumor growth and survival and angiogenesis. Beyond well-validated signaling targets such as VEGFR, VHL, and mTOR, additional pathways including Wnt/β-catenin and HGF/c-MET have emerged as important to RCC pathogenesis.

The premise of targeted therapy in oncology is the fundamental reliance of tumor cells on biological pathways to which drugs inhibiting those pathways can be applied. Creative Biogene, as a leading biotechnology company, is able to offer various renal cell carcinoma pathway related products including stable cell lines, viral particles and clones for your drug discovery projects.

References:

  1. Daniel S, et al. Molecular pathways in renal cell carcinoma: recent advances in genetics and molecular biology. Current Opinion in Oncology, 2015, 27(3):217-23.
  2. Banumathy G, Cairns P. Signaling pathways in renal cell carcinoma. Cancer Biology & Therapy, 2010, 10(7):658-664.
  3. The PI3K/AKT Pathway and Renal Cell Carcinoma. Journal of Genetics and Genomics, 2015, 42(7):343-353.
  4. Renal Cell Carcinoma. Lancet, 2009, 36:3252.

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