User:Brandon westmoreland/sandbox

Bladder cancer has effected over 80,000 people this year and is the 4th most common type of cancer for men (“Bladder Cancer: Statistics”). This disease has been seen, in correlation with the increasing FGFR3 production, but why it affects carcinogenesis is not well understood (Cao, et al.). Bladder cancer is usually a somatic mutation, but is only considered a somatic mutation when the cancer is found only in the bladder cells (FGFR3 Gene). Patients with mutations that led to increased productions of FGFR3, had much higher risk for developing bladder cancer, than someone who developed another type of mutation (Kang, et al.). When observing the mutations at exon 9 for FGFR3 these people did not show signs of cancer development, although patients with t1 bladder cancer did show both, signs of other mutations and increased FGFR3 production (Kang, et al.). FGFR3 can do a lot in the body such as bone growth, cell division, and angiogenesis(FGFR3 Gene). Scientist theorize that the fact that FGFR3 plays a part in cell division, the overproduction of FGFR3 causes the cells to divide rapidly, unchecked (Cao, et al.). It is also theorized that the same thing is happening with angiogenesis, supplying the new tumor with the blood it needs to survive (Cao, et al.). The Department of Urinary Surgery, The Second Affiliated Hospital of Harbin Medical University in China, did an experiment to see the result of underproduction of FGFR3 and over production of FGFR3 (Cao, et al.). When the production was limited to how much FGFR3 by INF-α, a type I interferon inhibitor, there was reduced angiogenesis leading to reduced tumor production on the bladder wall (Cao, et al.). When the cells were given more than enough FGFR3, they increased blood flow with more blood vessels becoming present around the cancer (Cao, et al.). They also looked into the PPI (Proton Pump Inhibitor) drug network for FGFR3 to look for connections there, and concluded that around 4 other proteins can play a part in carcinogenesis those being CSTF2, POLA1,HMOX2, and EFNB2 (Cao, et al.). Patients with CSTF2 AND POLA1 have a lower risk of reoccurring bladder cancer, while HMOX2 and EFNB2 had a higher risk of reoccurring bladder cancer (Cao, et al.). These proteins have different functions throughout the body; CSTF2 has been linked with the formation of lung cancer; POLA1 helps with the formation of new DNA, by helping start DNA replication with DNA polymerase; HMOX2 is thought to help develop cervical lymph node metastasis on the tongue; and EFNB2 is known to cause cancer in the esophagus (Cao, et al.). This confirmed to the department, that the PPI drug system of FGFR3 was probably a part of the reason that someone would develop cancer in their bladder (Cao, et al.). There are multiple forms of bladder cancer, but most forms of this cancer having to do with FGFR3 involve Ta, T1, and T2, like pTaG1, pTaG2, pTaG3, pT1G2, pT1G3, pT2-4 CIS (Neuzillet, et al.). While the other forms of bladder cancer involve mostly with the mutation of the TP53 gene, although some tumors are found with traits of both mutations, this is much rarer to find (Neuzillet, et al.). The mutations can often be seen without having to look at the genetic code, because they usually stay within the same size and stage (Neuzillet, et al.). To combat some of the reoccurring cases of bladder cancer the Administration of Neoadjuvant Chemotherapy tested a procedure called the Neoadjuvant Chemotherapy (Yang, et al.). In the procedure they gave randomized bladder cancer patients 2- 4 rounds of chemotherapy before surgery on the cancer, and the results showed a 5-8 percent increase to the patients overall survival (Yang, et al.). Even with all the progress we have made researching this gene and disease, there is still not much we really know about how the gene fully plays a role in developing the cancer, but research is still currently being done. Works cited 1.	 “Bladder Cancer: Statistics” Cancer.Net, 20 Oct. 2017, www.cancer.net/cancer-types/bladder-cancer/statistics.

2.	Cao, Wei et al. “Exploring the FGFR3-related oncogenic mechanism in bladder cancer using bioinformatics strategy” World journal of surgical oncology vol. 15,1 66. 20 Mar. 2017, doi:10.1186/s12957-017-1125-4

3.	“FGFR3 Gene, Fibroblast Growth Factor Receptor 3.” U.S. National Library of Medicine, National Institutes of Health, 6 Nov. 2018, ghr.nlm.nih.gov/gene/FGFR3#normalfunction.

4.	Kang, Ho Won et al. “Expression levels of FGFR3 as a prognostic marker for the progression of primary pT1 bladder cancer and its association with mutation status” Oncology letters vol. 14,3 (2017): 3817-3824.

5.	Neuzillet Y, et al. (2012) A Meta-Analysis of the Relationship between FGFR3 and TP53 Mutations in Bladder Cancer. PLoS ONE 7(12): e48993. https://doi.org/10.1371/journal.pone.0048993

6.	Yang, Zhao, et al. “Somatic FGFR3 Mutations Distinguish a Subgroup of Muscle-Invasive Bladder Cancers with Response to Neoadjuvant Chemotherapy” Ebiomedicine vol. 35, 198-203 September 2018, doi: https://doi.org/10.1016/j.ebiom.2018.06.011

User:Brandon westmoreland/New Sandbox

There are a few ways you can get bladder cancer but one common way is by having a mutated FGFR3 gene that causes the over production of the FGFR3 protein.(plcking) Most forms of this cancer having to do with FGFR3 involve Ta, T1, and T2, like pTaG1, pTaG2, pTaG3, pT1G2, pT1G3, pT2-4 CIS (Neuzillet, et al.). While alot of the other forms of bladder cancer involve mostly with the mutation of the TP53 gene, although some tumors are found with traits of both mutations, this is much rarer to find (Neuzillet, et al.). Bladder cancer is usually a somatic mutation, but is only considered a somatic mutation when the cancer is found only in the bladder cells, but this gene does a lot more in the body such as bone growth, cell division, and angiogenesis(FGFR3 Gene).Scientist theorize that the fact that FGFR3 plays a part in cell division, the overproduction of FGFR3 causes the cells to divide rapidly, unchecked, because when the production of FGFR3 was limmited by INF-α, a type I interferon inhibitor, there was reduced angiogenesis leading to reduced tumor production on the bladder wall (Cao, et al.). When the cells were given more than enough FGFR3, they increased blood flow with more blood vessels becoming present around the cancer (Cao, et al.). When looking into the PPI scientist saw around 4 other proteins that can play a part in carcinogenesis those being CSTF2, POLA1,HMOX2, and EFNB2 (Cao, et al.). Patients with CSTF2 AND POLA1 have a lower risk of reoccurring bladder cancer, while HMOX2 and EFNB2 had a higher risk of reoccurring bladder cancer (Cao, et al.).These proteins have different functions throughout the body; CSTF2 has been linked with the formation of lung cancer; POLA1 helps with the formation of new DNA, by helping start DNA replication with DNA polymerase; HMOX2 is thought to help develop cervical lymph node metastasis on the tongue; and EFNB2 is known to cause cancer in the esophagus (Cao, et al.).