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10.1002/cam4.1010 http://scihub22266oqcxt.onion/10.1002/cam4.1010 C5345671!5345671!28211617     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Med 2017 ; 6 (3): 619-30 Nephropedia Template TP {{tp|p=28211617|t=2017. Phosphorylation of pRb: mechanism for RB pathway inactivation in MYCN?amplified retinoblastoma |pdf=|usr=}}{{28211617}} gab.com Text Phosphorylation of pRb: mechanism for RB pathway inactivation in MYCN amplified retinoblastoma JO: Cancer Med http://www.kidney.de/pget.php?&tw=1&pmid=28211617 #FOAvip A small, but unique subgroup of retinoblastoma has been identified with no detectable mutation in the retinoblastoma gene (RB1) and with high levels of MYCN gene amplification. This manuscript investigated alternate pathways of inactivating pRb, the encoded protein in these tumors. We analyzed the mutation status of the RB1 gene and MYCN copy number in a series of 245 unilateral retinoblastomas, and the phosphorylation status of pRb in a subset of five tumors using immunohistochemistry. There were 203 tumors with two mutations in RB1 (RB1?/?, 83%), 29 with one (RB1+/?, 12%) and 13 with no detectable mutations (RB1+/+, 5%). Eighteen tumors carried MYCN amplification between 29 and 110 copies: 12 had two (RB1?/?) or one RB1 (RB1+/?) mutations, while six had no mutations (RB1+/+). Immunohistochemical staining of tumor sections with antibodies against pRb and phosphorylated Rb (ppRb) displayed high levels of pRb and ppRb in both RB1+/+ and RB1+/? tumors with MYCN amplification compared to no expression of these proteins in a classic RB1?/?, MYCN?low tumor. These results establish that high MYCN amplification can be present in retinoblastoma with or without coding sequence mutations in the RB1 gene. The functional state of pRb is inferred to be inactive due to phosphorylation of pRb in the MYCN?amplified retinoblastoma without coding sequence mutations. This makes inactivation of RB1 by gene mutation or its protein product, pRb, by protein phosphorylation, a necessary condition for initiating retinoblastoma tumorigenesis, independent of MYCN amplification. Twit Text FOAVip Phosphorylation of pRb: mechanism for RB pathway inactivation in MYCN amplified retinoblastoma ????Cancer Med http://www.kidney.de/pget.php?&tw=1&pmid=28211617 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28211617 #FOAvip English Wikipedia <ref>{{Cite pmid|28211617}}</ref> Phosphorylation of pRb: mechanism for RB pathway inactivation in MYCN?amplified retinoblastoma #MMPMID28211617 Ewens KG; Bhatti TR; Moran KA; Richards?Yutz J; Shields CL; Eagle RC; Ganguly A Cancer Med 2017[Mar]; 6 (3): 619-30 PMID28211617show ga A small, but unique subgroup of retinoblastoma has been identified with no detectable mutation in the retinoblastoma gene (RB1) and with high levels of MYCN gene amplification. This manuscript investigated alternate pathways of inactivating pRb, the encoded protein in these tumors. We analyzed the mutation status of the RB1 gene and MYCN copy number in a series of 245 unilateral retinoblastomas, and the phosphorylation status of pRb in a subset of five tumors using immunohistochemistry. There were 203 tumors with two mutations in RB1 (RB1?/?, 83%), 29 with one (RB1+/?, 12%) and 13 with no detectable mutations (RB1+/+, 5%). Eighteen tumors carried MYCN amplification between 29 and 110 copies: 12 had two (RB1?/?) or one RB1 (RB1+/?) mutations, while six had no mutations (RB1+/+). Immunohistochemical staining of tumor sections with antibodies against pRb and phosphorylated Rb (ppRb) displayed high levels of pRb and ppRb in both RB1+/+ and RB1+/? tumors with MYCN amplification compared to no expression of these proteins in a classic RB1?/?, MYCN?low tumor. These results establish that high MYCN amplification can be present in retinoblastoma with or without coding sequence mutations in the RB1 gene. The functional state of pRb is inferred to be inactive due to phosphorylation of pRb in the MYCN?amplified retinoblastoma without coding sequence mutations. This makes inactivation of RB1 by gene mutation or its protein product, pRb, by protein phosphorylation, a necessary condition for initiating retinoblastoma tumorigenesis, independent of MYCN amplification. äPhosphorylation of pRb: mechanism for RB pathway inactivation in MYCN?(epmc).pdf DeepDyve Pubget Overpricing