Pubmed abstracts for Protein-Protein Interaction search result :

Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Frequent co alterations of TP 53 , p16 / CDKN2A , p14ARF , PTEN tumor suppressor genes in human glioma cell lines . ^^^ In this study we established the simultaneous status of TP 53 , p 16 , p14ARF and PTEN tumor suppressor genes in 34 randomly chosen human glioma cell lines . ^^^ Mutations / deletions were found at the following frequencies : TP 53 ( 76 . 5 % ) , p14ARF ( 64 . 7 % ) , p 16 ( 64 . 7 % ) , PTEN ( 73 . 5 % ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Recent evidence has shown that P14ARF binds to MDM 2 leading to an increased availability of wild type TP 53 protein . ^^^ Assuming that 9p deletion occurs first , the common occurrence of p 53 and p14ARF alterations suggests that p14ARF inactivation is not functionally equivalent to abrogation of the TP 53 pathway by p 53 mutation . . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Seventy six percent of GBs ( 103 of 136 ) , 72 % of AAs ( 28 of 39 ) , and 67 % of As ( 10 of 15 ) had deregulated p 53 pathway either by mutation of TP 53 , amplification of MDM 2 , or homozygous deletion / mutation of p14ARF . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Analysis of the p16INK4 , p14ARF , p 15 , TP 53 , and MDM 2 genes and their prognostic implications in osteosarcoma and Ewing sarcoma . ^^^ We examined alterations of the p16INK4 , p14ARF , p 15 , TP 53 , and MDM 2 genes in 30 osteosarcomas and 24 Ewing sarcomas . ^^^ While TP 53 abnormalities were far more frequent in osteosarcoma than in Ewing sarcoma , alterations of p16INK4 , p14ARF , and p 15 were present at similar frequencies in the two types of sarcoma . ^^^ The event free survival ( EFS ) was worse in Ewing sarcoma patients with p16INK4 and p14ARF mutation / deletion than in those without the mutation / deletion ( P = 0 . 019 ) , and EFS was worse in osteosarcoma patients with TP 53 alterations than in those without TP 53 alterations ( P = 0 . 048 ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Cell growth regulators include proteins of the p 53 pathway encoded by the genes CDKN2A ( p 16 , p14arf ) , MDM 2 , TP 53 , and CDKN1A ( p 21 ) as well as proteins encoded by genes like RB 1 , E2F , and MYCL . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Different expression of P14ARF defines two groups of breast carcinomas in terms of TP 73 expression and TP 53 mutational status . ^^^ In 95 breast carcinomas , we investigated P14ARF and TP 73 mRNA expression and their relationship to TP 53 mutations , determined by an immunohistochemical method , studying several clinicopathologic features of the tumors . ^^^ The association of P14ARF and TP 73 overexpression was statistically significant , as was the association between positive TP 53 staining and TP 73 overexpression . ^^^ P14ARF was related to TP 53 only in those cases in which there was low expression of P14ARF . ^^^ Concomitant overexpression of P14ARF and TP 73 was statistically related to positive TP 53 immunostaining . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Mutational analysis of TP 53 ( exons 5 9 ) and exon 1beta of pl4ARF was performed by PCR SSCP and putative mutations were confirmed by sequencing . p14ARF mRNA expression was evaluated by RT PCR and the presence of HDM 2 gene amplification by differential PCR . ^^^ Among the cell lines , 7 / 14 ( 50 % ) harbored TP 53 mutations and 2 / 14 ( 14 % ) had a deletion ofp14ARF exon 1beta with no detectable p14ARF mRNA . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
In addition , p14ARF hypermethylation was predominantly found in tumors without a demonstrated TP 53 mutation . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Further , 50 % ( 10 / 20 ) of anaplastic oligodendrogliomas showed alterations in the TP 53 pathway through promoter hypermethylation or homozygous deletion of the p14ARF gene and , less frequently , through TP 53 mutation or MDM 2 amplification . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
HIF 1 mediated gene expression may be directly or indirectly modulated by alterations in oncogenes / tumor suppressor genes that occur during astrocytoma development , including PTEN , TP 53 , p 16 ( CDKN2A ) , p14ARF , EGFR , and PDGFR . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
To determine the frequency and timing of hypermethylation during carcinogenesis of astrocytic tumors , we analysed promoter methylation status of ten tumor associated genes ( MGMT , GSTP 1 , DAPK , p14ARF , THBS 1 , TIMP 3 , p 73 , p16INK4A , RB 1 and TP 53 ) in a series of 88 astrocytic gliomas , including 24 diffuse astrocytomas ; 21 anaplastic astrocytomas , and 43 glioblastomas ( 33 primary and 10 secondary ) , as well as two non neoplastic brain samples , by methylation specific PCR . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
TP 53 , p14ARF , p16INK4a and H ras gene molecular analysis in intestinal type adenocarcinoma of the nasal cavity and paranasal sinuses . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
We determined the frequency of aberrant CpG island methylation of several tumour associated genes : MGMT , GSTP 1 , DAPK , p14ARF , THBS 1 , TIMP 3 , p 73 , p16INK4A , RB 1 and TP 53 in 24 neurogenic tumours consisting of pilocytic astrocytomas ( n=13 ) and medulloblastomas ( n=11 ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Eleven GCAs occurring in 7 men and 4 women ranging in age from 46 to 75 years were investigated for genetic alterations of known significance in glial tumorigenesis , including LOH at 1p , 9p , 10q , 17p , and 19q , point mutations of TP 53 , deletions of p 16 ( CDKN2A ) and p14ARF , as well as EGFR amplifications . ^^^ TP 53 mutations were identified in 2 grade 4 GCAs , while combined p14ARF and p 16 ( CDKN2A ) homozygous deletions were noted in only one grade 4 lesion . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
The frequencies of aberrant methylation were : 64 % for thrombospondin 1 ( THBS 1 ) ; 30 % for tissue inhibitor of metalloproteinase 3 ( TIMP 3 ) ; 27 % for O 6 methylguanine DNA methyltransferase ( MGMT ) ; 25 % for p 73 ; 18 % for RB 1 ; 14 % for death associated protein kinase ( DAPK ) , p14ARF , p16INK4a and caspase 8 , and 0 % for TP 53 and glutathione S transferase P 1 ( GSTP 1 ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
We have determined the methylation status of the CpG island of 11 tumour related genes ( RB 1 , p14ARF , p16INK4a , p 73 , TIMP 3 , MGMT , DAPK , THBS 1 , caspase 8 , TP 53 and GSTP 1 ) in 18 neurofibromas ( including one plexiform neurofibroma ) and three neurofibrosarcomas , as well as two non neoplastic peripheral nerve sheath samples , using methylation specific polymerase chain reaction . ^^^ The incidence of aberrant methylation in the tumour samples was 52 % for THBS 1 , 43 % for MGMT , 33 % for TIMP 3 , 19 % each for p16INK4a and p 73 , 14 % for RB 1 , 5 % for p14ARF , and 0 % for DAPK , caspase 8 , TP 53 and GSTP 1 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Thus , in addition to these two genes , we determined the methylation status of the genes p16INK4a , glutathione S transferase P 1 ( GSTP 1 ) , O 6 methylguanine DNA methyltransferase ( MGMT ) , thrombospondin 1 ( THBS 1 ) , p14ARF , TP 53 , p 73 , and tissue inhibitor of metalloproteinase 3 ( TIMP 3 ) , in 18 brain metastases of solid tumors , with methylation specific PCR . ^^^ We detected methylation levels in the tumor samples of 83 % in p16INK4a , 72 % in DAP kinase , 56 % in THBS 1 , 50 % in RB 1 , 39 % in MGMT , 33 % in GSTP 1 and p14ARF each , 22 % in p 73 and TIMP 3 each , and 11 % in TP 53 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Expression of P14ARF , MDM 2 , and TP 53 proteins was assayed in the two WDL subtypes to establish whether distinct expression profiles correlated with cell ploidy . ^^^ Although a transcriptionally functional TP 53 was present in most tumors independent of their karyotype , type H cells were characterized by high levels of P14ARF and MDM 2 proteins . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
CDKN2A , 9p21 , encodes two alternatively spiked , functionally distinct , tumor suppressor proteins , P16INK4A and P14ARF , which play active roles in the RB 1 and TP 53 pathways , respectively . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
In a series of 11 microsatellite stable ( MSS ) and 9 microsatellite unstable ( MSI ) colon cancer cell lines and primary colon carcinomas ( 25 MSS and 28 MSI ) with known ploidy stem line and APC , KRAS , and TP 53 mutation status , we analyzed the promoter methylation of the following genes : hMLH 1 , MGMT , p16INK4a ( CDKN2A alpha transcript ) , p14ARF ( CDKN2A beta transcript ) , APC , and E cadherin ( CDH 1 ) . ^^^ Methylation of p14ARF , which indirectly inactivates TP 53 , was seen more frequently in tumors with normal TP 53 than in mutated samples , but the difference was not statistically significant . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Potentially prognostic histopathological markers vary among different entities and consist of assessment of necroses , mitoses , differentiation , vascular proliferation , and growth pattern , whereas immunohistochemical features include proliferation markers ( Ki 67 , MIB 1 ) , expression of oncogenes / tumor suppressor genes and their proteins ( TP 53 , c erbB 2 ) , growth factor and hormonal receptors ( VEGF , EGFR , HER 2 , HER 4 , ErbB 2 ) , cell cycle genes ( p 27 , p14ARF ) and cell adhesion molecules , as well as factors potentially related to therapeutic resistance ( DNA topoisomerase IIalpha , metallothionein , P glycoprotein , tenascin ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Promoter methylation of the p14ARF gene , another gene involved in the TP 53 pathway , was detected by methylation specific PCR in 5 / 49 ( 10 % ) low grade astrocytomas , 7 / 18 ( 39 % ) oligoastrocytomas , and 15 / 41 ( 37 % ) oligodendrogliomas . ^^^ Our previous and present data show alterations of at least one of TP 53 promoter methylation , p14ARF promoter methylation , and TP 53 mutations in 43 / 49 ( 88 % ) of low grade astrocytomas , 15 / 18 ( 83 % ) of oligoastrocytomas , and 35 / 42 ( 83 % ) oligodendrogliomas , suggesting that disruption of the TP53 / p14ARF pathway is frequent in all histological types of low grade glioma . . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
In cell lines with isolated CDKN2A ( Exon 2 ) mutations , coincident alterations in TP 53 or deletion of CDKN2A ( Exon 1 beta ) suggest that p 16 transcript may be preferentially targeted over the p14ARF transcript as additional p 53 pathway lesions are recruited . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Analysis of mRNA and protein levels in melanomas with 12q14 amplification demonstrated overexpression of target genes CDK 4 and MDM 2 without loss of CDKN2A P 16 ( P16INK4A ) or CDKN2A P14ARF ( P14ARF ) expression , important regulators of the RB 1 and TP 53 pathways , which are commonly lost or mutated in melanoma . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
However , INK 4 mRNA was expressed at high levels in 5 cell lines , and this was associated with deletion or inactivation of the retinoblastoma susceptibility gene product pRB but not with mutation of TP 53 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Several studies indicate that TP 53 ( 17p13 ) and p 16 ( Ink 4 ) / CDKN2 ( 9p21 22 ) gene loci abnormalities are frequent and early events in the pathogenesis of this neoplasm , in some cases preceding the onset of histological changes of invasion . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
To elucidate the mechanism of action of sodium butyrate ( NaB ) , we examined its effect on the expression of some cell cycle related proteins ( cyclins D 1 and E , p 16 ( ink 4 ) , p 21 ( waf 1 ) , p 27 ( kip 1 ) ) in 2 human non small cell lung cancer cell lines ( NCI 460 and NCI H 23 ) characterized by wild type and mutant TP 53 , respectively . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
MYCL 1 , FHIT , SPARC , p 16 ( INK 4 ) and TP 53 genes associated to lung cancer in idiopathic pulmonary fibrosis . ^^^ These alterations were found on markers previously associated with lung cancer located on 1p34 . 3 , 3p21 . 32 p21 . 1 , 5q32 q33 . 1 , 9p21 and 17p13 . 1 where MYCL 1 , FHIT , SPARC , p 16 ( Ink 4 ) and TP 53 genes have been mapped respectively . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
These inhibitors included the CDKIs of the CIP / KIP family ( p21CIP1 p27KIP1 , and p57KIP2 ) and the INK 4 family ( p15INK4b , p16INK4a , p18INK4c , and p19INK4d ) as well as the retinoblastoma protein family ( pRb , p 107 , and p 130 ) and the tumor suppressor p 53 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Advances in the understanding of pancreas cancer biology have been made over the past decade , including the discovery of critical mutations in oncogenes ( i . e . , K Ras ) as well as the loss of tumor suppressor genes , such as TP 53 and p 16 ( INK 4 ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Because Tp 53 mutations are a common feature of the multistep pre B cell transformation process mediated by Abelson murine leukemia virus ( Ab MLV ) , we examined the possibility that proteins encoded by the Ink4a / Arf locus also play a role in Abelson virus transformation . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
BACKGROUND : Abnormalities involving the p 16 ( also known as cyclin dependent kinase N 2 [ CDKN 2 ] , p 16 [ INK4a ] , or MTS 1 ) and p 53 ( also known as TP 53 ) tumor suppressor genes are highly prevalent in esophageal adenocarcinomas . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
SUMMARY : Karyotypic complexities associated with frequent loss or rearrangement of a number of chromosome arms , deletions , and mutations affecting the TP 53 region , and molecular alterations of the INK4A gene have been reported in sporadic and / or neurofibromatosis type 1 ( NF 1 ) related malignant peripheral nerve sheath tumors ( MPNSTs ) . ^^^ Thus , we investigated the occurrence of TP 53 and p 16 ( INK4A ) gene deregulation and the presence of microsatellite alterations at markers located at 17p , 17q , 9p21 , 22q , 11q , 1p , or 2q loci in MPNSTs and neurofibromas either related ( 14 cases ) or unrelated ( 14 cases ) to NF 1 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Methylation specific PCR detected no methylation for p 15 ( INK4B ) , von Hippel Lindau and TP 53 and only limited methylation for E Cadherin and p 16 ( INK4A ) in tumors . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
The tumor suppressor genes p 14 ( ARF ) , p 16 ( INK4a ) and Tp 53 are commonly inactivated in many tumors . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
The human Ink4a / Arf tumor suppressor locus encodes two distinct products : p 16 ( Ink4a ) which prevents phosphorylation and inactivation of the retinoblastoma protein and , p 14 ( Arf ) , a nucleolar protein which activates the function of the tumor suppressor p 53 protein in the nucleoplasm in response to oncogenic stimulation through an as yet ill defined mechanism . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Mutation analysis of the tumor suppressor genes showed that Y ML 1B is inactivated in TP 53 and RASSF1A , but not in p 14 ( ARF ) , p 16 ( INK4A ) , or RB . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Classical banding and interphase cytogenetic analyses targeting ATM , TP 53 , and P 16 ( INK4a ) genes and the D13S25 locus from 13 CD 5 ( + ) DLBLs were compared with 55 CD 5 ( ) DLBLs . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
TP 53 , CDKN2A ( p 16 ( INK4a ) ) , CDK 4 , MDM 2 , and EGFR . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
In this article we describe major genetic alterations of pancreatic cancer , mutations in the proto oncogene K RAS and the tumor suppressors INK4A , TP 53 and DPC4 / SMAD4 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Pancreatic cancer is characterized by the sequential acquisition of somatic mutations in the proto oncogene K RAS and the tumor suppressors INK4a , TP 53 and DPC4 / SMAD4 and by epigenetic alterations , including the overexpression of the `` epidermal growth factor ' ' receptor / ligand system . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
We have determined the promoter CpG island methylation status of O ( 6 ) methylguanine DNA methyltransferase ( MGMT ) , glutathione S transferase P 1 ( GSTP 1 ) , death associated protein kinase ( DAPK ) , p 14 ( ARF ) , thrombospondin 1 ( THBS 1 ) , tissue inhibitor of metalloproteinase 3 gene ( TIMP 3 ) , p 73 , p 16 ( INK4A ) , RB 1 , and TP 53 genes in three primary central nervous system lymphomas ( PCNSL ) . ^^^ These findings concur with previous data suggesting a frequent inactivation of p 16 ( INK4A ) and very limited involvement of TP 53 in PCNSL and also provide insights into the epigenetic molecular involvement of other tumor related genes in this neoplasm . . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Deletion of the tumor suppressor p 53 combined with abolition of p 16 ( Ink4a ) function failed to mimic the introduction of simian virus 40 large T antigen , indicating that large T antigen may target additional cellular functions . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Other abnormalities of the cell cycle G 1 phase regulatory pathway were detected , including loss of expression of p 53 ( JeKo 1 ) and p 16 ( INK4a ) ( SP 53 and Granta 519 ) , as well as TP 53 mutation ( Mino ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
The CDKN2A tumor suppressor gene in chromosome band 9p21 encoding CDKN2A ( also known as p 16 , INK4A ) , a negative regulator of cyclin dependent kinases , and p 14 ( ARF 1 ) , an activator of TP 53 , is inactivated in many human cancers by point mutations , promoter hypermethylation , or deletions . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
The frequencies of hypermethylation for the 10 genes were as follows , in oligodendrogliomas and ependymomas , respectively : 80 % and 28 % for MGMT ; 70 % and 28 % for GSTP 1 ; 66 % and 57 % for DAPK ; 44 % and 28 % for TP 14 ( ARF ) ; 39 % and 0 % for THBS 1 ; 24 % and 28 % for TIMP 3 ; 24 % and 14 % for TP 73 ; 22 % and 0 % for TP 16 ( INK4A ) ; 3 % and 14 % for RB 1 ; and 0 % in both neoplasms for TP 53 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Because of the close relationship between p 14 ( ARF ) and TP 53 and between p 15 ( INK4b ) / p16 ( INK4a ) and Rb , these results support a model of a coinactivation of TP 53 and Rb pathways in 75 % of MPNSTs , with functional consequences on cell growth control and apoptosis . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
PURPOSE : The chromosome 9p21 region harbors three tumor suppressor genes , p 14 ( ARF ) , p 15 ( INK4b ) , and p 16 ( INK4a ) , all of which can be targets for hypermethylation associated inactivation in low grade gliomas . p 16 ( INK4a ) and p 15 ( INK4b ) are critically involved in the RB 1 pathway , whereas p 14 ( ARF ) acts as an upstream regulator of the TP 53 pathway . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
EXPERIMENTAL DESIGN : We examined the DNA methylation status of 12 tumor related genes ( NF 2 , RB 1 , p 14 ( ARF ) , p 16 ( INK4a ) , p 73 , TIMP 3 , MGMT , DAPK , THBS 1 , caspase 8 , TP 53 , and GSTP 1 ) in 44 sporadic and / or NF 2 associated schwannomas using methylation specific PCR . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Loss of heterozygosity ( LOH ) 10q was the most frequent genetic alteration ( 69 % ) , followed by EGFR amplification ( 34 % ) , TP 53 mutations ( 31 % ) , p 16 ( INK4a ) deletion ( 31 % ) , and PTEN mutations ( 24 % ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
The CDKN2A tumor suppressor locus on chromosome band 9p21 , which encodes p 16 ( INK4A ) , a negative regulator of cyclin dependent kinases , and p 14 ( ARF 1 ) , an activator of TP 53 , is inactivated in many human cancers by point mutation , promoter hypermethylation , and , often , deletion . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
EXPERIMENTAL DESIGN : We determined the mRNA expression of p 1 ( INK4A ) , p 14 ( ARF ) , CDK 4 , RB 1 , MDM 2 , TP 53 , and E2F1 by quantitative reverse transcription PCR in 38 cases of GISTs and correlated the findings with clinicopathologic factors , including mutation analysis of KIT and PDGFRA . ^^^ GISTs with low mRNA expression of the CDKN2A transcripts p 16 ( INK4A ) and p 14 ( ARF ) but high mRNA expression of CDK 4 , RB 1 , MDM 2 , TP 53 , and E2F1 were associated with aggressive clinical behavior and unfavorable prognosis , whereas GISTs with a low mRNA expression of CDK 4 , RB 1 , MDM 2 , TP 53 , and E2F1 were not . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
The putative role of TP 53 and p 16 ( INK4A ) tumor suppressor genes and Ras oncogenes in the development and progression of salivary gland neoplasias was studied in 28 cases of pleomorphic adenomas ( PA ) , 4 cases of cystic adenocarcinomas , and 1 case of carcinoma ex PA . ^^^ Our analysis suggests that TP 53 mutations and p 16 ( INK4A ) promoter methylation , but not alterations in the H Ras and K Ras genes , might be involved in the malignant progression of PA into carcinoma . . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Presence and location of TP 53 mutation determines pattern of CDKN2A / ARF pathway inactivation in bladder cancer . ^^^ We examined 19 bladder cancer cell lines derived from 17 patients for alterations in TP 53 , RB 1 , CDKN2A , and ARF . ^^^ Another group of seven cell lines had a wild type TP 53 gene or a mutation in exons 1 4 of TP 53 and concomitant alterations in both CDKN2A and ARF in every case . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Association of p 19 ( ARF ) with Mdm 2 inhibits ubiquitin ligase activity of Mdm 2 for tumor suppressor p 53 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
An inverse correlation was noted between retention of the wild type Trp 53 allele and expression of p 19 ( ARF ) , providing further evidence of negative feedback control of the latter by p 53 . ^^^ However , expression of p 19 ( ARF ) does not appear to be counterselected in the absence of p 53 , and its integrity in Trp 53 ( + / ) tumors was indicated by its transcriptional upregulation on Trp 53 wild type allele loss in vitro in selected tumor cell lines . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
These included 3 genes coding for proteins in the p 53 pathway ( i . e . , TP 53 , p 14 ( ARF ) , and MDM 2 ) , 4 in the Rb 1 pathway ( i . e . , CDKN2A , CDKN2B , RB 1 , and CDK 4 ) , as well as PTEN and epidermal growth factor receptor . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
The TP 53 ARF tumor suppressor pathway is frequently disrupted in large / cell anaplastic medulloblastoma . ^^^ We analyzed the TP 53 and INK4A / ARF loci in 29 pediatric medulloblastomas . ^^^ Mutually exclusive mutation in TP 53 , methylation of P 14 ( ARF ) or deletion of INK4A / ARF were identified in 21 % ( 6 / 29 ) of tumors . ^^^ Our data provide the first evidence that alterations within the TP 53 ARF tumor suppressor pathway contribute to development of aggressive forms of medulloblastoma . . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Overall , activating mutations of BRAF and loss of functional p 16 and ARF were detected in the majority of melanomas ( 29 / 41 , 36 / 41 and 29 / 41 , respectively ) , while PTEN alterations / loss , NRAS and TP 53 mutations occurred less frequently ( 6 / 41 , 6 / 41 and 10 / 41 , respectively ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
In addition to ARF deletion , p 53 pathway disruption can result from dominant negative TP 53 mutations . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
These included three genes coding for proteins in the p 53 pathway ( TP 53 , p 14 ( ARF ) and MDM 2 ) , four in the Rb 1 pathway ( CDKN2A , CDKN2B , RB 1 and CDK 4 ) and PTEN and EGFR . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
PROCEDURE : Primary ependymomas at diagnosis or relapse from 24 children were analyzed for p 53 pathway , using a functional assay in yeast , RT PCR , Western blot analysis , and / or immunohistochemistry for TP 53 mutation , p 14 ( ARF ) deletion and promoter hypermethylation , MDM 2 and PAX 5 expression , respectively . p 53 mediated response to radiation induced DNA damage was evaluated using Western blot and flow cytometry analysis in two ependymoma xenograft models , IGREP 37 and IGREP 83 , derived from primary anaplastic childhood ependymomas . ^^^ RESULTS : No TP 53 , MDM 2 , p 14 ( ARF ) , PAX 5 gene abnormalities were detected in the primary ependymomas tumors and xenografts tested . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Remarkably , similar to human malignant mesotheliomas , tumors from Nf 2 ( + / ) mice showed frequent homologous deletions of the Cdkn2a / Arf locus and adjacent Cdkn2b tumor suppressor gene , as well as reciprocal inactivation of Tp 53 in a subset of tumors that retained the Arf locus . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
These alterations include deletions of negative regulatory elements ( TP 53 , CDKN 2 , MTS 2 ) and amplification of positive factors ( MDM 2 , CDK 4 ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Mutations in the CDKN 2 and p 53 ( also known as TP 53 ) genes were analyzed by single strand conformation polymorphism and DNA sequencing . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
The recurrent deletions encompass sites of tumor suppressor genes commonly inactivated in lung carcinomas , such as CDKN 2 ( 9p21 ) , RB 1 ( 13q14 ) , and TP 53 ( 17p13 ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
CONCLUSIONS : Genetic alterations at chromosomal sites containing putative tumor suppressor genes ( i . e . , 3p14 and the FHIT gene , 9p21 and the p 16 gene [ also known as CDKN 2 ] , and 17p13 and the p 53 gene [ also known as TP 53 ] ) occur frequently in the histologically normal or minimally altered bronchial epithelium of chronic smokers . . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
We evaluated the relationship between CDKN 2 deletions and the GBM subsets as defined by EGFR amplification or TP 53 mutation in 70 GBM . ^^^ The remaining 16 cases with CDKN 2 loss were divided between GBM with TP 53 mutations ( 6 cases ) and GBM with neither EGFR amplification nor TP 53 mutation ( 10 cases ) . ^^^ Thus , CDKN 2 deletions occur twice as commonly in GBM with EGFR amplification ( 71 % ) than in GBM with TP 53 mutation ( 29 % ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Inactivating mutations of the tumour suppressor genes TP 53 , CDKN 2 and SMAD 4 are also frequently observed and this constellation of genetic defects sets pancreatic cancer apart from other types of cancer , a feature which could have important implications for molecular diagnosis . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
A series of genetic changes are associated with the main histologic features of malignancy , such as TP 53 mutations , EGFR amplification , CDKN 2 deletion , etc . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
LOH on 3p , 9p , 13q , 17p and 18q occurred mainly within the loci of the VHL , CDKN 2 , Rb , TP 53 and DCC tumour suppressor genes respectively . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Mutations of TP 53 were found in three ( 25 % ) tumors , KRAS 2 in three ( 25 % ) tumors , and CDKN 2 in two ( 18 % ) tumors . ^^^ Four ( 50 % ) mutations ( one each in TP 53 and CDKN 2 and two in KRAS 2 ) were G : C to T : A transversions on the coding strand , a mutation accounting for approximately one third of mutations in smoking related tumors but uncommonly found in lung cancers not associated with smoking . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
These data suggest that LOH of BRCA 1 , or a closely linked locus , precedes the loss of CDKN 2 , TP 53 , and RB 1 , and imply that inactivation of a tumor suppressor gene in this region is an important early step in the development of these tumors . . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
We have analysed Li Fraumeni syndrome families , previously shown to be negative for mutations in TP 53 , for mutations to the tumour suppressor genes PTEN and CDKN 2 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Loss of 9p or homozygous deletion of the CDKN 2 gene or both are associated with anaplastic oligodendrogliomas , whereas loss of 17p or TP 53 gene mutations or both are frequent in astrocytomas , but rare in oligodendrogliomas . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
To evaluate whether gcGBM may also represent a genetically defined subgroup of GBM , we analyzed a series of 19 gcGBMs for mutations in the TP 53 gene for amplification of the EGFR and CDK 4 genes and for homozygous deletions in the CDKN2A ( p16 / MTS1 ) gene . ^^^ Seventeen of nineteen gcGBMs carried TP 53 mutations whereas EGFR and CDK 4 gene amplification was seen in only one tumor each and homozygous deletion of CDKN2A was not observed at all . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
We therefore sequenced exons 1alpha and 2 of CDKN2A using lymphocyte DNA isolated from index cases from 67 families with cancers at multiple sites , where the patterns of cancer did not resemble those attributable to known genes such as hMLH 1 , hMLH 2 , BRCA 1 , BRCA 2 , TP 53 or other cancer susceptibility genes . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
No evidence for linkage was found with markers near MSH 2 , MLH 1 , MCC , APC , HMPS , CDKN2A , JP 1 , PTEN , KRAS 2 , TP 53 , or LKB 1 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Frequent inactivation of CDKN2A and rare mutation of TP 53 in PCNSL . ^^^ Twenty primary central nervous system lymphomas ( PCNSL ) from immunocompetent patients ( nineteen B cell lymphomas and one T cell lymphoma ) were investigated for genetic alterations and / or expression of the genes BCL 2 , CCND 1 , CDK 4 , CDKN1A , CDKN2A , MDM 2 , MYC , RB 1 , REL , and TP 53 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Several TSGs , such as TP 53 , RB 1 and CDKN2A , encode proteins that are significant to the cell cycle . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Each pair of tumors was analyzed for TP 53 mutation , EGFR amplification , and loss of heterozygosity for tumor suppressor genes ( TP 53 , RB 1 , CDKN2A , PTEN , DMBT 1 ) and tumor suppressor gene regions ( 1p36 , 19q13 , 11p15 , 10p15 ) known to be frequently implicated in glioma tumorigenesis . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Therefore , we have analyzed molecular genetic alterations involving chromosomes 1p , 10q , and 19q and the TP 53 ( on chromosome 17p ) and CDKN2A ( on chromosome 9p ) genes , in addition to clinicopathologic features in 39 patients with anaplastic oligodendrogliomas for whom chemotherapeutic response and survival could be assessed . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
A series of molecular changes including loss of heterozygosity ( LOH ) at 17p ( TP 53 gene ) , 13q ( RB gene ) , 18q ( DCC gene ) , and 9p21 ( CDKN2a gene ) chromosomal regions have been identified in dysplasias , carcinomas in situ , and invasive carcinomas of the gallbladder , whereas mutations in K and N ras genes are rare . ^^^ We determined the presence of mutations in TP 53 , K and N ras genes , and LOH at five chromosomal regions ( 5q22 APC MCC region , RB , TP 53 , DCC and 9p21 CDKN2a ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
FISH analysis of BK 10 using chromosome arm specific paints , centromere probes , and oncogene / tumor suppressor gene specific probes revealed a deletion of CDKN2A ( p 16 ) in all copies of chromosome 9 , a low level amplification of MYC ( five copies ) , and loss of one copy of TP 53 ; detected the presence of the Y chromosome in a hidden translocation ; and detected four copies of ERBB 2 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Neoplastic progression in BE is associated with alterations in TP 53 ( also known as p 53 ) and CDKN2A ( also known as p 16 ) and non random losses of heterozygosity ( LOH ) . ^^^ We have previously shown in small numbers of patients that disruption of TP 53 and CDKN2A typically occurs before aneuploidy and cancer . ^^^ Here , we determine the evolutionary relationships of non random LOH , TP 53 and CDKN2A mutations , CDKN2A CpG island methylation and ploidy during neoplastic progression . ^^^ Diploid cell progenitors with somatic genetic or epigenetic abnormalities in TP 53 and CDKN2A were capable of clonal expansion , spreading to large regions of oesophageal mucosa . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Mutations of TP 53 , amplification of EGFR , MDM 2 and CDK 4 , and deletions of CDKN2A in malignant astrocytomas . ^^^ The genetic alterations analyzed were : deletion of CDKN2a / p16 gene , TP 53 mutations , and amplification of EGFR , MDM 2 and CDK 4 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
These findings demonstrate that oligodendroglial neoplasms usually have loss of 1p and 19q whereas astrocytomas of the progressive type frequently contain mutations of the TP 53 gene , and that 9p loss and CDKN2A deletions are associated with progression from well differentiated to anaplastic oligodendrogliomas . . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
More focussed molecular genetic analyses revealed neither aberrations of the TP 53 and CDKN2A tumor suppressor genes nor amplification of the EGFR , CDK 4 , and MDM 2 proto oncogenes . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
The scarcity of such cases generally requires that molecular analyses of PMAs are based on the utilization of paraffin embedded material , and here we have used 39 such specimens to examine the incidence and prognostic significance of oncogene and tumor suppressor gene alterations ( including amplifications of EGFR , CDK 4 , and MDM 2 as well as inactivating mutations of CDKN2A , TP 53 , and PTEN ) in these tumors . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Specific alterations of the EGFR , CDK 4 , CDKN2A , TP 53 , DMBT 1 , NF 2 , and PTEN genes were analyzed in addition . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Molecular analysis of the PTEN , TP 53 and CDKN2A tumor suppressor genes in long term survivors of glioblastoma multiforme . ^^^ Therefore , we compared 2 age and gender matched groups of GBM patients with different post operative time to tumor progression ( TTP ) , defined as ' short term ' for TTP of less than 6 months ( n = 21 ) , and ' long term ' for TTP of more than 24 months ( n = 21 ) for genetic alterations of the PTEN , CDKN2A and TP 53 genes as well as overexpression of the EGFR , p 53 and Mdm 2 proteins . ^^^ For the GBMs with ' short term ' TTP vs . ' long term ' TTP , the studies revealed PTEN mutations in 4 / 21 vs . 2 / 21 , TP 53 mutations in 5 / 21 vs . 8 / 21 , homozygous deletion of the CDKN2A gene in 5 / 21 vs . 6 / 21 , overexpression of EGFR in 7 / 20 vs . 10 / 20 , accumulation of p 53 protein in 9 / 20 vs . 7 / 20 and of Mdm 2 protein in 0 / 20 vs . 1 / 20 cases studied . ^^^ Taken together , our data indicate that mutations of the PTEN and TP 53 tumor suppressor genes , homozygous deletion of the CDKN2A gene as well as overexpression of the EGFR , p 53 and Mdm 2 proteins lack prognostic significance for overall survival time in patients with GBMs . . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Normal human diploid cells irradiated with 10 rays showed permanent cell cycle arrest and exhibited senescence like phenotypes including the expression of senescence associated beta galactosidase ( SA beta gal ) . 10 irradiation caused persistent phosphorylation of TP 53 at Ser 15 and accumulation of the TP 53 protein , followed by the induction of CDKN1A ( also known as p 21 ( Waf1 / Cip1 ) ) and CDKN2A ( also known as p 16 ) , preceded the expression of SA beta gal . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Overexpression of p 53 was observed in only one tumour , and a TP 53 mutation was present in this case . p 16 immunostaining was undetectable in 10 cases , and homozygous deletion of CDKN2A was observed in four of the six studied tumours . pRb expression was lost in four tumours . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
The molecular events involved in pancreatic cancer are becoming increasingly well characterized , with mutations in the dominant oncogene KRAS and the tumour suppressor genes TP 53 , CDKN2A and MADH 4 being typically observed . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
To determine the molecular genetic alterations in such `` glioblastomas with oligodendroglial component ' ' , we investigated 13 of these tumors for genetic alterations and / or expression of the TP 53 , CDKN2A , PTEN , and EGFR genes . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Correlation of histology and molecular genetic analysis of 1p , 19q , 10q , TP 53 , EGFR , CDK 4 , and CDKN2A in 91 astrocytic and oligodendroglial tumors . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Molecular genetic analysis of one tumor revealed no TP 53 mutation ( exons 4 10 ) , no loss of CDKN2A , and no amplification of EGFR , CDK 4 or MDM 2 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Molecular genetic abnormalities preceding , or occurring during , BC include overexpression of the BCR / ABL transcript , upregulation of the EVI 1 gene , increased telomerase activity , and mutations of the tumor suppressor genes RB 1 , TP 53 , and CDKN2A . ^^^ Apart from the strong phenotypic impact of addition of acute myeloid leukemia / myelodysplasia associated translocations and inversions , such as inv ( 3 ) ( q21q26 ) , t ( 3 ; 21 ) ( q 26 ; q 22 ) , and t ( 15 ; 17 ) ( q 22 ; q 12 21 ) , in CML BC , only a few significant differences between myeloid and lymphoid BC are discerned , with 1 ( 17q ) and TP 53 mutations being more common in myeloid BC and monosomy 7 , hypodiploidy , and CDKN2A deletions being more frequent in lymphoid BC . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
RESULTS : Microsatellite instability was present in 21 % , DNA nondiploidy in 15 % , and mutations in the PTEN , KRAS , CTNNB1 / beta catenin , TP 53 , and CDKN2A genes were detected in 32 , 11 , 13 , 17 , and 0 % of the tumors , respectively . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Molecular analysis showed no loss of heterozygosity for microsatellite markers at the tumor suppressor loci of TP 53 , CDKN2A ( p16 / INK4A ) , and MADH 4 ( Smad4 / DPC4 ) in the invasive carcinoma , although loss of heterozygosity was detected at one CDKN2A marker in the intraductal component . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Molecular genetic analysis of the TP 53 , PTEN , CDKN2A , EGFR , CDK 4 and MDM 2 tumour associated genes in supratentorial primitive neuroectodermal tumours and glioblastomas of childhood . ^^^ To identify molecular genetic markers that may distinguish sPNET and GBM , we investigated 12 cerebral sPNETs and six GBMs from paediatric patients for genetic alterations of the TP 53 , PTEN , CDKN2A , EGFR , CDK 4 and MDM 2 genes , as well as for allelic loss on chromosome arms 10q and 17p . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
To date , molecular genetic studies of CML BC have mainly focused on alterations of well known tumor suppressor genes ( e . g . , TP 53 , CDKN2A , and RB 1 ) and oncogenes ( e . g . , RAS and MYC ) , whereas limited knowledge is available about the molecular genetic correlates of the unbalanced chromosomal abnormalities . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
On surgical samples , TP 53 , Mdm 2 , CDKN2A / p16 p 14 alterations were studied by molecular biology techniques and by immunohistochemistry . ^^^ TP 53 mutations and Mdm 2 amplifications were mutually exclusive , whereas TP 53 mutations and CDKN2A / p14 inactivation coexisted in 5 cases . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Gene abnormalities in multiple myeloma ; the relevance of TP 53 , MDM 2 , and CDKN2A . ^^^ Since the incidence and clinical implications of abnormalities of TP 53 , CDKN2A ( encoding for p 16 and p 14 ) and MDM 2 genes ( chromosome 12 ) in multiple myeloma ( MM ) is not clear , we investigated allelic loss at the former two loci and gain at the latter locus in a series of 82 MM patients . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
This study indicates that BALB / c Prkdc and Cdkn2a alleles do modify tumor incidence in Trp 53 ( + / ) mice and highlights the complexity of gene interaction effects in determining cancer phenotypes but discounts these alleles as major recessive loci contributing to spontaneous mammary tumor susceptibility . . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
The most commonly identified genetic alterations associated with the FCL transformation are TP 53 gene mutations , inactivation of CDKN2A and CDKN2B genes and deregulation of the C MYC gene . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
TP 53 ( alias p 53 ) gene mutation was studied by a polymerase chain reaction ( PCR ) single strand conformation polymorphism sequencing ; CDKN2B ( alias p 15 ) and CDKN2A ( alias p 16 ) gene methylation by methylation specific PCR ; and genetic imbalances by comparative genomic hybridization ( CGH ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Tumor suppressor genes TP 53 and CDKN2A were downregulated and protooncogenes JUN and GRB 10 were upregulated . ^^^ Deregulation was found in pathways that contribute to genomic stability ( by downregulation of either TP 53 or CSE1L and by upregulation of GADD45A ) and regulate cell cycle progression ( by downregulation of CDKN2A and upregulation of RBBP 4 , CDC 37 , and NEDD 5 ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Selected SNPs belong to the following genes : ADH1B , ALDH 2 , APEX , CDKN2A , COMT , CYP1A1 , CYP1A2 , CYP1B1 , CYP2A6 , CYP2C19 , CYP2C9 , CYP2E1 , CYP3A4 , DRD 2 , DRD 4 , EPHX 1 , ERCC 1 , ERCC 2 , ERCC 4 , ERCC 5 , GRPR , GSTA 4 , GSTM 3 , GSTP 1 , GSTT 2 , LIG 3 , MDM 2 , MGMT , MPO , NAT 1 , NAT 2 , NQO 1 , OGG 1 , PCNA , POLB , SLC6A3 , SOD 2 , TP 53 , XRCC 1 , XRCC 2 , XRCC 3 , and XRCC 9 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Molecular alterations commonly observed in gliomas subtypes , including LOH 1p and 1q , LOH 19q , LOH 10p and 10q , LOH 9p , TP 53 and PTEN mutations , EGFR amplification , CDKN2A homozygous deletion and telomerase reactivation were systematically screened in the original and xenografted tumours . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
The screening of seven MPNSTs for subtle mutations in the CDKN2A and TP 53 genes proved negative , although the screening of 11 MPNSTs detected LOH involving either the TP 53 or the CDKN2A gene in a total of four tumors . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Allelic losses were nonrandomly distributed across the genome and most prevalent for chromosome arms 9p , 17p , and 18q ( > 60 % ) , sites of the known tumor suppressor genes CDKN2A , TP 53 , and MADH 4 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
TP 53 , MDM 2 and CDKN2A / p14ARF genes were unchanged . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Disruption of the gene Cdkn2a ( encoding p 16 and p 19 ) , but not of Trp 53 ( encoding p 53 ) , reconstituted cell transformation in Ppm1d null MEFs . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
They were characterized for their genetic alterations , including those considered as `` early ' ' alterations , namely loss of chromosome 1 + / loss of chromosome 19q , TP 53 mutation , and those considered as `` late ' ' alterations , namely loss of chromosome 10 , loss of chromosome 9p , EGFR genomic amplification , PTEN mutation , CDKN2A homozygous deletion , and telomerase reactivation . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
The TOV 21G , TOV 81D , OV 90 , and TOV 112D cell lines were derived from ovarian tumors ( TOV ) or ascites ( OV ) from chemotherapy and radiotherapy naive patients and were characterized by their mutation spectrum of BRCA 2 , TGFbeta RII , KRAS 2 , TP 53 , and CDKN2A . ^^^ In contrast , sensitivity to camptothecin or paclitaxel was not significantly different between all cell lines , irrespective of the mutation status of BRCA 1 , BRCA 2 , TGFbeta RII , KRAS 2 , TP 53 , and CDKN2A . ^^^ The observed responses to treatment are consistent with the current knowledge concerning BRCA 2 , TGFbeta RII , KRAS 2 , TP 53 , and / or CDKN2A aberrant function . . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
In fact , several tumor suppressors and oncogenes have been shown to be involved in melanoma pathogenesis , including CDKN2A , PTEN , TP 53 , RAS and MYC , though they have not been related to melanoma subtypes or validated as prognostic markers . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Genes that were frequently deleted included ( 56 . 7 % ) , FGFR 2 ( 66 . 7 % ) , MTAP ( 60 . 0 % ) , DMBT 1 CDKN2A ( p 16 ) / MTAP ( 50 . 0 % ) , PIK3CA ( 43 . 3 % ) , and EGR 2 ( 43 . 3 % ) , but deletion of RB 1 or TP 53 was rarely detected . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Mutation analysis of genes that control the G1 / S cell cycle in melanoma : TP 53 , CDKN1A , CDKN2A , and CDKN2B . ^^^ The aim of our study was to analyse mutations in TP 53 , CDKN1A , CDKN2A , and CDKN2B genes in melanoma tumors and melanoma cell lines METHODS : We analysed 39 primary and metastatic melanomas and 9 melanoma cell lines by single stranded conformational polymorphism ( SSCP ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Expressions of DUSP 6 , CDKN2A , TP 53 , and SMAD 4 were investigated by immunohistochemistry in a total of 206 lesions of dysplastic ductal precursors and carcinomas retrieved from 52 pancreata with invasive ductal carcinomas and 51 of those with intraductal papillary mucinous neoplasms . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Several cell lines showed deletions of the TP 53 ( alias p 53 ) , CDKN2A ( alias p 16 ) , and VHL genes . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Genomic alterations influencing the expression and / or activity of tumor suppressors or oncogenes such as KRAS 2 , CDKN2A , TP 53 , and DPC 4 have been directly implicated in the initiation and progression of human pancreatic adenocarcinoma . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
We sequenced BRAF and KRAS , analyzed for microsatellite instability ( MSI ) and 18q loss of heterozygosity ( LOH ) , and performed immunohistochemistry for TP 53 , cyclooxygenase 2 ( COX 2 ) , MLH 1 , O 6 methylguanine DNA methyltransferase ( MGMT ) , p 16 ( CDKN2A ) , and fatty acid synthase ( FASN ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Abrogation of CDKN2A occurs in low grade / early PanIN , whereas aberrations of TP 53 and SMAD 4 occur in high grade / late PanIN . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
We have developed a quantitative PCR / LDR / Universal Array assay that allows parallel evaluation of methylation status of 75 CpG dinucleotides in the promoter regions of 15 tumor suppressor genes ( CDKN2B , CDKN2A , CDKN2D , CDKN1A , CDKN1B , TP 53 , BRCA 1 , TIMP 3 , APC , RASSF 1 , CDH 1 , MGMT , DAPK 1 , GSTP 1 , and RARB ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
In contrast , other genetic alterations , such as TP 53 and PTEN mutations , EGFR amplification , and homozygous deletion of CDKN2A have been correlated with worse outcome in these tumors . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Moreover , several tumour suppressors and oncogenes have been shown to be involved in melanoma pathogenesis , including CDKN2A , PTEN , TP 53 , RAS and MYC , but have not been related to melanoma subtypes or validated as prognostic markers . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Finally , small regions of deletion and amplification , often including genes known to be involved in leukemia progression ( for example MYC , TP 53 , CDKN2A , and KIT ) , were identified . . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Gene therapy approaches include inhibition of activated oncogenes ( KRAS , LSM 1 ) with antisense and RNA interference strategies , replacement of inactivated tumour suppressor genes ( TP 53 , CDKN2A , CDKN1A ) , targeting of cell signalling pathways , gene directed prodrug activation therapies and the use of replication competent oncolytic viruses . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Many of the genetic lesions involved in BE neoplastic progression are known , including loss of CDKN2A ( p 16 ) and TP 53 ( p 53 ) and the development of tetraploidy and aneuploidy . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Some genes have been found altered in prostate cancer , such as PTEN , TP 53 , AR , RNASEL ( HPC 1 ) , ELAC 2 ( HPC 2 ) , CDKN2A and MSR 1 and those can be natural targets for new strategies of treatment . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
We comparatively evaluated 1 FISH patterns of chromosomes 3 , 7 , 9 , and 17 and of the CDKN2A and TP 53 loci in newly diagnosed superficial bladder lesions and in corresponding bladder washings , to verify representatives of the latter type of sampling and to improve the efficacy of 1 FISH follow up . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
To investigate the molecular mechanisms of tuberous sclerosis ( TSC ) histopathologic lesions , we have tested for loss of heterozygosity the two TSC loci ( TSC 1 and TSC 2 ) and seven tumor suppressor gene containing regions ( TP 53 , NF 1 , NF 2 , BRCA 1 , APC , VHL , and MLM ) in 20 hamartomas from 18 TSC patients . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Also in bladder carcinoma the study of cellular differentiation markers has been replaced by that of genotypic alterations , and , mainly with the help of immunohistochemistry , of the expression of genes involved in cell proliferation and death , such as MTS 1 , TP 53 , Rb , c myc , Bcl 2 , c erb B 2 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
A physical and functional interaction between the Ca ( 2+ ) binding protein Mts 1 ( S100A4 ) and the tumor suppressor p 53 protein is shown here for the first time . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Analysis of the p16INK4 and TP 53 tumor suppressor genes in bone sarcoma pediatric patients . ^^^ Recent data suggest that deletion of p16INK4 and mutation of TP 53 are among the most common genetic events in the development of human cancer , since the codified proteins act as brakes of the abnormal cell cycle . ^^^ As the molecular events leading to the development of pediatric bone sarcomas remain unclear , we analyzed 75 osteosarcoma and Ewing sarcoma samples from 43 pediatric patients to search for alterations at the TP 53 or p16INK4 tumor suppressor genes . ^^^ These data support the hypothesis that TP 53 alterations may play a role in the development of pediatric bone tumors and that the primary mechanism of inactivation of p16INK4 seems to be homozygous deletion rather than point mutation . . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Molecular analysis of tumor suppressor genes p16INK4 and TP 53 of osteosarcomas in Spanish children ] . ^^^ OBJECTIVE : Alterations affecting tumor suppressor genes , specifically p16INK4 and TP 53 , have been shown to be involved in the development of human cancer due to their important role in the control of normal cell cycle progression . ^^^ RESULTS : Our analysis showed that 18 . 4 % of the samples harbored mutations in the coding region of TP 53 and that 7 % had a homozygous deletion of the p16INK4 gene . ^^^ Our results suggest that p16INK4 deletions may constitute a bad prognostic factor and that TP 53 alterations may be correlated , although not statistically , with reduced survival time . ^^^ CONCLUSIONS : Mutations of the TP 53 and deletion of p16INK4 tumor suppressor genes seem to be involved in the development of pediatric osteosarcoma . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
PURPOSE : To analyze the genetic and epigenetic alterations affecting the RB 1 , TP 53 , p16INK4 , and p21WAF1 tumor suppressor genes , loss of heterozygosity ( LOH ) at 3q and 18q , and the clinical variables of a series of Spanish children with osteosarcoma . ^^^ The mutation and methylation status of p16INK4 , p21WAF1 , TP 53 , and RB 1 was screened as well as LOH at 3q and 18q . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Analysis of the involvement of the tumour suppressor genes TP 53 , p16INK4 , p21WAF1 , RB 1 and the drugs metabolizing enzymes in the development of bone tumours in children ] . ^^^ BACKGROUND : Several tumor suppressor genes such as p16INK4 , TP 53 , RB 1 y p21WAF1 are involved in cell cycle regulation in response to DNA damage and belong to the complex pathway that regulates cell proliferation and / or differentiation . ^^^ MATERIALS AND METHODS : By means of PCR based techniques , we have analyzed the presence of variations in the coding sequence of p16INK4 , TP 53 , RB 1 y p21WAF1 and of the Drug Metabolizing Enzymes in a group of 82 osteosarcomas and 47 Ewing ' s sarcomas as well as in a control group of 115 healthy children . ^^^ CONCLUSIONS : Alteration of TP 53 , p16INK4 and p21WAF1 seems to be involved in the development of pediatric bone tumors and to be an unfavourable prognostic factor in this type of tumors . . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
After whole genome amplification by improved primer extension and preamplification PCR ( 1 PEP PCR ) , microsatellite PCR based loss of heterozygosity analysis ( LOH ) of the tumor suppressor gene loci TP 53 , p16INK4 , and DPC 4 was performed . ^^^ One of 85 informative duct lesions ( 1 . 2 % ) had LOH of TP 53 , 1 of 76 duct lesions ( 1 . 3 % ) had LOH of DPC 4 , and 2 / 29 duct lesions ( 6 . 9 % ) showed LOH of p16INK4 . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Tumor suppressor p 53 is expressed in proliferating and newly formed neurons of the embryonic and postnatal rat brain : comparison with expression of the cell cycle regulators p21Waf1 / Cip1 , p27Kip1 , p57Kip2 , p16Ink4a , cyclin G 1 , and the proto oncogene Bax . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Cumulation of TP 53 mutations and p16INK4A / p15INK4B homozygous deletions in human papilloma virus type 16 positive scrotal cancer . ^^^ TP 53 , p16INK4A , and p15INK4B were reported as the transcription factors that regulate the cell cycle on the same pathway . ^^^ Here , the mutation pattern of TP 53 , p16INK4A , and p15INK4B genes and the homo / hemizygous deletion patterns of p16INK4A / p15INK4B genes are presented in four scrotal carcinoma cases . ^^^ Homozygous deletion in p16INK4A / p15INK4B genes and a codon 259 missense point mutation ( GAC > TAC ; Asp > Tyr ) in the TP 53 gene were observed in one human papilloma positive scrotal carcinoma case . ^^^ The cumulation of TP 53 mutations and p16INK4A / p15INK4B homozygous deletions in human papilloma virus type 16 positive scrotal carcinoma cases indicate that the alterations of TP 53 , p16INK4A , and p15INK4B genes have an important role in the progression of scrotal cancers , as well as other factors . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
In this study we evaluated whether the mutation rate of the TP 53 and p16INK4a genes of pancreatic cancers differs in pancreatic cancer patients with and without multiple primaries . ^^^ Furthermore , we investigated whether pancreatic cancer patients with multiple primaries carry germline mutations in either p16INK4a , TP 53 , or BRCA 2 tumor suppressor genes to detect a genetic alteration that predisposes to the development of different primaries . ^^^ Normal constitutional and tumor DNA of the 14 patients with a positive cancer history , but negative family history , were analyzed for p16INK4a , TP 53 , and BRCA 2 mutations by single strand conformational variant ( SSCV ) analysis and direct sequencing . ^^^ The frequency of somatic TP 53 and p16INK4a mutations in pancreatic cancer is similar in patients with and without multiple primaries . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
To test whether previously characterized tumor suppressor genes are affected by hypermethylation we performed MS PCR for p15INK4B , p16INK4A , VHL , TP 53 and E cadherin . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
The overall survival was shorter in aggressively treated leukemia patients than in aggressively treated lymphoma patients ( P = . 003 ) ; however , the incidence rates of TP 53 mutation , p16INK4a deletion , and p15INK4b deletion that were found in 6 ( 15 % ) of 40 , 3 ( 9 % ) of 35 , and 2 ( 6 % ) of 35 tumors , respectively , were similar between the 2 subtypes . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Hereditary TP 53 codon 292 and somatic P16INK4A codon 94 mutations in a Li Fraumeni syndrome family . ^^^ On the other hand , hereditary mutations of TP57KIP2 , P15INK4B , and P16INK4A , which affect the cell cycle similar to TP 53 , were observed in some types of cancer . ^^^ In a Turkish family with the diagnosis of Li Fraumeni syndrome , we analyzed the mutation pattern of TP 53 , P57KIP2 , P15INK4B , and P16INK4A in the peripheral blood , and loss of heterozygosity ( homo / hemizygous deletion ) pattern of TP 53 and P15INK4B / P16INK4A in two tumor tissues . ^^^ In the analyses of tumor tissues from the propositus and his daughter , a P16INK4A codon 94 missense point mutation ( GCG > GAG ; Ala > Glu ) was observed with the hereditary TP 53 mutation . ^^^ No other gene alteration in TP 53 , P57KIP2 , P15INK4B , and P16INK4A was observed . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
Our recent population based study in the Canton of Zrich , Switzerland , shows that primary glioblastomas develop in older patients ( mean age , 62 years ) and typically show LOH on chromosome 10q ( 69 % ) and other genetic alterations ( EGFR amplification , TP 53 mutations , p16INK4a deletion , and PTEN mutations ) at frequencies of 24 34 % . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
No prognostic significance was associated with genetic changes in epidermal growth factor receptor ( amplified in 17 of 41 patients ) , TP 53 ( mutated in 11 of 41 patients ) , p16INK4A ( deleted in 15 of 33 patients ) , or phosphatase and tensin homologue ( mutated in 15 of 41 patients ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
In glioblastomas , LOH 10q was the most frequent genetic alteration ( 69 % ) , followed by EGFR amplification ( 34 % ) , TP 53 mutations ( 31 % ) , p16INK4a deletion ( 31 % ) , and PTEN mutations ( 24 % ) . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
None of the tumors simultaneously showed LOH at TP 53 and RB 1 genes ( R= 0 . 211 , p=0 . 16 ; Spearman ' s rank correlation test ) . p16INK4A alterations ( LOH and gene deletion ) occurred concomitantly , with 3 tumors showing the TP 53 allelic loss , whereas the cyclin D1 / cdk4 complex was overexpressed in a case with TP 53 LOH . ^^^ Disruptions at p16INK4A and / or cdk4 / cyclin D 1 concomitantly occurring with TP 53 LOH may participate in the development of a subset of endometrioid type ECs . . ^^^
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA
Interacting proteins: Q8N726 and P04637	Pubmed	SVM Score :0.0
NA