| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| The tumor suppressor p 53 has been implicated in apoptosis induction and is mutated in human T ALL CCRF CEM cells . ^^^ |
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| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| TP 53 is the most commonly mutated gene in human cancer , but TP 53 mutations are present in less than 5 % of children with acute lymphoblastic leukemia ( ALL ) at initial presentation . ^^^ Mutations are detected more frequently in children with relapsed T cell ALL , but the potential role of TP 53 mutations in relapsed B lineage childhood ALL is not understood as well . ^^^ The authors determined the nucleotide sequence of amplified DNA from exons 5 to 8 of the TP 53 gene in leukemic cells obtained from 17 children with ALL at the time of first bone marrow relapse . ^^^ All 17 contained only germline TP 53 sequences . ^^^ Review of the published literature disclosed that TP 53 mutations have been found in 22 % of cases of relapsed ALL . ^^^ |
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| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| However , TP 53 mutations are uncommon in ALL . ^^^ It is possible that alternative mechanisms of regulation of the TP 53 apoptosis pathway , such as modulation of p 33 ( ING1b ) expression , may be important in ALL . ^^^ |
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| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| Relative to nonmethylated leukemia samples , TP 53 expression levels were decreased in all methylated samples in which TP 53 expression could be measured . ^^^ Methylation of CpG and CCWGG motifs in the promoter of TP 53 could represent a novel mechanism leading to functional impairment of this tumor suppressor gene in ALL . . ^^^ |
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| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| In this study , we have analysed : ( 1 ) the complete coding region , all intron exon junctions and noncoding regions of exons 1 11 of TP 53 by lexon DGGE ; ( 2 ) the methylation status of the 5 ' region of TP 53 and ( 3 ) the deletion of one or both alleles of the gene by fluorescence in situ hybridisation ( FISH ) in 57 ALL patients . ^^^ Using these techniques , we have found promoter methylation in 32 % of the cases , missense mutations in 8 . 8 % , and deletion of one allele in 7 . 5 % of the samples , with TP 53 being altered in 40 % of the ALL samples studied in this series . . ^^^ |
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| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| In the remaining 4 ALL tumors , apoptotic resistance was associated with a TP 53 mutation or with defective activation of p 53 . ^^^ |
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| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| We have analyzed the regulation and expression of ASPP members , genes implicated in the regulation of the apoptotic function of the TP 53 tumor suppressor gene , in acute lymphoblastic leukemia ( ALL ) . ^^^ Abnormal ASPP 1 expression was associated with normal function of the tumor suppressor gene TP 53 in ALL . ^^^ |
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| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| Our data suggest that the expression of the tumor suppressor p 53 is involved in the regulation of both normal and CML hemopoiesis and that the inhibition of p 53 expression could modulate the proliferation of CML hemopoietic cells and possibly of normal cells . . ^^^ |
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| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| The TP 53 gene has been extensively studied in patients with chronic myeloid leukemia ( CML ) , both in chronic phase and in blast crisis . ^^^ Since these samples had no TP 53 mutations , we believe that wild type TP 53 accumulates in blood cells of CML patients . ^^^ Accumulation of wild type TP 53 in CML cells may indicate an additional mechanism involving this gene in the pathogenesis of this disease . . ^^^ |
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| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| 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 . ^^^ |
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| Interacting proteins: P11274 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 . ^^^ |
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| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P11274 and P04637 |
Pubmed |
SVM Score :0.0 |
| NA |
|