Philadelphia chromosome Abnormal human chromosome 22 ,resultingfrom reciprocal translocation
a shortened chromosome 22resultingfrom a reciprocal translocation , t(9;22
1988).The BCR - ABL oncogeneresultsfrom a reciprocal t(9;22)chromosomal translocation
frequently develop liver cancer ,resultingfrom reciprocal translocation
The appearance of an aberrant chromosome 22 , the Philadelphia chromosomeresultingfrom a reciprocal translocation t(9;22
Chronic myelogenous leukemia ( CML ) is characterized by the presence of the Philadelphia chromosomeresultingfrom the reciprocal translocation
the disruption of CD40LG ... resulting in defective CD40L expression in the female patient with an extremely skewed X - inactivation pattern in T cells leading to the HIGM1 phenotype [ 17causedthe disruption of CD40LG ... resulting in defective CD40L expression in the female patient with an extremely skewed X - inactivation pattern in T cells leading to the HIGM1 phenotype [ 17
the so - called Philadelphia chromosome ( Ph(passive) is created bythe so - called Philadelphia chromosome ( Ph
a Mr 80,000 constitutively active tyrosine kinase protein , termed nucleophosminoriginatesa Mr 80,000 constitutively active tyrosine kinase protein , termed nucleophosmin
CML ... in which a piece of chromosome 9 containing the ABL1 oncogene is translocated to chromosome 22 and fused to the BCR gene(passive) is caused byCML ... in which a piece of chromosome 9 containing the ABL1 oncogene is translocated to chromosome 22 and fused to the BCR gene
in theshort arm of chromosome 1 ... band 3resultsin theshort arm of chromosome 1 ... band 3
in fusion of the Ewing sarcoma 1 ( EWS1 ) gene on chromosome 22 and WT1 on chromosome 11resultingin fusion of the Ewing sarcoma 1 ( EWS1 ) gene on chromosome 22 and WT1 on chromosome 11
h3createsh3
to fusion of depositsleadingto fusion of deposits
partial T18causespartial T18
to a kf protein with altered transcrip- tional propertiesleadingto a kf protein with altered transcrip- tional properties
to the transfer of the tyrosine kinase c - abl from chromosome 9 into the ber gene on chromosome 22leadsto the transfer of the tyrosine kinase c - abl from chromosome 9 into the ber gene on chromosome 22
in no net loss of genic material between daughter cellsresultsin no net loss of genic material between daughter cells
two abnormal chromosomes one elongated and longer chromosome 9 called “ derivative chromosome ” , and one shorted chromosome 22 called “ truncated chromosomecreatestwo abnormal chromosomes one elongated and longer chromosome 9 called “ derivative chromosome ” , and one shorted chromosome 22 called “ truncated chromosome
to fusion with AK6ledto fusion with AK6
pairing between two non - homologous chromosomes during meiosiswould causepairing between two non - homologous chromosomes during meiosis
in fusion of GOLGA5 with the RET oncogene found in radioactivity - induced thyroid carcinomasresultingin fusion of GOLGA5 with the RET oncogene found in radioactivity - induced thyroid carcinomas
in LRRFIP1-MET fusion in an atypical Spitz tumourresultingin LRRFIP1-MET fusion in an atypical Spitz tumour
to a terminal 6q duplication and partial monosomy of another chromosomeleadingto a terminal 6q duplication and partial monosomy of another chromosome
in the fusion of DGKG ( chromosome 3 ; light grey ) and BST1 ( chromosome 4 ; dark greyresultedin the fusion of DGKG ( chromosome 3 ; light grey ) and BST1 ( chromosome 4 ; dark grey
in a fusion of the EWS gene to the Fli1 generesultsin a fusion of the EWS gene to the Fli1 gene
in an elongated chromosome 9 ( 9q+resultingin an elongated chromosome 9 ( 9q+
irreversible aggregation and precipitationto preventirreversible aggregation and precipitation
reduced fertility in heterozygotes ( data not shown ; van Harten 1998causesreduced fertility in heterozygotes ( data not shown ; van Harten 1998
in a fusion with RARA gene encoding retinoic acid receptor alpharesultedin a fusion with RARA gene encoding retinoic acid receptor alpha
from double - strand breaks in both chromosomes 6 and 9 produced chromosomes 96 and 69resultingfrom double - strand breaks in both chromosomes 6 and 9 produced chromosomes 96 and 69
from the integration of GFP - tailswap T - DNAsoriginatingfrom the integration of GFP - tailswap T - DNAs
in the Philadelphia chromosome ( Ph1resultingin the Philadelphia chromosome ( Ph1
a fusion protein between the EWS gene on chromosome 22 and the FLI1 gene on chromosome 11createsa fusion protein between the EWS gene on chromosome 22 and the FLI1 gene on chromosome 11
in a RARα fusion protein and subsequent RARα functional impairment ( 25 , 26resultedin a RARα fusion protein and subsequent RARα functional impairment ( 25 , 26
binding between the promoter and RNA polymerasepreventedbinding between the promoter and RNA polymerase
in the EWSR1-ATF1 fusion generesultingin the EWSR1-ATF1 fusion gene
the A. thaliana chromosomes IV and V ( between AL6 and AL7creatingthe A. thaliana chromosomes IV and V ( between AL6 and AL7
in the fusion of EWS to an ETS transcription factorresultingin the fusion of EWS to an ETS transcription factor
in the formation of Philadelphia chromosomeresultingin the formation of Philadelphia chromosome
in diploid cellsresultingin diploid cells
to the Philadelphia chromosome ( Ph+ ) with a fusion gene BCR - ABL , the molecular hallmark of CML and Ph - positive acute lymphoblastic leukaemia ( LALleadingto the Philadelphia chromosome ( Ph+ ) with a fusion gene BCR - ABL , the molecular hallmark of CML and Ph - positive acute lymphoblastic leukaemia ( LAL
into the Philadelphia ( Ph ) chromosome and formation of the BCR / ABL fusion generesultinginto the Philadelphia ( Ph ) chromosome and formation of the BCR / ABL fusion gene
in a fusion of the PML protein to the retinoic acid receptor αresultingin a fusion of the PML protein to the retinoic acid receptor α
to the expression of the Bcr - Abl fusion proteinleadingto the expression of the Bcr - Abl fusion protein