THE PH1-CHROMOSOME: TRANSLOCATION TO CHROMOSOME 9

The Lancet ◽  
1973 ◽  
Vol 302 (7836) ◽  
pp. 1030-1031 ◽  
Author(s):  
H. Van Den Berghe
Keyword(s):  
Chromosome Translocation ◽  
Chromosome 9

scholarly journals Chromosome 3q21 abnormalities associated with hyperactive thrombopoiesis in acute blastic transformation of chronic myeloid leukemia

Blood ◽  
1986 ◽  
Vol 68 (3) ◽  
pp. 652-657 ◽  
Author(s):  
R Bernstein ◽  
A Bagg ◽  
M Pinto ◽  
D Lewis ◽  
B Mendelow
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
De Novo ◽  
Chromosome Translocation ◽  
Chromosome 9 ◽  
Chromosome 3 ◽  
Acute Megakaryoblastic Leukemia ◽  
Blastic Transformation ◽  
Megakaryoblastic Leukemia ◽  
Platelet Counts

Abstract Two patients with acute blastic transformation of chronic myeloid leukemia (CML) associated with strikingly elevated platelet counts showed abnormalities of chromosome 3q in addition to the standard Philadelphia (Ph1) chromosome translocation. The first patient had an inversion of chromosome 3 (q21q26) cytologically identical to an inversion 3 previously reported in de novo acute megakaryoblastic leukemia, and the second patient showed a translocation between chromosome 3q and the chromosome 9 homologue not involved in the Ph1 translocation, [t(3;9)(q21;q34)]. Previous studies had incriminated either 3q21 or 3q26 as the locus for a regulatory thrombopoietic gene, but the current study suggests that 3q21 is the relevant site.

The (6;9) chromosome translocation, associated with a specific subtype of acute nonlymphocytic leukemia, leads to aberrant transcription of a target gene on 9q34

1990 ◽  
Vol 10 (8) ◽  
pp. 4016-4026
Author(s):  
M von Lindern ◽  
A Poustka ◽  
H Lerach ◽  
G Grosveld
Keyword(s):  
Long Range ◽  
Cdna Cloning ◽  
Target Gene ◽  
Chromosomal Translocation ◽  
Chromosome Translocation ◽  
Chromosome 9 ◽  
Chromosome 6 ◽  
Acute Nonlymphocytic Leukemia ◽  
Chromosome Walking ◽  
Chromosome Isolation

The specific (6;9)(p23;q34) chromosomal translocation is associated with a defined subtype of acute nonlymphocytic leukemia (ANLL). The 9q34 breakpoint is located at the telomeric side of the c-abl gene. Through a combination of chromosome jumping, long-range mapping, and chromosome walking, the chromosome 9 breakpoints of several t(6;9) ANLL patients were localized within a defined region of 8 kilobases (kb), 360 kb telomeric of c-abl. Subsequent cDNA cloning revealed that this region represented an intron in the middle of a gene, called Cain (can), encoding a 7.5-kb transcript. Disruption of the can gene by the translocation resulted in the expression of a new 5.5-kb can mRNA from the 6p- chromosome. Isolation of chromosome 6 sequences showed that breakpoints on 6p23 also clustered within a limited stretch of DNA. These data strongly suggest a direct involvement of the translocation in the leukemic process of t(6;9) ANLL.

scholarly journals Chromosome 3q21 abnormalities associated with hyperactive thrombopoiesis in acute blastic transformation of chronic myeloid leukemia

Blood ◽  
1986 ◽  
Vol 68 (3) ◽  
pp. 652-657
Author(s):  
R Bernstein ◽  
A Bagg ◽  
M Pinto ◽  
D Lewis ◽  
B Mendelow
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
De Novo ◽  
Chromosome Translocation ◽  
Chromosome 9 ◽  
Chromosome 3 ◽  
Acute Megakaryoblastic Leukemia ◽  
Blastic Transformation ◽  
Megakaryoblastic Leukemia ◽  
Platelet Counts

Two patients with acute blastic transformation of chronic myeloid leukemia (CML) associated with strikingly elevated platelet counts showed abnormalities of chromosome 3q in addition to the standard Philadelphia (Ph1) chromosome translocation. The first patient had an inversion of chromosome 3 (q21q26) cytologically identical to an inversion 3 previously reported in de novo acute megakaryoblastic leukemia, and the second patient showed a translocation between chromosome 3q and the chromosome 9 homologue not involved in the Ph1 translocation, [t(3;9)(q21;q34)]. Previous studies had incriminated either 3q21 or 3q26 as the locus for a regulatory thrombopoietic gene, but the current study suggests that 3q21 is the relevant site.

CYTOLOGY AND GENETICS OF T(9,11) IN THE GERMAN COCKROACH, AND ITS RELATIONSHIP TO OTHER CHROMOSOME 9 TRAITS

1974 ◽  
Vol 16 (3) ◽  
pp. 639-649 ◽  
Author(s):  
Donald G. Cochran ◽  
Mary H. Ross
Keyword(s):  
Sex Differences ◽  
Linkage Group ◽  
Blattella Germanica ◽  
German Cockroach ◽  
Chromosome Translocation ◽  
Chromosome 9 ◽  
Linkage Data ◽  
Wild Type ◽  
Cytological Data ◽  
Cockroach Blattella Germanica

A new chromosome translocation in the German cockroach, Blattella germanica, was studied. Cytologically, it involves chromosomes 9 and 11 and was designated T(9,11). The approximate positions of the breakpoints were determined. In chromosome 9, the distance between the breakpoint and Df(9)Pw was measured. Genetically, linkage of T(9,11) with the chromosome 9 marker, ru, was estimated at 1.1 ± 0.6%. The new chromosome 9 breakpoint and available linkage data were used to approximate the location of the linkage group on the chromosome. An attempt to correlate map and chromosome distances indicated chromosome 9 probably has a total of at least 50 crossover units.Crosses between T(9, 11) heterozygotes and wild type showed significant sex differences in oothecal size and percent hatch. In males, the hatch data suggested preferential alternate disjunction. This was confirmed cytologically by examination of metaphase I and prophase II cells. In females, the hatch data suggested random disjunction. Similar hatch and cytological data are included for T(9,10)Pw and T(2,11)Cu. Intercrosses of T(9,11) were largely sterile, precluding the attempt to test for a viable homozygote.

scholarly journals Searching for Genes for Cleft Lip and/or Palate Based on Breakpoint Analysis of a Balanced Translocation t(9;17)(q32;q12)

2009 ◽  
Vol 46 (5) ◽  
pp. 532-540 ◽  
Author(s):  
Junichiro Machida ◽  
Têmis M. Félix ◽  
Jeffrey C. Murray ◽  
Koh-ichiro Yoshiura ◽  
Mitsuyo Tanemura ◽  
...  
Keyword(s):  
Positional Cloning ◽  
Cleft Lip ◽  
Cleft Lip And Palate ◽  
Chromosome Translocation ◽  
Chromosome 9 ◽  
Chromosome 17 ◽  
Nucleotide Polymorphisms ◽  
Balanced Translocation ◽  
Japanese Family ◽  
Chemokine Ligand

Objective: Identification of the breakpoints of disease-associated chromosome rearrangements can provide informative clues to a positional cloning approach for genes responsible for inherited diseases. Recently, we found a three-generation Japanese family segregating balanced chromosome translocation t(9;17)(q32;q12). One of the subjects had cleft lip and palate. We examined whether regions near the breakpoint could be associated with cleft lip and/or palate. Methods: We determined the breakpoints involved in the translocation by fluorescence in situ hybridization analysis and subsequent long-range polymerase chain reaction. In order to study the role of these disrupted regions in nonsyndromic cleft lip and/or palate, we performed mutation analysis and a haplotype-based transmission disequilibrium test using tagging single-nucleotide polymorphisms in the flanking regions of the breakpoints in white and Filipino nonsyndromic cleft lip and/or palate populations. Results: Sequence analysis demonstrated that two genes, SLC31A1 (solute carrier family 31 member 1) on chromosome 9 and CCL2 (chemokine ligand 2) on chromosome 17, were rearranged with the breaks occurring within their introns. It is interesting that SLC31A1 lies closed to BSPRY (B-box and SPRY domain), which is a candidate for involvement with cleft lip and/or palate. Some of the variants in BSPRY and CCL2 showed significant p values in the cleft lip and/or palate population compared with the control population. There was also statistically significant evidence of transmission distortion for haplotypes on both chromosomes 9 and 17. Conclusions: The data support previous reports that genes on chromosomal regions of 9q and 17q play an important role in facial development.

scholarly journals The (6;9) chromosome translocation, associated with a specific subtype of acute nonlymphocytic leukemia, leads to aberrant transcription of a target gene on 9q34.

1990 ◽  
Vol 10 (8) ◽  
pp. 4016-4026 ◽  
Author(s):  
M von Lindern ◽  
A Poustka ◽  
H Lerach ◽  
G Grosveld
Keyword(s):  
Long Range ◽  
Cdna Cloning ◽  
Target Gene ◽  
Chromosomal Translocation ◽  
Chromosome Translocation ◽  
Chromosome 9 ◽  
Chromosome 6 ◽  
Acute Nonlymphocytic Leukemia ◽  
Chromosome Walking ◽  
Chromosome Isolation

The specific (6;9)(p23;q34) chromosomal translocation is associated with a defined subtype of acute nonlymphocytic leukemia (ANLL). The 9q34 breakpoint is located at the telomeric side of the c-abl gene. Through a combination of chromosome jumping, long-range mapping, and chromosome walking, the chromosome 9 breakpoints of several t(6;9) ANLL patients were localized within a defined region of 8 kilobases (kb), 360 kb telomeric of c-abl. Subsequent cDNA cloning revealed that this region represented an intron in the middle of a gene, called Cain (can), encoding a 7.5-kb transcript. Disruption of the can gene by the translocation resulted in the expression of a new 5.5-kb can mRNA from the 6p- chromosome. Isolation of chromosome 6 sequences showed that breakpoints on 6p23 also clustered within a limited stretch of DNA. These data strongly suggest a direct involvement of the translocation in the leukemic process of t(6;9) ANLL.

A Unique, Complex Variant Philadelphia Chromosome Translocation in a Patient With Typical Chronic Myelogenous Leukemia

2001 ◽  
Vol 125 (3) ◽  
pp. 437-439
Author(s):  
Raida Oudat ◽  
Zebunnisa Khan ◽  
Armand B. Glassman
Keyword(s):  
Chronic Myelogenous Leukemia ◽  
Chromosomal Abnormalities ◽  
Philadelphia Chromosome ◽  
Chronic Phase ◽  
Chromosome Translocation ◽  
Chromosome 9 ◽  
Myelogenous Leukemia ◽  
Chromosome 11 ◽  
Ph Chromosome ◽  
Conventional Cytogenetics

Abstract The Philadelphia (Ph) chromosome [der(22) t(9;22)(q34;q11)] is the characteristic chromosomal abnormality found in chronic myelogenous leukemia (CML). This chromosome has been reported in patients with other chromosomal abnormalities. In this study, we describe a patient with hematologically typical chronic-phase CML with an unusual and complex translocation involving chromosomes 9, 11, and 22. These complex translocations were identified by G-banded conventional cytogenetics and confirmed by fluorescence in situ hybridization (FISH) using whole chromosome painting probes (wcp). To the best of our knowledge, these are unique translocations involving the short and the long arms of chromosome 9 in 4 different translocations with the short arm of chromosome 11 and the long arm of chromosome 22.

Examination of the dynamics of global DNA methylation pattern establishment during spermatogenesiss

2007 ◽  
Vol 30 (4) ◽  
pp. 90
Author(s):  
Kirsten Niles ◽  
Sophie La Salle ◽  
Christopher Oakes ◽  
Jacquetta Trasler
Keyword(s):  
Dna Methylation ◽  
Germ Cell ◽  
Germ Cells ◽  
Epigenetic Modification ◽  
Methylation Pattern ◽  
Chromosome 9 ◽  
Specific Gene ◽  
Global Methylation ◽  
Dna Methylation Pattern ◽  
Methylation Patterns

Background: DNA methylation is an epigenetic modification involved in gene expression, genome stability, and genomic imprinting. In the male, methylation patterns are initially erased in primordial germ cells (PGCs) as they enter the gonadal ridge; methylation patterns are then acquired on CpG dinucleotides during gametogenesis. Correct pattern establishment is essential for normal spermatogenesis. To date, the characterization and timing of methylation pattern acquisition in PGCs has been described using a limited number of specific gene loci. This study aimed to describe DNA methylation pattern establishment dynamics during male gametogenesis through global methylation profiling techniques in a mouse model. Methods: Using a chromosome based approach, primers were designed for 24 regions spanning chromosome 9; intergenic, non-repeat, non-CpG island sequences were chosen for study based on previous evidence that these types of sequences are targets for testis-specific methylation events. The percent methylation was determined in each region by quantitative analysis of DNA methylation using real-time PCR (qAMP). The germ cell-specific pattern was determined by comparing methylation between spermatozoa and liver. To examine methylation in developing germ cells, spermatogonia from 2 day- and 6 day-old Oct4-GFP (green fluorescent protein) mice were isolated using fluorescence activated cell sorting. Results: As compared to liver, four loci were hypomethylated and five loci were hypermethylated in spermatozoa, supporting previous results indicating a unique methylation pattern in male germ cells. Only one region was hypomethylated and no regions were hypermethylated in day 6 spermatogonia as compared to mature spermatozoa, signifying that the bulk of DNA methylation is established prior to type A spermatogonia. The methylation in day 2 spermatogonia, germ cells that are just commencing mitosis, revealed differences of 15-20% compared to day 6 spermatogonia at five regions indicating that the most crucial phase of DNA methylation acquisition occurs prenatally. Conclusion: Together, these studies provide further evidence that germ cell methylation patterns differ from those in somatic tissues and suggest that much of methylation at intergenic sites is acquired during prenatal germ cell development. (Supported by CIHR)

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