Spatial Relationship between Ph and Normal Chromosome 22 at Somatic Metaphase in Chronic Myelogenous Leukemia

Oncology ◽  
1990 ◽  
Vol 47 (3) ◽  
pp. 267-268
Author(s):  
M. Krishna ◽  
R.S. Verma
Keyword(s):  
Chronic Myelogenous Leukemia ◽  
Spatial Relationship ◽  
Normal Chromosome ◽  
Myelogenous Leukemia ◽  
Chromosome 22 ◽  
Somatic Metaphase

scholarly journals Analysis of breakpoints within the bcr gene and their correlation with the clinical course of Philadelphia-positive chronic myelogenous leukemia

Blood ◽  
1988 ◽  
Vol 72 (2) ◽  
pp. 485-490 ◽  
Author(s):  
M Shtalrid ◽  
M Talpaz ◽  
R Kurzrock ◽  
H Kantarjian ◽  
J Trujillo ◽  
...  
Keyword(s):  
Clinical Outcome ◽  
Chronic Myelogenous Leukemia ◽  
Clinical Course ◽  
Philadelphia Chromosome ◽  
Chronic Phase ◽  
Myelogenous Leukemia ◽  
Chromosome 22 ◽  
Blastic Crisis ◽  
Phase Duration ◽  
Dna Fragment

Abstract Chronic myelogenous leukemia (CML) is characterized by a reciprocal translocation between chromosomes 9 and 22. The breakpoints on chromosome 22 are clustered within a 5.8-kilobase (kb) DNA fragment known as the breakpoint cluster region (bcr), which encodes part of a functionally active gene. We analyzed the bcr in DNAs from 108 consecutive, unselected Philadelphia chromosome-positive CML patients by Southern blot and determined five restriction enzyme fragments within which breaks occur on chromosome 22. The exact sublocalization was determined in the DNA of 100 patients. It was found to be within the 5.8-kb in 99 patients and outside the bcr in only one. Within the bcr, most of the breakpoints occurred in fragments 1, 2, and 3. Overall, laboratory and clinical features of CML did not correlate with specific breakpoint fragments, but chronic-phase duration was longer in patients with a breakpoint in fragment 2 of the bcr. Large 3′ bcr deletions were found in nine patients but did not influence clinical outcome. DNA from one of six patients analyzed both during chronic phase and blastic crisis showed an additional aberrant fragment, which suggested that a second abnormal clone developed in blastic crisis.

Position of the Y-chromosome at somatic metaphase in patients with chronic myelogenous leukemia (CML)

1986 ◽  
Vol 42 (4) ◽  
pp. 440-441 ◽  
Author(s):  
R. S. Verma ◽  
S. Thomas ◽  
M. Coleman ◽  
R. T. Silver ◽  
H. Dosik
Keyword(s):  
Y Chromosome ◽  
Chronic Myelogenous Leukemia ◽  
Myelogenous Leukemia ◽  
Somatic Metaphase

scholarly journals Variable breakpoints on the Philadelphia chromosome in chronic myelogenous leukemia

Blood ◽  
1985 ◽  
Vol 66 (1) ◽  
pp. 243-245 ◽  
Author(s):  
D Leibowitz ◽  
K Schaefer-Rego ◽  
DW Popenoe ◽  
JG Mears ◽  
A Bank
Keyword(s):  
Chronic Myelogenous Leukemia ◽  
Southern Blotting ◽  
Philadelphia Chromosome ◽  
Dna Probes ◽  
Chromosome 9 ◽  
Myelogenous Leukemia ◽  
Chromosome 22 ◽  
Human Dna ◽  
Translocation Breakpoints ◽  
The Creation

Abstract The abl oncogene is translocated from chromosome 9 to 22 in the creation of the Philadelphia (Ph1) chromosome. This article describes new translocation breakpoints identified in two patients with chronic myelogenous leukemia using Southern blotting and cloned human DNA probes from chromosome 9. The translocation breakpoints on chromosome 9 in both of these patients lie closer to the human cellular abl (c-abl) gene, and the chromosome 22 breakpoints are distributed more widely than previously reported. These data help to define more clearly the chromosomal span of the breakpoints and indicate that some translocations include very little chromosome 9 sequence located 5′ to the c-abl gene.

scholarly journals Analysis of breakpoints within the bcr gene and their correlation with the clinical course of Philadelphia-positive chronic myelogenous leukemia

Blood ◽  
1988 ◽  
Vol 72 (2) ◽  
pp. 485-490
Author(s):  
M Shtalrid ◽  
M Talpaz ◽  
R Kurzrock ◽  
H Kantarjian ◽  
J Trujillo ◽  
...  
Keyword(s):  
Clinical Outcome ◽  
Chronic Myelogenous Leukemia ◽  
Clinical Course ◽  
Philadelphia Chromosome ◽  
Chronic Phase ◽  
Myelogenous Leukemia ◽  
Chromosome 22 ◽  
Blastic Crisis ◽  
Phase Duration ◽  
Dna Fragment

Chronic myelogenous leukemia (CML) is characterized by a reciprocal translocation between chromosomes 9 and 22. The breakpoints on chromosome 22 are clustered within a 5.8-kilobase (kb) DNA fragment known as the breakpoint cluster region (bcr), which encodes part of a functionally active gene. We analyzed the bcr in DNAs from 108 consecutive, unselected Philadelphia chromosome-positive CML patients by Southern blot and determined five restriction enzyme fragments within which breaks occur on chromosome 22. The exact sublocalization was determined in the DNA of 100 patients. It was found to be within the 5.8-kb in 99 patients and outside the bcr in only one. Within the bcr, most of the breakpoints occurred in fragments 1, 2, and 3. Overall, laboratory and clinical features of CML did not correlate with specific breakpoint fragments, but chronic-phase duration was longer in patients with a breakpoint in fragment 2 of the bcr. Large 3′ bcr deletions were found in nine patients but did not influence clinical outcome. DNA from one of six patients analyzed both during chronic phase and blastic crisis showed an additional aberrant fragment, which suggested that a second abnormal clone developed in blastic crisis.

scholarly journals C-sis and C-abl expression in chronic myelogenous leukemia and other hematologic malignancies

Blood ◽  
1986 ◽  
Vol 67 (3) ◽  
pp. 839-841
Author(s):  
P Romero ◽  
M Blick ◽  
M Talpaz ◽  
E Murphy ◽  
J Hester ◽  
...  
Keyword(s):  
Chronic Myelogenous Leukemia ◽  
Chromosomal Rearrangements ◽  
Philadelphia Chromosome ◽  
Chronic Phase ◽  
Hematologic Malignancies ◽  
Chromosome 9 ◽  
Myelogenous Leukemia ◽  
Chromosome 22 ◽  
Aberrant Expression

Cellular oncogenes have been localized at the breakpoints of characteristic chromosomal rearrangements occurring in certain hematologic malignancies. This has been reported to result in aberrant expression of the involved oncogenes. Over 90% of chronic myelogenous leukemia (CML) is characterized by a reciprocal translocation that brings c-abl from chromosome 9 to chromosome 22, and c-sis from chromosome 22 to chromosome 9. To investigate the possible role of these two oncogenes in the leukemic process, we studied their expression in a number of fresh samples obtained from patients with various forms of leukemia, by Northern blot analysis using c-onc probes. Seven of 24 samples obtained from patients with either CML or chronic myelomonocytic leukemia expressed a normal 4.0-kilobase (kb) c- sis transcript. C-sis expression was found only in the accelerated/blast phases but not in the chronic phase of CML. All of the CML Philadelphia chromosome-positive (Ph1+) samples expressed an aberrant 8-kb c-abl transcript. The expression of c-sis in

scholarly journals C-sis and C-abl expression in chronic myelogenous leukemia and other hematologic malignancies

Blood ◽  
1986 ◽  
Vol 67 (3) ◽  
pp. 839-841 ◽  
Author(s):  
P Romero ◽  
M Blick ◽  
M Talpaz ◽  
E Murphy ◽  
J Hester ◽  
...  
Keyword(s):  
Chronic Myelogenous Leukemia ◽  
Chromosomal Rearrangements ◽  
Philadelphia Chromosome ◽  
Chronic Phase ◽  
Hematologic Malignancies ◽  
Chromosome 9 ◽  
Myelogenous Leukemia ◽  
Chromosome 22 ◽  
Aberrant Expression

Abstract Cellular oncogenes have been localized at the breakpoints of characteristic chromosomal rearrangements occurring in certain hematologic malignancies. This has been reported to result in aberrant expression of the involved oncogenes. Over 90% of chronic myelogenous leukemia (CML) is characterized by a reciprocal translocation that brings c-abl from chromosome 9 to chromosome 22, and c-sis from chromosome 22 to chromosome 9. To investigate the possible role of these two oncogenes in the leukemic process, we studied their expression in a number of fresh samples obtained from patients with various forms of leukemia, by Northern blot analysis using c-onc probes. Seven of 24 samples obtained from patients with either CML or chronic myelomonocytic leukemia expressed a normal 4.0-kilobase (kb) c- sis transcript. C-sis expression was found only in the accelerated/blast phases but not in the chronic phase of CML. All of the CML Philadelphia chromosome-positive (Ph1+) samples expressed an aberrant 8-kb c-abl transcript. The expression of c-sis in

scholarly journals Variable breakpoints on the Philadelphia chromosome in chronic myelogenous leukemia

Blood ◽  
1985 ◽  
Vol 66 (1) ◽  
pp. 243-245
Author(s):  
D Leibowitz ◽  
K Schaefer-Rego ◽  
DW Popenoe ◽  
JG Mears ◽  
A Bank
Keyword(s):  
Chronic Myelogenous Leukemia ◽  
Southern Blotting ◽  
Philadelphia Chromosome ◽  
Dna Probes ◽  
Chromosome 9 ◽  
Myelogenous Leukemia ◽  
Chromosome 22 ◽  
Human Dna ◽  
Translocation Breakpoints ◽  
The Creation

The abl oncogene is translocated from chromosome 9 to 22 in the creation of the Philadelphia (Ph1) chromosome. This article describes new translocation breakpoints identified in two patients with chronic myelogenous leukemia using Southern blotting and cloned human DNA probes from chromosome 9. The translocation breakpoints on chromosome 9 in both of these patients lie closer to the human cellular abl (c-abl) gene, and the chromosome 22 breakpoints are distributed more widely than previously reported. These data help to define more clearly the chromosomal span of the breakpoints and indicate that some translocations include very little chromosome 9 sequence located 5′ to the c-abl gene.

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