Treatment of Chronic and Acute Phase Chronic Myelogenous Leukemia with Interferon-α2b and, Interferon-γ

1988 ◽  
pp. 119-128 ◽  
Author(s):  
N. Niederle ◽  
O. Kloke ◽  
R. Osieka ◽  
D. May ◽  
U. B. Wandl ◽  
...  
Keyword(s):  
Chronic Myelogenous Leukemia ◽  
Acute Phase ◽  
Interferon Γ ◽  
Myelogenous Leukemia ◽  
Interferon Α2b

Chromosome changes in a patient achieving complete remission in the acute phase of chronic myelogenous leukemia

1979 ◽  
Vol 6 (2) ◽  
pp. 155-161 ◽  
Author(s):  
Ronald Stern ◽  
Julie Sorenson ◽  
Doris H. Wurster-Hill ◽  
Gibbons G. Cornwell ◽  
O. Ross McIntyre
Keyword(s):  
Complete Remission ◽  
Chronic Myelogenous Leukemia ◽  
Acute Phase ◽  
Myelogenous Leukemia

scholarly journals CML-T1: a cell line derived from T-lymphocyte acute phase of chronic myelogenous leukemia

Blood ◽  
1989 ◽  
Vol 74 (4) ◽  
pp. 1381-1387 ◽  
Author(s):  
K Kuriyama ◽  
RP Gale ◽  
M Tomonaga ◽  
S Ikeda ◽  
E Yao ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Line ◽  
Chronic Myelogenous Leukemia ◽  
Acute Phase ◽  
T Lymphocyte ◽  
Messenger Rna ◽  
Chromosome 9 ◽  
Myelogenous Leukemia ◽  
Hematopoietic Stem ◽  
Ph Chromosome

Abstract Most data suggest that malignant transformation in chronic myelogenous leukemia (CML) occurs in hematopoietic stem cell that is the progenitor of myelopoiesis and of B but not T lymphopoiesis. We established a T- lymphoid cell line (CML-T1) from a person with Ph-chromosome-negative CML in acute phase. Evidence of its T-lymphocyte origin includes the pattern cytochemical reactivity, reactivity with anti-T-cell monoclonal antibodies (MoAbs), and rearrangement of the beta-T-cell receptor (TCRB) gene. CML-T1 cells have features of type IV thymocytes. Cytogenetic analyses indicate a 47,XX, del(11), t(6;7)(q23;q24), +mar karyotype. CML-T1 cells exhibit molecular changes typical of CML, including translocation of the ABL protooncogene from chromosome 9 to 22, rearrangement of the BCR gene, and transcription of a chimeric BCR- ABL messenger RNA (mRNA). The ABL insertion on chromosome 22 appears interstitial, similar to other cases of Ph-chromosome-negative CML. These data clearly indicate that T cells can be involved in acute-phase CML. CML-T1 should be useful in studying this process as well as that underlying Ph-chromosome-negative CML.

scholarly journals p53 in chronic myelogenous leukemia in acute phase.

1991 ◽  
Vol 88 (14) ◽  
pp. 6293-6297 ◽  
Author(s):  
E. Feinstein ◽  
G. Cimino ◽  
R. P. Gale ◽  
G. Alimena ◽  
R. Berthier ◽  
...  
Keyword(s):  
Chronic Myelogenous Leukemia ◽  
Acute Phase ◽  
Myelogenous Leukemia

Interferon-α2b in Chronic Myelogenous Leukemia: Experience with Two Treatment Regimen

1990 ◽  
pp. 515-524
Author(s):  
M. Freund ◽  
P. von Wussow ◽  
F. Hild ◽  
F. Buchholz ◽  
Th. Buhr ◽  
...  
Keyword(s):  
Treatment Regimen ◽  
Chronic Myelogenous Leukemia ◽  
Myelogenous Leukemia ◽  
Interferon Α2b

Rearrangements in the p53 gene in Philadelphia chromosome positive chronic myelogenous leukemia [see comments]

Blood ◽  
1989 ◽  
Vol 74 (7) ◽  
pp. 2318-2324 ◽  
Author(s):  
Z Kelman ◽  
M Prokocimer ◽  
S Peller ◽  
Y Kahn ◽  
G Rechavi ◽  
...  
Keyword(s):  
Chronic Myelogenous Leukemia ◽  
Acute Phase ◽  
Southern Blot Analysis ◽  
Philadelphia Chromosome ◽  
P53 Gene ◽  
Myelogenous Leukemia ◽  
Chromosome 17 ◽  
Blastic Crisis ◽  
Significant Incidence ◽  
Philadelphia Chromosome Positive

Molecular structural analysis of the p53 gene in patients with Philadelphia chromosome-positive chronic myelogenous leukemia (CML) indicates a significant incidence of gene rearrangements in patients at either accelerated phase or blastic crisis. Southern blot analysis of genomic DNA hybridizing with either genomic or cDNA p53 specific probes indicated that 30% of the CML patients at blastic crisis phase exhibited rearrangements, mostly mapping downstream to the first non- coding exon. This is compatible with the observation that the progression of CML from the chronic to the acute phase involves frequent aberrations in chromosome 17, to which the p53 oncogene has been mapped. Therefore, we suggest that one of the pathways of development of CML to the acute phase is associated with aberrations in the p53 nuclear oncogene.

HLA class II–restricted antigen presentation of endogenous bcr-abl fusion protein by chronic myelogenous leukemia–derived dendritic cells to CD4+ T lymphocytes

Blood ◽  
2001 ◽  
Vol 98 (5) ◽  
pp. 1498-1505 ◽  
Author(s):  
Masaki Yasukawa ◽  
Hideki Ohminami ◽  
Kensuke Kojima ◽  
Takaaki Hato ◽  
Atsuhiko Hasegawa ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
T Lymphocytes ◽  
Fusion Protein ◽  
Chronic Myelogenous Leukemia ◽  
T Lymphocyte ◽  
Class Ii ◽  
Interferon Γ ◽  
Fusion Peptide ◽  
Hla Class Ii ◽  
Myelogenous Leukemia

Bcr-abl fusion peptide–specific CD4+ T-lymphocyte clones have recently been shown to augment colony formation by chronic myelogenous leukemia (CML) cells in a bcr-abl type-specific and HLA class II–restricted manner without addition of exogenous antigen. These findings suggest that CML cells can naturally process and present endogenous bcr-abl fusion protein to CD4+ T lymphocytes in the context of HLA class II molecules. To verify this possibility, the ability of CML-derived dendritic cells (DCs) to present endogenous bcr-abl fusion protein to bcr-abl fusion peptide–specific CD4+ T-lymphocyte clones was investigated. The bcr-abl b3a2 peptide–specific and HLA-DRB1*0901–restricted CD4+T-lymphocyte clones produced interferon-γ in response to stimulation with monocyte-derived DCs from HLA-DRB1*0901+ patients with b3a2 type CML. In contrast, DCs from patients with HLA-DRB1*0901− or b2a2 type CML and those from healthy individuals did not exert stimulatory activity on bcr-abl–specific CD4+ T-lymphocyte clones. The response of CD4+T-lymphocyte clones to CML-derived mature DCs was higher than that to immature DCs and was inhibited by anti–HLA-DR monoclonal antibody. These data suggest that CML-derived DCs can process and present endogenous bcr-abl fusion protein to CD4+ T lymphocytes.

scholarly journals Rearrangements in the p53 gene in Philadelphia chromosome positive chronic myelogenous leukemia [see comments]

Blood ◽  
1989 ◽  
Vol 74 (7) ◽  
pp. 2318-2324 ◽  
Author(s):  
Z Kelman ◽  
M Prokocimer ◽  
S Peller ◽  
Y Kahn ◽  
G Rechavi ◽  
...  
Keyword(s):  
Chronic Myelogenous Leukemia ◽  
Acute Phase ◽  
Southern Blot Analysis ◽  
Philadelphia Chromosome ◽  
P53 Gene ◽  
Myelogenous Leukemia ◽  
Chromosome 17 ◽  
Blastic Crisis ◽  
Significant Incidence ◽  
Philadelphia Chromosome Positive

Abstract Molecular structural analysis of the p53 gene in patients with Philadelphia chromosome-positive chronic myelogenous leukemia (CML) indicates a significant incidence of gene rearrangements in patients at either accelerated phase or blastic crisis. Southern blot analysis of genomic DNA hybridizing with either genomic or cDNA p53 specific probes indicated that 30% of the CML patients at blastic crisis phase exhibited rearrangements, mostly mapping downstream to the first non- coding exon. This is compatible with the observation that the progression of CML from the chronic to the acute phase involves frequent aberrations in chromosome 17, to which the p53 oncogene has been mapped. Therefore, we suggest that one of the pathways of development of CML to the acute phase is associated with aberrations in the p53 nuclear oncogene.

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