scholarly journals Blast crisis

2021 ◽  
Author(s):  
Yuranga Weerakkody
Keyword(s):  
Blast Crisis

Electron Microscopic identification of Pre-B Lymphocytes in the Bone Marrow of a Patient with Chronic Myelocytic Leukemic in Blast Crisis

1982 ◽  
Vol 40 ◽  
pp. 346-347
Author(s):  
T. Mullin ◽  
G. Yee ◽  
M. Aheam ◽  
J. Trujillo
Keyword(s):  
Blast Crisis ◽  
Immunoglobulin M ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Transformation Theory ◽  
Electron Microscopic ◽  
Chemotherapeutic Sensitivity ◽  
Microscopic Studies ◽  
Hematopoietic Precursor ◽  
Lymphoblastic Transformation ◽  
B Lineage

There have been numerous reports in the current literature suggesting that hematopoietic precursor cells in some human chronic myelocytic leukemias (CML) undergo lymphoblastic transformation at the time of the acute blast crisis (BC) stage. The primary evidence offered in support of this transformation theory--lymphoblastic appearing morphology, increased terminal deoxynucleotidyl transferase (TdT) activity, and chemotherapeutic sensitivity to vincristine and prednisone--has been indirect, however, since these features may occur in nonlymphoid cells. More direct support for the Pre-B lineage of these cells has recently been provided by immunofluorescent light microscopic studies demonstrating the presence of intracytoplasmic immunoglobulin M (IgM) in these CML-BC cells.

Expression of a Multidrug Resistance Gene in Blast Crisis of Chronic Myelogenous Leukemia

1989 ◽  
Vol 1 (2) ◽  
pp. 141-144 ◽  
Author(s):  
Robert Pirker ◽  
Lori J. Goldstein ◽  
Heinz Ludwig ◽  
Werner Linkesch ◽  
Christina Lechner ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Resistance Gene ◽  
Chronic Myelogenous Leukemia ◽  
Blast Crisis ◽  
Myelogenous Leukemia ◽  
Multidrug Resistance Gene

Meningeal Leukemia following Lymphoid Blast Crisis in Chronic Myeloid Leukemia: Therapeutic Implications

1982 ◽  
Vol 68 (3) ◽  
pp. 257-263 ◽  
Author(s):  
Mario Cazzola ◽  
Giulio Nalli ◽  
Ercole Brusamolino ◽  
Maurizio Daccò ◽  
Angela Ghizzi ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Chronic Myeloid Leukemia ◽  
Complete Remission ◽  
Myeloid Leukemia ◽  
Lymphoblastic Leukemia ◽  
Blast Crisis ◽  
Early Prevention ◽  
Therapeutic Implications ◽  
Therapeutic Protocol ◽  
Meningeal Leukemia

Five of 40 patients with chronic myeloid leukemia (CML) had lymphoid blast crisis and 4 of them achieved complete remission of metamorphosis with vincristine and prednisone. While in hematologic remission, two of these subjects developed meningeal leukemia. Clinical and biologic data indicated that the course of the disease after lymphoid blast crisis was very similar to that of acute lymphoblastic leukemia (ALL). It is suggested that patients with CML who develop lymphoid blast crisis should be treated with an intensive therapeutic protocol including early prevention of meningeal leukemia.

Pernio as the presenting sign of blast crisis in acute lymphoblastic leukemia

2017 ◽  
Vol 35 (1) ◽  
pp. e74-e75 ◽  
Author(s):  
Kelly K. Park ◽  
Bailey Tayebi ◽  
Lily Uihlein ◽  
Jodi Speiser ◽  
Adnan Mir ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Lymphoblastic Leukemia ◽  
Blast Crisis

scholarly journals Clonal evolution and clinical implications of genetic abnormalities in blastic transformation of chronic myeloid leukaemia

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yotaro Ochi ◽  
Kenichi Yoshida ◽  
Ying-Jung Huang ◽  
Ming-Chung Kuo ◽  
Yasuhito Nannya ◽  
...  
Keyword(s):  
Chronic Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Kinase Inhibitors ◽  
Blast Crisis ◽  
Clonal Evolution ◽  
Chronic Phase ◽  
Genetic Alterations ◽  
Prognostic Impact ◽  
Genetic Abnormalities ◽  
Prior Use

AbstractBlast crisis (BC) predicts dismal outcomes in patients with chronic myeloid leukaemia (CML). Although additional genetic alterations play a central role in BC, the landscape and prognostic impact of these alterations remain elusive. Here, we comprehensively investigate genetic abnormalities in 136 BC and 148 chronic phase (CP) samples obtained from 216 CML patients using exome and targeted sequencing. One or more genetic abnormalities are found in 126 (92.6%) out of the 136 BC patients, including the RUNX1-ETS2 fusion and NBEAL2 mutations. The number of genetic alterations increase during the transition from CP to BC, which is markedly suppressed by tyrosine kinase inhibitors (TKIs). The lineage of the BC and prior use of TKIs correlate with distinct molecular profiles. Notably, genetic alterations, rather than clinical variables, contribute to a better prediction of BC prognosis. In conclusion, genetic abnormalities can help predict clinical outcomes and can guide clinical decisions in CML.

Myeloid Neoplasm with t(8;22)(p11;q11): A Mimicker of Chronic Myeloid Leukaemia in Blast Crisis

2020 ◽  
Author(s):  
Gargi Kapatia ◽  
Arun Sasikumar Nair Remani ◽  
Shano Naseem ◽  
Mayur Parihar ◽  
Sreejesh Sreedharanunni
Keyword(s):  
Chronic Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Blast Crisis ◽  
Myeloid Neoplasm

RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR-ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance

Blood ◽  
2008 ◽  
Vol 111 (7) ◽  
pp. 3735-3741 ◽  
Author(s):  
Catherine Roche-Lestienne ◽  
Lauréline Deluche ◽  
Sélim Corm ◽  
Isabelle Tigaud ◽  
Sami Joha ◽  
...  
Keyword(s):  
Dna Binding ◽  
High Frequency ◽  
Trisomy 21 ◽  
De Novo ◽  
Blast Crisis ◽  
Clonal Evolution ◽  
Chronic Phase ◽  
Chromosome 21 ◽  
Imatinib Resistance ◽  
Molecular Abnormalities

Abstract Acquired molecular abnormalities (mutations or chromosomal translocations) of the RUNX1 transcription factor gene are frequent in acute myeloblastic leukemias (AMLs) and in therapy-related myelodysplastic syndromes, but rarely in acute lymphoblastic leukemias (ALLs) and chronic myelogenous leukemias (CMLs). Among 18 BCR-ABL+ leukemias presenting acquired trisomy of chromosome 21, we report a high frequency (33%) of recurrent point mutations (4 in myeloid blast crisis [BC] CML and one in chronic phase CML) within the DNA-binding region of RUNX1. We did not found any mutation in de novo BCR-ABL+ ALLs or lymphoid BC CML. Emergence of the RUNX1 mutations was detected at diagnosis or before the acquisition of trisomy 21 during disease progression. In addition, we also report a high frequency of cryptic chromosomal RUNX1 translocation to a novel recently described gene partner, PRDM16 on chromosome 1p36, for 3 (21.4%) of 14 investigated patients: 2 myeloid BC CMLs and, for the first time, 1 therapy-related BCR-ABL+ ALL. Two patients presented both RUNX1 mutations and RUNX1-PRDM16 fusion. These events are associated with a short survival and support the concept of a cooperative effect of BCR-ABL with molecular RUNX1 abnormalities on the differentiation arrest phenotype observed during progression of CML and in BCR-ABL+ ALL.

Sign in / Sign up

Export Citation Format

Share Document