scholarly journals CCN3 suppresses mitogenic signalling and reinstates growth control mechanisms in Chronic Myeloid Leukaemia

2011 ◽  
Vol 6 (1) ◽  
pp. 27-35 ◽  
Author(s):  
Lynn McCallum ◽  
Wanhua Lu ◽  
Susan Price ◽  
Noureddine Lazar ◽  
Bernard Perbal ◽  
...  
Keyword(s):  
Chronic Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Growth Control ◽  
Control Mechanisms ◽  
Mitogenic Signalling

Haematological Disease Pattern at Specialized HOPD - A study in Bangabandhu Sheikh Mujib Medical University

2018 ◽  
Vol 2 (02) ◽  
pp. 39-41
Author(s):  
Md. Rafiquzzaman Khan ◽  
Arifur Rahman ◽  
Khaza Amirul Islam ◽  
AQM Ashraful Haque ◽  
Masuda Begum
Keyword(s):  
Iron Deficiency ◽  
Chronic Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Iron Deficiency Anaemia ◽  
Beta Thalassemia ◽  
Female Ratio ◽  
Deficiency Anaemia ◽  
Beta Thalassaemia ◽  
Hb E ◽  
Medical University

The aim of this retrospective observational study was to observe the pattern and frequency of haematological disorders among the patients attending in the specialized Haematology outpatient Department (HOPD) in Bangabandhu Sheikh Mujib Medical University. Consecutive 201 patients over the period of one year were enrolled. Their age ranged from 01 to 72 years with a mean age of 36.76 years. Most of the patients (34.3%) were in between the ages of 31 to 45 years followed by 16 to 30 years (27.9%). Male to female ratio was 0.65. Iron deficiency anaemia is the most common (24.9%) followed by chronic myeloid leukaemia (11.9%), Hb E beta thalassaemia (9.5%), idiopathic thrombocytopenic purpura (9.5%), beta thalassaemia trait (7.0%), Hb E trait (5.5 %), aplastic anaemia (5.0%), multiple myeloma (3.5%), acute lymphoblastic leukaemia (3.0%). Acute myeloid leukaemia, autoimmune haemolytic anaemia, chronic lymphocytic leukaemia, anaemia of chronic disease, non-Hodgkin lymphoma, polycythaemia, beta thalassemia major and alpha thalassemia was 2.5%, 2.5%, 2.0%, 1.5%, 1.5%, 1.5%, 1.0% and 1.0%, respectively. In the present study, we observed that iron deficiency anaemia the most common non-malignant disease and chronic myeloid leukaemia is the common haematological malignancy.

Chronic Myeloid Leukaemia

2017 ◽  
Vol 1 (01) ◽  
pp. 16-22
Author(s):  
Mohiuddin Ahmed Khan ◽  
Mafruh Akter ◽  
Muhammad Kamruzzaman
Keyword(s):  
Chronic Myeloid Leukaemia ◽  
Myeloid Leukaemia

TKI dose reduction can effectively maintain major molecular remission in patients with chronic myeloid leukaemia

2020 ◽  
Author(s):  
Simone Claudiani ◽  
Jane F. Apperley ◽  
Richard Szydlo ◽  
Afzal Khan ◽  
George Nesr ◽  
...  
Keyword(s):  
Chronic Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Dose Reduction ◽  
Molecular Remission

CHRONIC MYELOID LEUKÆMIA: A STUDY OF 86 PATIENTS

1959 ◽  
Vol 2 (3) ◽  
pp. 75-84
Author(s):  
C. K. Hamblt ◽  
T. I. Robertson
Keyword(s):  
Chronic Myeloid Leukaemia ◽  
Myeloid Leukaemia

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.

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