Abstract 1946
Background
Bone marrow aspiration and biopsy at presentation is important to demonstrate the phase of the disease, to provide material for cytogenetic studies and to demonstrate the myelofibrosis, which have prognostic and therapeutic implications. In the current era of molecular diagnostics, the role of bone marrow examination is questionable. The present study was designed to identify the role of bone marrow examination on phase migration, karyotyping and myelofibrosis.
Methods
Data of newly diagnosed CML patients seen between January 2013 and June 2018 was retrospectively analysed. CML was confirmed by demonstration of BCR-ABL fusion gene by PCR or FISH. Patients were stratified into chronic phase (CP), accelerated phase (AP) and blast phase (BP) according to WHO diagnostic criteria (2016).
Results
Of 749 patients, 541 patients had evaluable data. The male female ratio was 1.52:1 The median age at presentation was 37 years (range, 9-80 years). According to EUTOS risk stratification, 406 (75.1%) patients were low risk and 135(24.9%) were high risk. Based on bone marrow blasts criterion, phase migration occurred in 16 (2.9%). Of these 16 patients, phase migration from CP to AP, CP to BP and AP to BP were seen in 8 (50%), 4(25%) and 4 (25%) patients, respectively. Data on karyotyping was available in 195 (36%) patients. Of 195 patients, additional cytogenetic abnormalities were detected in 30 (15.3%) which includes, major route abnormalities in 11 (5.6%) patients. Of these 11 patients, 6 patients were in CP, 4 patients were in AP and 1 patient in BP. Myelofibrosis was demonstrated in 264 (48.7%) patients of which grade 1, grade 2, grade 3 and grade 4 were seen in 72 (13.3%), 100 (18.5%), 70 (12.9%); 20 (3.7%) patients respectively.
Conclusions
Bone marrow examination at presentation in CML patients results in phase migration, provides adequate material for cytogenetic studies and demonstrates presence of myelofibrosis. Hence, bone marrow examination is indispensable in newly diagnosed CML patients.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
Nizam’s Institute of Medical Sciences.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.
Resources from the same session
3309 - Heat Shock Protein 90 chaperones and Protein Kinase D3 regulates androgen-independent prostate cancer development
Presenter: Attila Varga
Session: Poster Display session 1
Resources:
Abstract
3441 - The SWI/SNF driven reprograming for the AR cistrome is NSD2 dependent
Presenter: Katia Ruggero
Session: Poster Display session 1
Resources:
Abstract
1659 - IGF1R inhibition affects the survival of HT29 cancer cells by alterations of the TLR9- and autophagy signaling
Presenter: Györgyi Műzes
Session: Poster Display session 1
Resources:
Abstract
1379 - Characterization of atypical dMMR (deficient MisMatch Repair) tumors: a study from a large cohort of 4948 cases
Presenter: Marion Jaffrelot
Session: Poster Display session 1
Resources:
Abstract
1657 - Modulation of TLR9-dependent autophagy response via inhibition of c-Met signaling influences the survival of HT29 cancer cells
Presenter: Ferenc Sipos
Session: Poster Display session 1
Resources:
Abstract
3045 - Positive Feedback Activation of Notch Signal by Obesity Enhances Colorectal Tumorigenicity
Presenter: Dake Chu
Session: Poster Display session 1
Resources:
Abstract
2285 - The Pathological and Functional Roles of BRPF1 in Hepatocellular Carcinoma
Presenter: Lai Hung Carol Cheng
Session: Poster Display session 1
Resources:
Abstract
3210 - Protein tyrosine phosphatase non-receptor type 3 (PTPN3) could be a new therapeutic target for pancreatic cancer.
Presenter: Akio Yamasaki
Session: Poster Display session 1
Resources:
Abstract
3920 - A Novel bispecific BCMAxCD3 T cell engaging antibody that treat multiple myeloma (MM) with minimal cytokine serection
Presenter: Zhenyu Li
Session: Poster Display session 1
Resources:
Abstract
2691 - Quantitative spatial profiling of lymphocyte-activation gene 3 (LAG-3)/major histocompatibility complex class II (MHC II) interaction in gastric and urothelial tumors
Presenter: Cyrus Hedvat
Session: Poster Display session 1
Resources:
Abstract