scholarly journals Megakaryocytes harbour the del(5q) abnormality despite complete clinical and cytogenetic remission induced by lenalidomide treatment

2018 ◽  
Vol 180 (4) ◽  
pp. 526-533 ◽  
Author(s):  
Christian Scharenberg ◽  
Monika Jansson ◽  
Leonie Saft ◽  
Eva Hellström-Lindberg
Keyword(s):  
Cytogenetic Remission

scholarly journals Polyclonal hematopoiesis in interferon-induced cytogenetic remissions of chronic myelogenous leukemia

Blood ◽  
1992 ◽  
Vol 79 (4) ◽  
pp. 997-1002 ◽  
Author(s):  
D Claxton ◽  
A Deisseroth ◽  
M Talpaz ◽  
C Reading ◽  
H Kantarjian ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Gene Polymorphism ◽  
Chronic Myelogenous Leukemia ◽  
Myelogenous Leukemia ◽  
Hematopoietic Stem ◽  
Clonality Analysis ◽  
Ifn Therapy ◽  
Cytogenetic Remission ◽  
The One

Interferon (IFN) therapy of early chronic myelogenous leukemia (CML) frequently produces partial or complete cytogenetic remission of the disease. Patients with complete cytogenetic remission often continue on therapy for several years with bone marrow showing only diploid (normal) metaphases. We studied hematopoiesis in five female patients with major cytogenetic remissions from CML during IFN therapy. Clonality analysis using the BstXI PGK gene polymorphism showed that granulocytes were nonclonal in all patients during cytogenetic remission. BCR region studies showed rearrangement only in the one patient whose remission was incomplete at the time of sampling. Granulopoiesis is nonclonal in IFN-induced remissions of CML and may be derived from normal hematopoietic stem cells.

scholarly journals Nilotinib after resistance to imatinib in CML patients with Wolf-Parkinson White syndrome

2015 ◽  
Vol 4 (2S) ◽  
pp. 7-11
Author(s):  
Massimo Breccia
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Kinase Inhibitor ◽  
Standard Dose ◽  
Cytogenetic Response ◽  
Qtc Prolongation ◽  
Trisomy 8 ◽  
Optimal Response ◽  
White Syndrome ◽  
Cytogenetic Remission

We report a case of a young man affected by Wolf-Parkinson White syndrome, who was diagnosed as having chronic myeloid leukemia. He started imatinib at standard dose of 400 mg/day and he reached a partial cytogenetic response at 6 months, a sub-optimal response according to European LeukemiaNet criteria of 2006. For this reason he increased imatinib dose to 600 mg/day, but after 3 months he suddenly lost his hematologic response. Cytogenetic analysis performed at this time showed a cytogenetic relapse and acquisition of an additional cytogenetic abnormality (trisomy 8). Considering the patient as a failure at this time, he switched to second-generation tyrosine kinase inhibitor, nilotinib at the dose of 800 mg/day. He reached complete cytogenetic remission after 3 months and nilotinib was safely administered without further QTc prolongation.

Chronic myeloid leukaemia

2020 ◽  
pp. 93-112
Author(s):  
Tariq I. Mughal
Keyword(s):  
Chronic Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Kinase Inhibitors ◽  
Treatment Algorithm ◽  
Chromosome 9 ◽  
Balanced Translocation ◽  
Optimal Monitoring ◽  
Advanced Phase ◽  
Cytogenetic Remission ◽  
Initial Choice

Chronic myeloid leukaemia (CML) was recognized in the 1970s by Janet Rowley to be a genetically simple malignancy; resulting as a consequence of a balanced translocation between chromosome 9 and 22. This provided vital insights into the molecular aberration, in the 1990s, which ushered in the current ‘precision medicine’ era, not only for patients of CML, but for cancers in general. As a result, today, a personalized treatment algorithm is available for all newly diagnosed patients with CML. Treatment involves a choice of three first-line orally administered tyrosine kinase inhibitors (TKIs) and two effective next-line TKIs that should be used based on risk stratification, comorbidities, the side effects profile, and the BCR-ABL1 genotype. Regardless of the initial choice of TKI, the vast majority of patients achieve a durable complete cytogenetic remission, with a lifespan approaching that of the general population. In most instances the medication must be continued indefinitely, and a principal challenge now, is to develop strategies to stop TKIs safely and effectively. Challenges remain in how to achieve optimal monitoring of patients with CML on treatment and in achieving a better understanding of the mechanisms and treatment of patients with advanced phase disease. This chapter addresses these questions as well as the concomitant topical issues in CML.

scholarly journals Discontinuation of imatinib mesylate could improve renal impairment in chronic myeloid leukemia

Open Medicine ◽  
2018 ◽  
Vol 14 (1) ◽  
pp. 22-24 ◽  
Author(s):  
Umit Y. Malkan ◽  
Ibrahim C. Haznedaroglu
Keyword(s):  
Pleural Effusion ◽  
Chronic Myeloid Leukemia ◽  
Serum Creatinine ◽  
Imatinib Mesylate ◽  
Myeloid Leukemia ◽  
Laboratory Tests ◽  
Fluid Retention ◽  
X Ray ◽  
Cytogenetic Remission

AbstractWe aim to report a CML case that had fluid retention and serum creatinine increase under long-term imatinib mesylate (IM) treatment. A 68-year-old woman was diagnosed with chronic myeloid leukemia, and IM was started in 2002 with a dose of 400 mg/day. She had achieved complete hematological, molecular and cytogenetic remission under IM treatment. In September 2015, her creatinine level was 1.7 mg/dl. In May 2016, she was admitted to our hospital with dyspnea. Hypervolemia secondary to fluid retention was detected in our patient. Her laboratory tests results showed hemoglobin 9.7 gr/dl, white blood cell 7.6x103/μl, platelet 157x103/μl, creatinine 3.2 mg/dl, blood urea nitrogen (BUN) 88 mg/dl. In her X-ray chest film, bilateral pleural effusion was detected. The effusion was detected as transuda. The other reasons of pleural effusion were excluded and the development of pleural effusion was considered secondary to IM. IM was also considered responsible for the acute rise of serum creatinine levels of our patient. Therefore for these two reasons IM was stopped. After the discontinuation of IM, her creatinine levels decreased to 1.6 mg/dl and her pleural effusions disappeared. IM treatment was considered as the reason of serum creatinine elevation since serum creatinine levels decreased after the discontinuation of IM. All of the side-effects disappeared after discontinuation of IM.

scholarly journals Targeted FGFR inhibition results in a durable remission in an FGFR1-driven myeloid neoplasm with eosinophilia

2020 ◽  
Vol 4 (13) ◽  
pp. 3136-3140 ◽  
Author(s):  
Monica Kasbekar ◽  
Valentina Nardi ◽  
Paola Dal Cin ◽  
Andrew M. Brunner ◽  
Meghan Burke ◽  
...  
Keyword(s):  
Small Molecule ◽  
Gene Rearrangement ◽  
Small Molecule Inhibitor ◽  
Myeloid Neoplasm ◽  
Molecule Inhibitor ◽  
Key Points ◽  
Fgfr1 Gene ◽  
Cytogenetic Remission ◽  
Fgfr Inhibition ◽  
Durable Remission

Key Points A novel PCM1-FGFR1 gene rearrangement was identified in a patient with a myeloid neoplasm with eosinophilia. Futibatinib, an oral selective small molecule inhibitor of FGFR1-4, resulted in a durable complete hematologic and cytogenetic remission.

scholarly journals Donor leukocyte transfusions for treatment of recurrent chronic myelogenous leukemia in marrow transplant patients

Blood ◽  
1990 ◽  
Vol 76 (12) ◽  
pp. 2462-2465 ◽  
Author(s):  
HJ Kolb ◽  
J Mittermuller ◽  
C Clemm ◽  
E Holler ◽  
G Ledderose ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Transplantation ◽  
Chronic Myelogenous Leukemia ◽  
Adoptive Immunotherapy ◽  
Marrow Transplant ◽  
Buffy Coat ◽  
Myelogenous Leukemia ◽  
Graft Versus Host ◽  
Transplant Patients ◽  
Cytogenetic Remission

Abstract Three patients with hematologic relapse after bone marrow transplantation for chronic myelogenous leukemia were treated with interferon alpha and transfusion of viable donor buffy coat. All had complete hematologic and cytogenetic remission, which persisted 32 to 91 weeks after treatment. In two patients graft-versus-host disease developed and was treated by immunosuppression. These results are an example of adoptive immunotherapy without cytoreductive chemotherapy or radiotherapy in human chimeras.

scholarly journals Polyclonal hematopoiesis in interferon-induced cytogenetic remissions of chronic myelogenous leukemia

Blood ◽  
1992 ◽  
Vol 79 (4) ◽  
pp. 997-1002 ◽  
Author(s):  
D Claxton ◽  
A Deisseroth ◽  
M Talpaz ◽  
C Reading ◽  
H Kantarjian ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Gene Polymorphism ◽  
Chronic Myelogenous Leukemia ◽  
Myelogenous Leukemia ◽  
Hematopoietic Stem ◽  
Clonality Analysis ◽  
Ifn Therapy ◽  
Cytogenetic Remission ◽  
The One

Abstract Interferon (IFN) therapy of early chronic myelogenous leukemia (CML) frequently produces partial or complete cytogenetic remission of the disease. Patients with complete cytogenetic remission often continue on therapy for several years with bone marrow showing only diploid (normal) metaphases. We studied hematopoiesis in five female patients with major cytogenetic remissions from CML during IFN therapy. Clonality analysis using the BstXI PGK gene polymorphism showed that granulocytes were nonclonal in all patients during cytogenetic remission. BCR region studies showed rearrangement only in the one patient whose remission was incomplete at the time of sampling. Granulopoiesis is nonclonal in IFN-induced remissions of CML and may be derived from normal hematopoietic stem cells.

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