scholarly journals CHRONIC MYELOID LEUKEMIA IN PREGNANCY

2018 ◽  
Vol 24 (3) ◽  
pp. 286
Author(s):  
Rosa Dwi Wahyuni ◽  
Agus Alim Abdullah ◽  
Mansyur Arif
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Blast Crisis ◽  
Philadelphia Chromosome ◽  
Peripheral Blood Smear ◽  
Chromosome 9 ◽  
Translocation Chromosome ◽  
Laboratory Evaluation ◽  
Abnormal Growth ◽  
In Pregnancy

Chronic Myeloid Leukemia (CML) is one of leukemias characterized by abnormal growth of myeloid cells in bone marrow. The Philadelphia chromosome is diagnostic parameter for CML. This chromosome is t(9;22) (q32;q21), a translocation chromosome 9 and 22 relocates a portion of proto-oncogene c-ABL from chromosome 9 to BCR on chromosome 22. Chronic myeloid leukemia consisting of three phases; Chronic, Accelerating and the Blast crisis phase. The clinicaling symptoms of CML are hypercatabolism, splenomegaly, anemia, bruising and sign of Gout. Chronic myeloid leukemia in pregnancy shows a better prognosis than acute leukemia in pregnancy. Chronic myeloid leukemia has the risk of leukocytosis which can lead to uteroplacental insufficiency giving rise to various consequences: fetal growth retardation and perinatal mortality. Moreover, the therapy of CML should be carefully administered considering the fetal effects.  Both sexes have the same risk, mostly in the range of 40 to 60 years old. In this case report, a 38-year-old pregnant female (G1P0A0) with 37 weeks of gestational age was diagnosed as CML on August 2013 and was treated with 500 mg of Cytodrox/Hydroxyurea twice to three times a day until January 2014. Laboratory evaluation on November 10th, 2014, showed leucocytes 449500/µL, erythrocytes 2.58.106/µL, hemoglobin 8.0 g/dL, thrombocytes 437,000/µL and hematocrit 23%. The peripheral blood smear showed normocytic normochromic erythrocytes, anisocytosis, ovalocytes, significantly increased leucocyte count, predominance polymorphonuclear series, all maturation series of myelocytes, 7% myeloblast, normal thrombocyte count and morphology. Based on these evaluations, the patient was diagnosed as CML. The evaluation of Neutrophil Alkaline Phosphatase (NAP) scored 1.

THE CASE VARIANT TRANSLOCATION T(3;9;22)(P24;Q34;Q11) IN CHRONIC MYELOID LEUKEMIA

2018 ◽  
Vol 64 (6) ◽  
pp. 810-814
Author(s):  
Kodirzhon Boboev ◽  
Yuliana Assesorova ◽  
Kh. Karimov ◽  
B. Allanazarova
Keyword(s):  
Adverse Effect ◽  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Fusion Gene ◽  
Genetic Locus ◽  
Philadelphia Chromosome ◽  
Chromosome 9 ◽  
Banding Technique ◽  
Variant Translocation

This paper presents a case of chronic myeloid leukemia with an earlier unknown variant translocation t (3; 9; 22) (p24; q34; q11) detected by cytogenetic research using the GTG-banding technique. Despite the absence of the classical Philadelphia chromosome, the presence of chromosome 9 and 22 derivatives, as well as the BCR-ABL fusion gene, allow this translocation to be considered pathogenetic for CML. A good response of the patient to the treatment with glivec is that there is no adverse effect on the pathogenesis of the disease of an additional genetic locus (3p24) involved in complex restructuring.

scholarly journals Pathological Fracture: An Unusual Presentation in Childhood Chronic Myeloid Leukemia

2019 ◽  
Vol 13 (4) ◽  
pp. 140
Author(s):  
Mururul Aisyi ◽  
Ayu Hutami Syarif ◽  
Anita Meisita ◽  
Agus Kosasih ◽  
Achmad Basuki ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Pathological Fracture ◽  
Hematological Malignancy ◽  
Blast Crisis ◽  
Philadelphia Chromosome ◽  
Molecular Response ◽  
Invasive Treatment ◽  
Non Invasive ◽  
Blast Count

Introduction: Chronic Myeloid Leukemia is a hematological malignancy driving from myeloproliferative process. It is typified by the presence of the Philadelphia chromosome manifesting in certain distinct complications, including pathological fracture. Pathological fracture is recognized as an extramedullary disease that occurs as a result of transformation of CML into blast crisis phase.Case Presentation: Here, we report a case of pediatric male CML. After being failed with imatinib therapy, he turned to nilotinib and was unable to achieve a major molecular response. He presented with high blast count and pain in the left arm. He was diagnosed with pathological fracture and blast crisis phase CML. Taken the young age and displacement of fracture into consideration, he was conservatively treated by a combination of immobilization and a higher dose of targeted therapy, nilotinib. The 2-month evaluation revealed clinical union and reduction of blast cells.Conclusions: Regarding the minimal displacement and age presentation, pathological fracture in pediatric CML requires non-invasive treatment and optimization of antileukemic therapy.

scholarly journals Basophils (Bsp-1+) derive from the leukemic clone in human myeloid leukemias involving the chromosome breakpoint 9q34

Blood ◽  
1989 ◽  
Vol 73 (3) ◽  
pp. 777-781 ◽  
Author(s):  
MP Bodger ◽  
CM Morris ◽  
MA Kennedy ◽  
JA Bowen ◽  
JM Hilton ◽  
...  
Keyword(s):  
Toluidine Blue ◽  
Myeloid Leukemia ◽  
Blast Crisis ◽  
Interleukin 2 ◽  
Philadelphia Chromosome ◽  
Chronic Phase ◽  
Normal Karyotype ◽  
Buffy Coat ◽  
Chromosome 9 ◽  
Leukemic Clone

Abstract The monoclonal antibody (MoAb) Bsp-1 was used to purify basophilic cells from leukemic blood of five patients with Philadelphia chromosome (Ph′) positive chronic myeloid leukemia (CML) and two patients with acute myeloid leukemia (AML) characterized by the chromosomal translocation t(6;9)(p23;q34). When cultured, Bsp-1 positive cells from all CML and AML patients showed the same clonal karyotype changes observed in diagnostic buffy coat preparations, indicating that the basophilic cells were of leukemic origin. In contrast, T lymphocytes from four of five CML patients cultured in the presence of interleukin- 2 (IL-2) showed a normal karyotype and were therefore not derived from the leukemic clone. Bsp-1 staining correlated with toluidine blue- positive basophils in chronic phase CML and with toluidine blue- negative blast cells expressing an immature myeloid phenotype in blast crisis CML and AML. Chromosome in situ hybridization showed that the ABL oncogene was translocated from chromosome 9 to chromosome 22 in the CML patients but remained on chromosome 9 in the AML patients. These results indicate that the breakpoint at 9q34 in CML is 5′ of ABL, whereas the breakpoint at 9q34 in AML is 3′ of ABL. Field inversion gel electrophoresis showed that the 9q34 breakpoint was not within 200 kb 3′ of ABL in one of the AML patients, nor was there any rearrangement of the PIM oncogene locus at 6p21.

A Translocation (9;22)(p24;q11.2) In a Patient With CML

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 5184-5184
Author(s):  
Daniele Costa Abreu ◽  
Ana Paula Castilho, Bachelor ◽  
Vivian Dionísio Niewiadonski, Bachelor ◽  
Mauricio Drummond ◽  
Nelson Gaburo
Keyword(s):  
Bone Marrow ◽  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Medical Information ◽  
Conflicts Of Interest ◽  
Philadelphia Chromosome ◽  
Chromosome Analysis ◽  
Chromosome 9 ◽  
Fish Analysis ◽  
Ph Chromosome

Abstract Introduction In January 2013 was received in our lab service a bone marrow sample for cytogenetic analysis. The 61 years old female patient presents an elevated white blood cell count (118,000 x10³/mm³) and clinical diagnosis as Chronic Myeloid Leukemia (CML). According the medical information the treatment began with hydroxyurea 3g daily and allopurinol 300mg daily. Methods We proceeded with cytogenetic examination of the patient’s bone marrow aspirate by conventional G-banding analysis performed on unstimulated short-term cultures (24 hrs). FISH for BCR/ABL translocation was tested using a dual fusion dual color probe. Because of the sample stability we were unable to performed RT-PCR test. Results Chromosome analysis showed the translocation (9;22)(p24;q11.2) as a sole abnormality in 100% (20/20) of analyzed metaphases. Chronic myeloid leukemia presents as a specific chromosomal abnormality the Philadelphia chromosome, t(9;22)(q34;q11) which is different from the results obtained where the region of translocation of chromosome 9 was p24 instead of the classic q34. This result suggests it is BCR/JACK2 translocation. The FISH analysis showed the presence of a complex Ph chromosome: ABL con BCRx1 (one fusion) and BCRx2;ABLx2. Conclusion The patient took imatinib without answer. She is still in clinical monitoring with persistent hyperleucocytosis and the treatment is following with hydroxyurea 500mg daily and Interferon 5000 UI three times a week. Further molecular and cytogenetic tests will be performed in a second sample to contribute with evaluation of disease progression and monitoring treatment response. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Detection of the BCR-ABL Gene By the Real-Time PCR Method in Patients with Chronic Myeloid Leukemia in Rio Grande Do Norte, Brazil

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 5432-5432
Author(s):  
Aldair Sousa Paiva ◽  
Hugo Diogenes De Oliveira Paiva ◽  
Geraldo Barroso Cavalcanti ◽  
Gioconda DR Leão ◽  
Marcos Dias Leão ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Real Time ◽  
Real Time Pcr ◽  
Myeloid Leukemia ◽  
Conflicts Of Interest ◽  
Rna Extraction ◽  
Philadelphia Chromosome ◽  
Genetic Material ◽  
Chromosome 9 ◽  
The Real

Abstract Background: The Philadelphia chromosome is a cytogenetic change resulting from a reciprocal translocation of genetic material between ABL genes from chromosome 9 and BCR from chromosome 22 or t(9; 22) (q34; 11), forming the chimeric gene BCR- ABL, being associated with chronic myeloid leukemia (CML), acute lymphoid leukemia (ALL) and acute myeloid leukemia (AML). The p190 variant is usually associated with acute forms of leukemia, including AML and ALL, whereas the p210 variant is associated with the chronic phases of CML. Due to the high sensitivity and specificity, nucleic acid amplification techniques by real-time PCR have replaced the conventional cytogenetic techniques for the identification of the Philadelphia chromosome and its p190 and p210 variants. Molecular analysis has been indicated in the initial diagnostic phase and also for the therapeutic monitoring defining the percentage of neoplastic cells present in the patients during the different phases of the treatment (Minimum Residual Disease or MRD).The aim of this study was the transcript BCR-ABL identification in patients with suspected of CML and evaluation of the gene frequency in these patients. Methods: The presence of BCR-ABL gene was investigated in blood samples from 42 patients with suspected CML. The RNA extraction was performed by phenol/chloroform method. The cDNA was submitted to PCR, using specific primers for and BCR-ABL genes by Real time PCR. Results: From all studied patients, 16 (38.10%) were negative, and 26 (59.09%) positive for one of rearrangements: p210 b3a2 and b2a2 in 18 cases (40.91%) and p190 a1a2 in 2 cases (4,76%) and double positive p120/190 in 6 cases (14,28%). We observed that the most common rearrangement was the p210 b3a2, and the molecular results were compatible with clinical and hematologic suspicion. Conclusions: The Real-timePCR, because of its specificity and sensitivity, can be considered the most used technique in routine diagnosis and investigation of MRD of CML patients. Disclosures No relevant conflicts of interest to declare.

scholarly journals T cell lineage involvement in lymphoid blast crisis of chronic myeloid leukemia

Blood ◽  
1985 ◽  
Vol 66 (5) ◽  
pp. 1155-1161 ◽  
Author(s):  
M Allouche ◽  
A Bourinbaiar ◽  
V Georgoulias ◽  
R Consolini ◽  
A Salvatore ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Blast Crisis ◽  
Interleukin 2 ◽  
Philadelphia Chromosome ◽  
Cell Lineage ◽  
Virtual Absence ◽  
Hodgkin's Lymphomas

Cytochemical and immunologic analysis of cells obtained from two patients with chronic myeloid leukemia (CML) during blast crisis reveals markers suggestive of an immature lymphoid phenotype. Peripheral blood mononuclear cells from both patients generated spontaneous lymphoblastoid colonies in methylcellulose, a phenomenon observed in T cell acute lymphoblastic leukemias and T cell non- Hodgkin's lymphomas but not in any other type of leukemia. Colonies derived from one patient were composed predominantly of OKT3+ cells (89%), whereas those from the second patient displayed 42% OKT3+ and OKT6+ cells. In the second patient's colonies, each of five mitoses contained the Philadelphia chromosome (Ph1) and two of five displayed the same additional karyotypic abnormalities as the blast crisis cells. Cells obtained from the two patients during remission still gave rise to spontaneous T cell colonies (greater than 85% OKT3+) and Ph1 was detected in 33% and 60% of the metaphases, respectively. However, when colony growth was induced by an interleukin 2-containing conditioned medium, less than 5% of mitoses were Ph1-positive. These data suggest that: (1) the T cell lineage might be involved in CML; (2) a subset of T cells may remain unaffected by the leukemic process, as demonstrated by the virtual absence of Ph1 in induced T cell colonies; and (3) the spontaneous colony assay seems to select for the growth of malignant T cells.

Duplication of chromosome 9 carrying a BCR/ABL chimeric gene in Philadelphia chromosome negative chronic myeloid leukemia

1996 ◽  
Vol 89 (2) ◽  
pp. 166-169 ◽  
Author(s):  
Naoto Takahashi ◽  
Ikuo Miura ◽  
Atsushi Ohshima ◽  
Seiko Utsumi ◽  
Takashi Nimura ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Philadelphia Chromosome ◽  
Chimeric Gene ◽  
Chromosome 9
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