Different cell clones in bone marrow and spleen of a patient with chronic myelocytic leukemia (CML) in blastic phase

Olinici, C D; Petrov, L. N.; Macavei, I; Dobay, O

doi:10.1002/1097-0142(197812)42:6<2707::aid-cncr2820420627>3.0.co;2-5

Cited by 5 publications

(4 citation statements)

References 15 publications

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“…In this study, we report a unique Ph+ chromosome case in the accelerated phase with additional chromosome of trisomy +19 and +22 der chromosome, 48XY,t(9;22) (q34;q11.2),+19,+der (22) [22]; previously, only one case before has been reported so far [49].…”

Section: Discussionmentioning

confidence: 79%

Molecular, Cytogenetic, and Hematological Analysis of Chronic Myeloid Leukemia Patients and Discovery of Two Novel Translocations

Asif

Hussain

Wali

et al. 2021

Analytical Cellular Pathology

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Chronic myeloid leukemia (CML) is a disease of hematopoietic stem cells and is caused by the balanced translocations among the long arms of chromosomes 9 and 22, which are called the Philadelphia (Ph) chromosome. In this study, 131 CML patients were enrolled. Complete blood cell count was performed at the time of diagnosis for all the patients. Cytogenetic (karyotyping) examination using bone marrow samples was conducted on 76 CML patients for the confirmation of Ph-positive (9;22)(q34;q11) standard translocation, complex variant translocation, and additional chromosome abnormalities. FISH was performed on 38 patients for diagnostic purposes and on 39 patients for monitoring purposes. Twenty-two samples of CML patients were evaluated by reverse transcriptase PCR and real-time PCR for the patients who failed to respond against imatinib mesylate. In this study, 72 (54.96%) were males and 59 (45.03%) were females with a median age of 38.5 years. CBC values in the diagnosis process showed that 75 patients had high values of WBC being > 100 × 10 3 / μ l , while 71 (58.01) patients exhibited reduced values of hemoglobin, i.e., <10.00 mg/dl, and high values of PLTs > 100 were observed in 40 (30.53%) patients. Cytogenetic results show that standard translocation was developed in 63 (82.89%), development of complex variant translocations in 4 (5.32%), additional chromosomal abnormalities (ACAs) in 3 (3.94%), and ACAs together with complex variant translocations in 1 (1.31%) patient. At the time of diagnosis, 61 (92.95%) patients were in the chronic phase, 4 (5.63%) were in the accelerated phase, and only 1 (1.40%) was in the blast crisis. Out of twenty-two patients, only 6 CML patients who were shifted from imatinib mesylate to nilotinib showed BCR-ABL-positive amplification. However, only 7 out of twenty-one patients exhibit BCR-ABL gene values ≥ 1 after three months of follow-up when analyzed by the quantitative real-time PCR. In conclusion, we found a novel five-way translocation 46XX,t(1;2;2;17;9;22)(p36.3,q21;q11.2,q21,q34,q11.2) and a novel four-way complex variant translocation 48XY,+8(8;17)(9;22),+der(22)(q11.2;q23)(q34;q11.2) in the accelerated phase.

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Section: Discussionmentioning

confidence: 79%

Molecular, Cytogenetic, and Hematological Analysis of Chronic Myeloid Leukemia Patients and Discovery of Two Novel Translocations

Asif

Hussain

Wali

et al. 2021

Analytical Cellular Pathology

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“…The natural history of the disease in this patient is consistent with the concept of clonal evolution of malignant cell populations [7, 121. The persistence of the original leukemic clone is not inconsistent with the view that variant subclones may evolve from it, and this may explain the phenomenmon of biclonal blast crises in CML [13].…”

Section: Discussionmentioning

confidence: 95%

Coexistence of myeloid and lymphoid neoplastic subpopulations in chronic myelogenous leukemia

Hutchinson

Rosenstock

Nowell̀

et al. 1981

Med. Pediatr. Oncol.

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Serial cytogenetic studies have been performed on a child with Philadelphia chromosome (Ph1)-positive chronic myelogenous leukemia (CML) and correlated with clinical, morphologic, and cytochemical data in an attempt to elucidate further the natural history of leukemia progression observed in this disease. Once the initial blast crisis had occurred, two genetically different leukemic clones of cells, one presumably having arisen from the other, coexisted throughout the remainder of the patient's course. The initial clone comprised differentiating myeloid cells, while the second clone appeared on morphologic and cytochemical grounds to be lymphoid and blastic. A dynamic equilibrium existed between these two populations of cells, with the balance altered by chemotherapy and/or other selective pressures. The leukemic progression demonstrated in this case is consistent with the concept of clonal evolution of malignant cell populations. In planning therapy, it may be necessary to consider each of these coexistent clones and their different therapeutic requirements.

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“…These results suggest the possibility of using the micronucleus test for a quantitative appreciation of the cytogenetic effects of radiation in tumour cells, micronuclei being generally derived from acentric chromosome fragments . In a previous paper we have reported the effects of X-irradiation on the incidence of micronuclei in Ehrlich tumour ascites cells and have shown a dose-effect relationship (Olinici, Almasan and Dobay 1978) .…”

mentioning

confidence: 92%

Effect of Misonidazole (Ro-07-0582) on the Incidence of Micronuclei in Irradiated Ehrlich Tumour Ascites Cells

Olinici¹,

Mustea²

1978

International Journal of Radiation Biology and Related Studies

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Different cell clones in bone marrow and spleen of a patient with chronic myelocytic leukemia (CML) in blastic phase

Cited by 5 publications

References 15 publications

Molecular, Cytogenetic, and Hematological Analysis of Chronic Myeloid Leukemia Patients and Discovery of Two Novel Translocations

Molecular, Cytogenetic, and Hematological Analysis of Chronic Myeloid Leukemia Patients and Discovery of Two Novel Translocations

Coexistence of myeloid and lymphoid neoplastic subpopulations in chronic myelogenous leukemia

Effect of Misonidazole (Ro-07-0582) on the Incidence of Micronuclei in Irradiated Ehrlich Tumour Ascites Cells

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