2013, Number 3
<< Back Next >>
Rev Esp Med Quir 2013; 18 (3)
Cytogenetic Diagnosis and Molecular Following in the Chronic Myeloid Leukemia
Cruz VJ, Arcos FDM, Chávez JMS, Sánchez HMP, Sánchez MDM, Galicia GS, Espinoza ZJR, Cervera CEE
Language: Spanish
References: 29
Page: 253-259
PDF size: 634.46 Kb.
ABSTRACT
In the last decade, therapy for Philadelphia chromosome
positive (Ph) has been amended due to global imatinib mesylate
(Gleevec
™, Glivec
™, Novartis, Basel, Switzerland). IM is a
potent inhibitor of TK activity (tyrosine kinase) protein-selective
chimeric BCR/ABL, preventing their activation and phosphorylation
of tyrosine residues involved in the activation of important
signaling pathways as apoptosis, proliferation and cell adhesion.
The latest report from IRIS (International Randomized
Study Imatinib
vs interferon alpha) was the first to demonstrate
the effectiveness of MI as a first line therapy in patients with
Ph positive chronic myeloid leukemia chronic phase; the study
indicated that over 90% of patients with MI show improvement
and a progression of five years free of disease. Recent studies
of patients with MI showed a significant correlation between
the percentage of Ph positive metaphases in bone marrow and
the levels of BCR/ABL in peripheral blood by quantitative polymerase
chain reaction. During therapy, in some patients can be
observed additional chromosomal metaphases Ph chromosome
positive, which should be monitored during follow-up, however,
recognition of these additional changes may also happen in Ph
negative metaphases. The clinical significance of these alterations
is currently unknown. These findings suggest performing a
bone marrow cytogenetic monitoring from 3 to 6 months, in order
to obtain a better understanding of the incidence and clinical
significance of clonal cytogenetic abnormalities in metaphases
Ph-negative/Ph-positive.
REFERENCES
Sans-Sabrafen J. Hematología clínica. 4ª ed. Barcelona: Harcourt, 2001;319-330.
Huret JL. Chronic myelogenous leukaemia (CML). Atlas Genet Cytogenet Oncol Haematol. December 1997. URL: http://www.infobiogen.fr/services/chromcancer/Anomalies/ CML.html Turhan A.G. Chronic myelogenous leukaemia (CML). Atlas Genet Cytogenet Oncol Haematol. October 2000. URL: http://www.infobiogen.fr/services/chromcancer/ Anomalies/CML. html
Savage GD, Antman KH. Imatinib mesylate-anem oral targeted therapia. N Engl J Med 2002;346:683-693.
Sandberg Avery A. The chromosomes in human cancer and leukemia. 2nd ed. New York: Elsevier, 1990;427-457.
Mitelman F, Sverre H. Cancer cytogenetics. New York: Wiley-Liss, 1995;33-68.
Rowley JD. The role of chromosome translocations in leukemogenesis. Semin Hematology 1999;36:59-72.
Turhan AG. ABL Atlas Genet Cytogenet Oncol Haematol. April2001.URL:http://www.infobiogen.fr/services/chromcancer/ genes/ABL.html
Alistair R, Gribble MS, Huntly B, Andrews MK, Campbell L. Variant Philadelphia translocations in chronic myeloid leukemia can mimic typical blast crisis chromosome abnormalities or classic t(9;22): a report of two cases. Br J Haematol 2001;113:439-442.
Melo Junia V. The diversity of BCR-ABL fusion proteins and their relationship to leukemia phenotype. Blood 1996;88:2375-2384.
Kolomietz E, Al-Maghrabi J, Brennan S, Karaskova J, et al. Primary chromosomal rearrangements of leukemia are frequently accompanied by extensive submicroscopic deletions and may lead to altered prognosis. Blood 2001;97:3281-3588.
Huret JL. ABL Atlas Genet Cytogenet Oncol Haematol. October 1997 URL: http://www.infobiogen.fr/services/ chromcancer/genes/ABL.html
Huret JL. BCR (Breakpoint cluster region). Atlas Genet Cytogenet Oncol Haematol. October 1997 URL: http://www. infobiogen.fr/services/chromcancer/genes/BCR.html
Turhan AG. BCR (Breakpoint cluster region). Atlas Genet Cytogenet Oncol Haematol. April 2001. URL: http://www. infobiogen.fr/services/chromcancer/genes/BCR.html
Laurent E, Talpaz M, Kantarjian H, Kurzrock R. The BCR gene and Philadelphia chromosome-positive leukemogenesis. Cancer Res 2001;61:2343-2355.
Román J, Jiménez A, Saglio G, Rocchi M, et al. Implicación de las alteraciones moleculares en el diagnóstico, tratamiento y monitorización de los pacientes con leucemia mieloide crónica. Haematologica 2001;86:115-122.
Shet A, Jahagirdar BN, Verfaillie CM. Chronic myelogenous leukemia: mechanisms underlying disease progression. Leukemia 2002;16:1402-1411.
Saglio G, Guerrasio A, Rosso C, Zaccaria A, et al. New type of BCR-ABL junction in Philadelphia chromosome positive chronic myelogenous leukemia: mechanisms underlying disease progression. Blood 1990;76:1819-1824.
Wada H, Mizutani S, Nishimura J, Usuki Y, et al. Establishment and molecular characterization of a novel leukemic cell line with Philadelphia chromosome expressing p230 BCR/ABL fusion protein. Cancer Res 1995;55:3192-3196.
Pane F, Frigeri F, Sidona M, Luciano L, et al. Neutrophilicchronic myeloid leukemia: a distinct disease with a specific molecular marker (BCR-ABL with c3a2 junction). Blood 1996;88:2410-2414.
Briz M, Vilches C, Cabrera R, Flores R, Fernández M. Typical chronicmyelogenous leukemia with e19a2 junction BCR/ABL transcript. Blood 1997;90:5024-5025.
Scheijen B, Griffin JD. Tyrosin kinase oncogenes in normal hematopoiesis and hematological disease. Oncogene 2002;21:3314-3333.
Deininger M, Goldman J, Melo Junia V. The molecular biology of chronic myeloid leukemia. Blood 2000;96:3343- 3356.
Sánchez-Izquierdo M, Odero M, Solé F, Gutiérrez NC. Aplicaciones clínicas de las nuevas técnicas de citogenética molecular en Hematooncología. Haematologica 2001;96:180-185.
Reuter H, Abbott GmbH and Co. KG. FISH for therapymolecular technologies. Business Briefing: European Pharmacotherapy 2003:1-3.
Swiger R, Tucker JD. FISH: a brief review. Environ Mol Mutagen 1996;27:245-254.
Cunneo A, Bigoni R, Emmanuel B, Smit E, et al. Fluorescence in situ hybridization for the detection and monitoring of the Ph-positive clone in chronic myelogenous leukemia: comparison with metaphase banding analysis. Leukemia 1998;12:1718-1723.
Seong CM. Monitoring the course of chronic myelogenous leukemia by FISH. Hematology 2002;76:53-57.
Müller C, Hennig E, Franke C, Leiblein S, et al. Letter to the editor. The BCR-ABL extra signal fluorescence in situ hybridization system reliably detects deletions upstream of the ABL locus: implications for reporting of results and follow up of chronic myelogenous leukemia patients. Cancer Genet Cytogen 2002;136:149-150.
Lee DS, Kim EC, Yoon BH, Kim WH, et al. Can minor BCRABL translocation in acute leukemia be discriminated from major BCR-ABL by extra signal FISH analysis? Haematologica 2001;86:991-992.