Isabel Giere

Academia Nacional de Medicina, Buenos Aires, Buenos Aires, Buenos Aires F.D., Argentina

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Publications (6)8.06 Total impact

  • Article: Planned pregnancy in a chronic myeloid leukemia patient in molecular remission.
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    ABSTRACT: Excellent response rates and a good quality of life have been observed since the introduction of tyrosine kinase inhibitors (TKIs) in chronic myeloid leukemia (CML) treatment. Consequently, some challenges began to appear in CML women in child-bearing age wishing to become pregnant. Currently, many women around the world are in stable major/complete molecular response MMR/CMR (MMR: <0.1% BCR-ABL/ABL and CMR: undetectable BCR-ABL mRNA by RQ-PCR transcript levels on the international scale). The condition of stable MMR/CMR is linked to a long-term virtual absence of progression to the accelerated and blastic phase and to the possibility of stopping the TKI treatment with the maintenance of a condition of CMR in a proportion of cases. Imatinib teratogenic and prescribing information prohibits the use of it during pregnancy. We describe the case of a 36-year-old female patient with CML in chronic phase who stopped imatinib after 2 years in major molecular response (MMR) to plan a pregnancy. Molecular monitoring by RQ-PCR was performed quarterly. She achieved a safe pregnancy and delivery maintaining an optimal molecular response throughout the pregnancy. Isolated literature reports have been described, but no formal advice has been described at present time.
    Case reports in hematology. 01/2012; 2012:624590.
  • Article: Molecular monitoring of imatinib in chronic myeloid leukemia patients in complete cytogenetic remission: does achievement of a stable major molecular response at any time point identify a privileged group of patients? A multicenter experience in Argentina and Uruguay.
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    ABSTRACT: Monitoring minimal residual disease (MRD) by real-time quantitative polymerase chain reaction (RT-PCR) in chronic myeloid leukemia (CML) patients is mandatory in the era of tyrosine kinase inhibitors. Achieving a major molecular response (MMR) at 12 and 18 months predicts a better progression and event-free survival. The objective of this prospective, multicentric study was to evaluate MRD by standardized RT-PCR in 178 patients with chronic-phase CML who were treated with imatinib at different institutions in Argentina and Uruguay and to determine if achievement of a stable MMR (BCR-ABL transcript levels < 0.1%) identifies a low-risk cytogenetic relapse group. The median age of the patients was 50 years, and 55% of them had received imatinib as first-line therapy. BCR-ABL transcript levels were measured after achievement of complete cytogenetic remission (CCyR) and at 6-month intervals. MMR was detected in 44% patients at the start of the study. This value increased to 79% at month 36 of evaluation. Complete molecular response (CMR) also increased from 24% to 52% of patients. Not achieving a stable MMR determined a higher risk of cytogenetic relapse (9% of MMR patients not achieving an MMR vs. 1% of patients who achieved MMR). Patients with sustained MMR had a significantly better cytogenetic relapse-free survival at 48 months (97% vs. 87%; P = .008) but showed no differences in overall survival. Patients who did not remain in CCyR changed treatment. A stable MMR is a strong predictor for a durable CCyR. Standardized molecular monitoring could replace cytogenetic analysis once CCyR is obtained. These results emphasize the validity and feasibility of molecular monitoring in all standardized medical centers of the world.
    Clinical lymphoma, myeloma & leukemia 06/2011; 11(3):280-5.
  • Article: Complex Karyotype with PH1 Chromosome in Myelodysplasia: Cytogenetic and Molecular Studies
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    ABSTRACT: We report here a patient with Ph1-positive myelodysplasia with a complex karyotype. The patient presented with severe refractory anemia and ineffective erythropoiesis. In addition to t(9;22), chromosomes no. 1, 11, 12 and X also showed structural aberrations. Serial chromosome analyses revealed an increase of the Ph1-positive cell line along with the evolution of the disease (50% to 100%). Southern blot analysis showed a breakpoint cluster region (bcr) rearrangement as described for chronic myeloid leukemia (CML). The disease evolved into an acute leukemia after 4 years without any clinical evidences of CML.
    06/2009; 6(4-5):401-406.
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    Article: Increased immature hematopoietic progenitor cells CD34+/CD38dim in myelodysplasia.
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    ABSTRACT: Myelodysplastic syndromes (MDS) are clonal disorders affecting hematopoietic progenitor cells (HPC). Despite the relevance of clonal CD34+ cells in developing MDS, only few studies analyze the phenotype of this cell population. The aim of this study was to evaluate phenotypic changes on HPC in MDS that could reflect abnormalities in the differentiation process of stem cells. We analyzed the expression of CD38 and HLA-DR on CD34+ cells by flow cytometry in 36 patients with MDS, as well as in healthy donors (n = 12) and patients with other hematological disorders: non-Hodgkin lymphomas and multiple myeloma, both in complete remission (CR) (n = 32); acute lymphoblastic leukemia in CR (n = 17); de novo acute myeloblastic leukemia (AML) at diagnosis (n = 22) and in CR (n = 37); and AML secondary to MDS at diagnosis (n = 19). Cases with available karyotype were grouped according to the International Prognostic Scoring System (IPSS). Compared to normal BM, the fraction of immature HPC, characterized as CD34+bright, intermediate FSC/SSC, and CD38dim, was significantly increased in high risk MDS and secondary AML, but not in low risk MDS, (P < or = 0.001, P = 0.03, and P = 0.7). De novo AML showed decreased immature HPC. High numbers of immature HPC correlated with higher IPSS risk groups (P = 0.05) and showed significant impact on disease progression (P = 0.03). Our study confirms that evaluation of CD38 expression pattern on HPC is an easy and reproducible test that allows evaluating the immature subset of progenitor cells. Increased immature HPC in high risk MDS and secondary AML may reflect blocked differentiation of CD34+ cells in these diseases.
    Cytometry Part B Clinical Cytometry 03/2006; 70(2):63-70. · 2.53 Impact Factor
  • Article: Structural aberrations of chromosomes 17 and 12 in chronic B-cell disorders.
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    ABSTRACT: Genomic aberrations can now be identified in approximately 80% of chronic lymphocytic leukemia, small lymphocytic lymphoma (CLL/SLL) patients. In the present study, four new structural changes involving chromosomes 17 and 12 in CLL/SLL patients are described. Five patients were selected for inclusion in the present report among a total of 92 cases with diagnosis of CLL/SLL. Cytogenetic studies and fluorescence in situ hybridization (FISH) analysis to detect some of the most frequent cryptic aberrations occurring in CLL/SLL patients were performed. Clinical studies are also described. Four cases showed structural rearrangements of chromosome 17. A psu dic(17;2)(p11.2;p21), leading to p53 deletion, was observed in a patient who developed a mixed cellularity Hodgkin's disease coexisting with the CLL/SLL in the same lymph node. Epstein Barr virus was detected in the Reed-Sternberg cells. Two cases had a balanced translocation t(2;17)(p21;q23). Both patients showed trisomy 12 and clonal evolution and one of them also had 11q deletion. In addition, a der(17)t(12;17)(q13;q25) as a part of a complex karyotype, and a complex translocation t(5;12;19) (q15;p11;q13) were also found. Four patients had an adverse clinical outcome and died because of disease progression. Four unreported nonrandom chromosome aberrations in CLL/SLL patients, one of them who might represent a new recurrent abnormality, are described. These uncommon abnormalities, mostly associated with evolving disease, may have implications for the understanding of genetic events associated with disease progression in this pathology.
    European Journal Of Haematology 01/2004; 71(6):433-8. · 2.61 Impact Factor
  • Article: Molecular study of the interferon genes in chronic myeloid leukemia
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    ABSTRACT: The interferons α, β, and w (IFNA, IFNB, IFNW), are a family of genes that have been mapped on the short arm of chromosome 9 (9p21–22). Deletions of genetic material on 9p are frequently observed in hematological diseases, particularly in lymphoid neoplasias. In this paper we have performed the molecular studies of IFNA and IFNB genes in chronic myeloid leukemia (CML) in order to determine if the deletions of these genes are prevalent in this pathology. Forty CML patients, Philadelphia positive or with rearrangement, were studied at diagnosis. The analysis of IFNA and IFNB genes was performed by Southern and dot blot techniques. Homozygous or hemizygous deletions of IFNA and IFNB genes could not be detected, indicating that deletions of these genes would not be present or would be a very infrequent event in the chronic phase of the CML patients.
    Leukemia Research 09/1995; · 2.92 Impact Factor

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Institutions

  • 2009
    • Academia Nacional de Medicina, Buenos Aires
      Buenos Aires, Buenos Aires F.D., Argentina