scholarly journals Treatment of Acute Lymphoid Leukemia Refractory to Classic First-Line and Rescue Protocols

2020 ◽  
Author(s):  
Flávia Tobaldini Russo ◽  
Maria Cristina Martins de Almeida Macedo ◽  
Pedro Amoedo Fernades1 ◽  
Larissa Yukari Okada ◽  
Lucas Augusto Monetta da Silva ◽  
...  
Keyword(s):  
Case Report ◽  
Acute Lymphoblastic Leukemia ◽  
Gold Standard ◽  
Lymphoblastic Leukemia ◽  
Lymphocytic Leukemia ◽  
Lymphoid Cells ◽  
Response To Treatment ◽  
First Line ◽  
Lymphoid Leukemia ◽  
No Gold Standard

Acute Lymphoblastic Leukemia is a very aggressive malignant disorder of lymphoid cells in adults, with recurrence (30 to 60% of the cases) after the initial treatment. Until this moment, there is no gold standard therapy for the treatment of adult patients with acute relapsed/refractory lymphoblastic leukemia. In this case report, we describe two cases of relapsed leukemia: one of lymphocytic leukemia B and one of trilineage leukemia, which presented a satisfactory response to treatment with Bortezomib associated with Vincristine, Dexamethasone, and Bendamustine.

scholarly journals Lactate dehydrogenase isoenzymes in normal and malignant human lymphoid cells

Blood ◽  
1982 ◽  
Vol 60 (2) ◽  
pp. 491-494 ◽  
Author(s):  
J Blatt ◽  
RJ Spiegel ◽  
NM Papadopoulos ◽  
SA Lazarou ◽  
IT Magrath ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Lactate Dehydrogenase ◽  
T Cell ◽  
Lymphoblastic Leukemia ◽  
Diagnostic Category ◽  
Lymphocytic Leukemia ◽  
Lymphoid Cells ◽  
Lymphoid Malignancies ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Isoenzyme Patterns

Abstract Intracellular lactate dehydrogenase (LD) isoenzyme patterns were studied in the malignant cells of patients with a variety of lymphoid malignancies. These were compared with intracellular LD isoenzyme patterns of normal lymphoid cells and were also correlated with immunologic cell surface marker characteristics. Results showed that, in general, the malignant B cells of Burkitt's lymphoma and the lymphoblasts of T-cell acute lymphoblastic leukemia had isoenzyme patterns similar to those of normal B and T cells, respectively. The isoenzyme patterns of malignant lymphoid cells from patients with non- T, and non-B acute lymphoblastic leukemia, cutaneous T-cell lymphoma, and chronic lymphocytic leukemia were more heterogeneous. These data, although based on small numbers of patients, are consistent with the hypothesis that LD isoenzymes may reflect differences in the maturational status of cells within a single diagnostic category.

scholarly journals TdT Negativity and ETP Phenotype in Young Patients with Acute T- Lymphoid Leukemia: A Case Report

2021 ◽  
Vol 8 (4) ◽  
Author(s):  
Cetin D ◽  
◽  
Midik MM ◽  
Karadag FK ◽  
Ozsan N ◽  
...  
Keyword(s):  
Case Report ◽  
Acute Lymphoblastic Leukemia ◽  
Poor Prognosis ◽  
Treatment Process ◽  
Lymphoblastic Leukemia ◽  
Young Patients ◽  
Case Series ◽  
Common Condition ◽  
Lymphoid Leukemia ◽  
Young Adult Patient

TdT is generally positive in patients with T-Acute Lymphoblastic Leukemia/ Lymphoma (T-ALL/LBL) and can often become negative after chemotherapy. TdT negativity at the time of diagnosis is not a common condition and is evaluated in favor of a poor prognosis. Due to its infrequent occurrence, there are not enough clinical studies, and there are often publications on the basis of case and case series. While its incidence increases in young people and children, the possibility of accompanying Early T Precursor (ETP) phenotype also increases. The presence of the ETP phenotype has negative repercussions on prognosis. Here, we will describe the diagnosis and treatment process of a young adult patient with TdT negative T-ALL accompanied by the ETP phenotype.

scholarly journals Lactate dehydrogenase isoenzymes in normal and malignant human lymphoid cells

Blood ◽  
1982 ◽  
Vol 60 (2) ◽  
pp. 491-494
Author(s):  
J Blatt ◽  
RJ Spiegel ◽  
NM Papadopoulos ◽  
SA Lazarou ◽  
IT Magrath ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Lactate Dehydrogenase ◽  
T Cell ◽  
Lymphoblastic Leukemia ◽  
Diagnostic Category ◽  
Lymphocytic Leukemia ◽  
Lymphoid Cells ◽  
Lymphoid Malignancies ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Isoenzyme Patterns

Intracellular lactate dehydrogenase (LD) isoenzyme patterns were studied in the malignant cells of patients with a variety of lymphoid malignancies. These were compared with intracellular LD isoenzyme patterns of normal lymphoid cells and were also correlated with immunologic cell surface marker characteristics. Results showed that, in general, the malignant B cells of Burkitt's lymphoma and the lymphoblasts of T-cell acute lymphoblastic leukemia had isoenzyme patterns similar to those of normal B and T cells, respectively. The isoenzyme patterns of malignant lymphoid cells from patients with non- T, and non-B acute lymphoblastic leukemia, cutaneous T-cell lymphoma, and chronic lymphocytic leukemia were more heterogeneous. These data, although based on small numbers of patients, are consistent with the hypothesis that LD isoenzymes may reflect differences in the maturational status of cells within a single diagnostic category.

scholarly journals Acute Lymphoblastic Leukemia after previously treated, relapsed Chronic Lymphocytic Leukemia: A Case Report

2015 ◽  
Vol 53 (2) ◽  
pp. 184-188 ◽  
Author(s):  
Elena Andrus ◽  
Anca Nicolescu ◽  
H. Bumbea ◽  
Ana-Maria Vlădăreanu
Keyword(s):  
Bone Marrow ◽  
Case Report ◽  
Acute Lymphoblastic Leukemia ◽  
Chronic Lymphocytic Leukemia ◽  
Bone Marrow Aspirate ◽  
Lymphoblastic Leukemia ◽  
Infectious Complications ◽  
Lymphocytic Leukemia ◽  
Previously Treated ◽  
One Year

Abstract We present the case of a 71-year-old woman diagnosed with chronic lymphocytic leukemia who received multiple chemotherapeutic lines and evolved to acute lymphoblastic leukemia. The patient was Rai stage 0 at the time of the diagnosis and was monitored for almost 9 years. After that, the disease progressed and the patient began chemotherapy (fludarabine/cyclophosphamide combination), obtained complete remission and relapsed one year later after finishing treatment. She received multiple therapeutic regimens, accompanied by multiple infectious complications. After 8 years of evolution since she started chemotherapy, bone marrow aspirate and immunophenotyping revealed acute lymphoblastic leukemia. The occurrence of acute leukemia in CLL is rare and may arise from the same clone; however, most cases appear after patients have received chemotherapy, suggesting that they are therapy-related.

Targeting Kinase-activating Genetic Lesions to Improve Therapy of Pediatric Acute Lymphoblastic Leukemia

2018 ◽  
Vol 25 (24) ◽  
pp. 2811-2825 ◽  
Author(s):  
Raffaella Franca ◽  
Natasa K. Kuzelicki ◽  
Claudio Sorio ◽  
Eleonora Toffoletti ◽  
Oksana Montecchini ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Fusion Gene ◽  
Hematologic Malignancy ◽  
Lymphoblastic Leukemia ◽  
Point Of View ◽  
Lymphoid Cells ◽  
Gene Encoding ◽  
Pediatric All ◽  
Blast Cells ◽  
Tk Inhibitors

Acute lymphoblastic leukemia (ALL) is the most common hematologic malignancy in children, characterized by an abnormal proliferation of immature lymphoid cells. Thanks to risk-adapted combination chemotherapy treatments currently used, survival at 5 years has reached 90%. ALL is a heterogeneous disease from a genetic point of view: patients’ lymphoblasts may harbor in fact several chromosomal alterations, some of which have prognostic and therapeutic value. Of particular importance is the translocation t(9;22)(q34;q11.2) that leads to the formation of the BCR-ABL1 fusion gene, encoding a constitutively active chimeric tyrosine kinase (TK): BCR-ABL1 that is present in ~3% of pediatric ALL patients with B-immunophenotype and is associated with a poor outcome. This type of ALL is potentially treatable with specific TK inhibitors, such as imatinib. Recent studies have demonstrated the existence of a subset of BCR-ABL1 like leukemias (~10-15% of Bimmunophenotype ALL), whose blast cells have a gene expression profile similar to that of BCR-ABL1 despite the absence of t(9;22)(q34;q11.2). The precise pathogenesis of BCR-ABL1 like ALL is still to be defined, but they are mainly characterized by the activation of constitutive signal transduction pathways due to chimeric TKs different from BCR-ABL1. BCR-ABL1 like ALL patients represent a group with unfavorable outcome and are not identified by current risk criteria. In this review, we will discuss the design of targeted therapy for patients with BCR-ABL1 like ALL, which could consider TK inhibitors, and discuss innovative approaches suitable to identify the presence of patient’s specific chimeric TK fusion genes, such as targeted locus amplification or proteomic biosensors.

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