Acute Lymphocytic Leukemia

BACKGROUNDModern intensive chemotherapy regimens have improved the prognosis for patients with adult acute lymphocytic leukemia (ALL). With these regimens, the complete response rates are now reported to be > 80%, and the long-term survival rates range from 30% to 45%. The current analysis updated the long-term results with the original hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone (Hyper-CVAD) program, with a median follow-up time of 63 months.Modern intensive chemotherapy regimens have improved the prognosis for patients with adult acute lymphocytic leukemia (ALL). With these regimens, the complete response rates are now reported to be > 80%, and the long-term survival rates range from 30% to 45%. The current analysis updated the long-term results with the original hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone (Hyper-CVAD) program, with a median follow-up time of 63 months.METHODSBetween 1992 and 2000, 288 patients were treated with Hyper-CVAD. The median age of the patients was 40 years, and 59 patients (20%) were ≥ age 60 years. The incidence of Philadelphia chromosome (Ph)-positive ALL was 17%, and the incidence of of T-cell ALL was 13%.Between 1992 and 2000, 288 patients were treated with Hyper-CVAD. The median age of the patients was 40 years, and 59 patients (20%) were ≥ age 60 years. The incidence of Philadelphia chromosome (Ph)-positive ALL was 17%, and the incidence of of T-cell ALL was 13%.RESULTSA complete response (CR) was achieved in 92% of patients. The induction mortality rate was 5% (2% if the patient's age was < 60 years, and 15% if the patient's age was ≥ 60 years). With a median follow-up time of 63 months, the 5-year survival rate was 38% and the 5-year CR duration rate was 38%. Multivariate analysis of prognostic factors for CR duration identified the following adverse factors: age ≥ 45 years, leukocytosis ≥ 50 × 109/L, poor performance status (an Eastern Cooperative Oncology Group score of 3–4), Ph-positive disease, French–American–British L2 morphology, > 1 course to achieve CR, and Day 14 bone marrow blasts > 5%. Patients were divided into low-risk (risk score 0–1; 37%), intermediate risk (risk score 2–3; 36%), and poor-risk groups (risk score ≥ 4; 27%) with 5-year CR duration rates of 52%, 37%, and 10%, respectively.A complete response (CR) was achieved in 92% of patients. The induction mortality rate was 5% (2% if the patient's age was < 60 years, and 15% if the patient's age was ≥ 60 years). With a median follow-up time of 63 months, the 5-year survival rate was 38% and the 5-year CR duration rate was 38%. Multivariate analysis of prognostic factors for CR duration identified the following adverse factors: age ≥ 45 years, leukocytosis ≥ 50 × 109/L, poor performance status (an Eastern Cooperative Oncology Group score of 3–4), Ph-positive disease, French–American–British L2 morphology, > 1 course to achieve CR, and Day 14 bone marrow blasts > 5%. Patients were divided into low-risk (risk score 0–1; 37%), intermediate risk (risk score 2–3; 36%), and poor-risk groups (risk score ≥ 4; 27%) with 5-year CR duration rates of 52%, 37%, and 10%, respectively.CONCLUSIONSCompared with the previous VAD regimens, Hyper-CVAD was associated with significantly better CR rates, CR duration, and survival. The long-term follow-up results of Hyper-CVAD were favorable. Comparison of Hyper-CVAD with other established adult ALL regimens is warranted. Cancer 2004. © 2004 American Cancer Society.Compared with the previous VAD regimens, Hyper-CVAD was associated with significantly better CR rates, CR duration, and survival. The long-term follow-up results of Hyper-CVAD were favorable. Comparison of Hyper-CVAD with other established adult ALL regimens is warranted. Cancer 2004. © 2004 American Cancer Society.

This work is licensed under Creative Commons Attribution 4.0 License OJCAM.MS.ID.000659. Opinion Leukemia is classified into four categories depending on if it is acute or chronic, and whether it is myeloid or lymphocytic: Acute myeloid leukemia (AML), Chronic myeloid leukemia (CML), Acute lymphoblastic leukemia (ALL), and Chronic lymphocytic leukemia (CLL). AML is characterized by the clonal expansion of immature myeloid precursor cells that compromises the formation of normal blood cells. Although the pathophysiology of AML remains unknown, medical researchers believe that other hematological ailments, chemical contaminants, radiation, and mutations, are significant risk factors for the disease [1,2]. For long, 7 + 3 combination

Key Points BM-derived MSC can become cancer associated fibroblasts and transfer mitochondria to rescue B-ALL cells from ROS-inducing chemotherapy. Rescue of B-ALL cells is overcome by microtubule inhibitors which interrupt the tunnelling nanotubes used for mitochondrial transfer.

CUTE MYELOID leukemia (AML) in adults is respon- A sive to chemotherapy in approximately 65% of the patients. To date only 30% to 35% of the patients can be cured with chemotherapy alone because of the emergence of malignant cell populations, which are resistant to all clini- cally available anticancer drugs. One cause of tumor cell resistance to natural product

Purpose To improve treatment outcome for childhood acute lymphoblastic leukemia (ALL), we designed the Malaysia-Singapore ALL 2003 study with treatment stratification based on presenting clinical and genetic features and minimal residual disease (MRD) levels measured by polymerase chain reaction targeting a single antigen-receptor gene rearrangement. Patients and Methods Five hundred fifty-six patients received risk-adapted therapy with a modified Berlin-Frankfurt-Münster–ALL treatment. High-risk ALL was defined by MRD ≥ 1 × 10−3 at week 12 and/or poor prednisolone response, BCR-ABL1, MLL gene rearrangements, hypodiploid less than 45 chromosomes, or induction failure; standard-risk ALL was defined by MRD ≤ 1 × 10−4 at weeks 5 and 12 and no extramedullary involvement or high-risk features. Intermediate-risk ALL included all remaining patients. Results Patients who lacked high-risk presenting features (85.7%) received remission induction therapy with dexamethasone, vincristine, and as...

Objective: To determine the relationship of cholesterol and triglycerides serum levels with the response to induction chemotherapy treatment in patients with acute lymphocytic leukemia. Material and Methods: The sample consisted in 25 patients 2 through 18 years-old admitted to the Neoplasia Diseases Institute with a recent diagnosis of acute lymphocytic leukemia in whom serum concentrations of total cholesterol, HDL-cholesterol, LDL-cholesterol and triglycerides were determine, before and after the first phase of the induction chemotherapy. Results: Only 23 patients responded to the treatment and in them we observe an increment from 19,24 ± 4,49 mg/dL to 46,84 ± 15,38 mg/dL for the HDL-cholesterol, and a descent from 153,66 ± 36,39 mg/dL to 79,79 ± 34,53 mg/dL for the triglycerides (p&lt;0,0001). On the contrary, in the patients that didn&#x27;t respond to the treatment, an increment was obtained from 14,64 ± 2,46 mg/ dL to 23,13 ± 14,23 mg/dL for HDL-cholesterol and an increment f...

Chemotherapy of the central nervous system may cause neurotoxicity in children with acute lymphocytic leukemia. We evaluated regional blood flow in a 6-year-old child presenting with akinetic mutism, using 99mTc-HMPAO single photon emission tomography (SPECT) following high-dose intravenous methotrexate therapy. While findings in X-ray computerized tomography were decreased density in bilateral basal ganglia and thalamic nuclei with diffusely decreased attenuation of the periventricular white matter, a global, frontal dominant profoundly abnormal perfusion pattern involving both gray and white matter was observed in the SPECT study. Treatment of the central nervous system with high dose intravenous chemotherapy may cause profound abnormalities in white and gray matter blood flow and early assessment of the neurotoxicity may be identified by 99mTc-HMPAO SPECT in the pediatric age group.

Human leukemic T cells carrying a t(10;14)(q24;q11) chromosome translocation were fused with mouse leukemic T cells, and the hybrids were examined for genetic markers of human chromosomes 10 and 14. Hybrids containing the human 10q+ chromosome had the human genes for terminal deoxynucleotidyltransferase that has been mapped at 10q23-q25 and for C alpha [the constant region of TCRA (the alpha-chain locus of the T-cell antigen receptor gene)], but not for V alpha (the variable region of TCRA). Hybrids containing the human 14q- chromosome retained the V alpha genes. Thus the 14q11 breakpoint in the t(10;14) chromosome translocation directly involves TCRA, splitting the locus in a region between the V alpha and the C alpha genes. These results suggest that the translocation of the C alpha locus to a putative cellular protooncogene located proximal to the breakpoint at 10q24, for which we propose the name TCL3, results in its deregulation, leading to T-cell leukemia. Since hybrids with t...

Hyperglycemia has been described as a common event occurring during acute lymphocytic leukemia chemotherapy. It is associated with the synergistic effect of L-asparaginase and glucocorticoids, and related to poor outcome. Our goal was to compare clinical and laboratory findings between hyperglycemic episodes occurring during childhood acute lymphocytic leukemia induction chemotherapy. Here we describe 12 (3.8%) high-risk patients of 311 total patients, 9 (75%) of who are female. The 12 patients presented with 16 hyperglycemic episodes classified into adverse or satisfactory categories. There were no differences in clinical or laboratory variables among groups, although the majority of episodes occurred in pubescents, regardless of the type of glucocorticoid employed. Despite the fact that only 1 patient was overweight, pancreatitis was not diagnosed. Although we could not determine whether hyperglycemia predicts an adverse outcome, glucose evaluation played an important role during ...

Background: The etiology of multiple myeloma (MM) remains obscure, al- though reports of familial clustering have implicated both a host susceptibil- ity factor and environmental effects. Here we describe the medical histories of members of a family prone to MM. Methods: We developed a pedigree for an MM-prone family by using informa- tion obtained from a questionnaire. Protein immunoelectrophoresis of