Survival of Mexican Children with Acute Myeloid Leukaemia Who Received Early Intensification Chemotherapy and an Autologous Transplant

Abstract

Background. In Mexico and other developing countries, few reports of the survival of children with acute leukaemia exist. Objective. We aimed at comparing the disease-free survival of children with acute myeloid leukaemia who, in addition to being treated with the Latin American protocol of chemotherapy and an autologous transplant, either underwent early intensified chemotherapy or did not undergo such treatment. Procedure. This was a cohort study with a historical control group, forty patients, less than 16 years old. Group A (20 patients), diagnosed in the period 2005–2007, was treated with the Latin American protocol of chemotherapy with an autologous transplant plus early intensified chemotherapy: high doses of cytarabine and mitoxantrone. Group B (20 patients), diagnosed in the period 1999–2004, was treated as Group A, but without the early intensified chemotherapy. Results. Relapse-free survival for Group A was 90% whereas that for Group B it was 60% (P = 0.041). Overall survival for Group A (18, 90%) was higher than that for Group B (60%). Complete remission continued for two years of follow-up. Conclusions. Relapse-free survival for paediatric patients treated with the Latin American protocol of chemotherapy with an autologous transplant plus early intensified chemotherapy was higher than that for those who did not receive early intensified chemotherapy.

MiR-29 Induces K562 Cell Apoptosis by Down-Regulating FoxM1

“…In this study, we investigated the regulating effect of miR-29 on K562 cells and its possible mechanism. The results showed that miR-29 overexpression inhibits human leukemia K562 cells growth and proliferation, and promotes K562 cells apoptosis, which is consistent with previous results [ 5 ].…”

“…At present, miRNAs with clearly defined functions includes miR-29, miR-150, miR-150, miR-181a, miR-23a, miR-148/152, miR-221/222, miR-483-3p, miR-30e, miR-397, and miR-126 [ 4 ]. Our study speculated that miR-29 may play a role through regulating transcription factors, while the other miRNAs’ regulating effect is unclear [ 3 – 5 ]. The miR-29 family comprises 3 isoforms arranged in 2 clusters: miR-29b-1/miR-29a in chromosome 7q32 and mir-29b-2/miR-29c in chromosome 1q23.…”

“…Interestingly, chromosome 7q32 is a frequent region of deletion in myelodysplasia and therapy-related acute myeloid leukemia (AML). In fact, miR-29 family members have been shown to be downregulated in CLL, lung cancer, invasive breast cancer, AML, and cholangiocarcinoma [ 3 – 5 ]. miR-29 can inhibit breast cancer cell growth.…”

A greater birthweight increases the risk of acute leukemias in Mexican children—experience from the Mexican Interinstitutional Group for the Identification of the Causes of Childhood Leukemia (MIGICCL)

“…Great advances have been achieved in the last 20 years in the knowledge on the biology of leukemia [7][8][9], and there has also been an increase in long-term survival E. Jiménez-Hernández et al A Greater Birth Weight and Childhood Leukemias through improvements in treatment regimens and supportive care [10][11][12]. However, there is little known of its etiology, with the existence of different morphological subtypes, great heterogeneity in pathophysiology, clinical manifestations, variability in response to treatment and prognosis, all of these suggesting different etiologies [13][14][15]. Epidemiological investigations have proposed many potential risk factors [16][17][18][19][20] although few have been confirmed, mainly for acute myeloid leukemia (AML) [21][22][23].…”

Pro-inflammatory-Related Loss of CXCL12 Niche Promotes Acute Lymphoblastic Leukemic Progression at the Expense of Normal Lymphopoiesis

“…Despite the notable progression in the disease management (9, 10), the emergence of mixed-lineage leukemias, chemoresistance, and minimal residual disease decreases the probabilities for therapy success and determines relapse in more than 20% of the treated patients. As observed for the normal hematopoietic progenitors, neither premalignant cells nor leukemic blasts work as independent and autonomous entities, but they are rather surrounded in all dimensions by bone marrow (BM) niche components that provide regulatory cues essential for their cell fate decisions such as proliferation and survival (11–14).…”