Acute leukemia in early childhood

Area of Science:

• Pediatric Oncology
• Hematology
• Cancer Etiology

Background:

• Infant acute leukemia is biologically and clinically distinct from childhood leukemia.
• Specific immunophenotypes (pro-B, CD10 negative) and genetic alterations (MLL gene rearrangements) are characteristic of infant acute leukemia.
• The TEL/AML1 fusion gene is more common in children over 24 months.

Purpose of the Study:

• To summarize recent findings on the biology of early childhood leukemias, focusing on infant acute leukemia in Brazil.
• To highlight the role of prenatal genetic events and environmental exposures in infant acute leukemia.
• To present molecular data from a Brazilian cohort of infant acute leukemia patients.

Main Methods:

• Review of recent scientific literature on infant acute leukemia.
• Analysis of molecular data from a Brazilian cohort (0-23 months) identifying specific genetic alterations (TEL/AML1, E2A/PBX1, PML/RARA, AML1/ETO).
• Examination of epidemiological studies on maternal exposures and their association with infant acute leukemia risk.

Main Results:

• A Brazilian cohort revealed specific genetic alterations: TEL/AML1 (N=9), E2A/PBX1 (N=4), PML/RARA (N=4), and AML1/ETO (N=2).
• The majority of genetic events in infant acute leukemia are believed to originate prenatally.
• Maternal exposures to dipyrone, pesticides, and hormones were associated with increased odds of infant acute leukemia.

Conclusions:

• Infant acute leukemia biology is significantly influenced by prenatal genetic alterations.
• Environmental exposures during pregnancy are critical factors in the etiology of infant acute leukemia.
• Further research into prenatal exposures can elucidate the causes of infant acute leukemia.