Acute lymphoid leukemia etiopathogenesis

Mol Biol Rep. 2021 Jan;48(1):817-822. doi: 10.1007/s11033-020-06073-3. Epub 2021 Jan 13.

Abstract

Acute lymphoid leukemia (ALL) is a type of hematological neoplasm that affects the precursor cells of strains B, T and NK, with a higher incidence in the pediatric range. The pathophysiology of ALL is characterized by chromosomal abnormalities and genetic alterations involved in the differentiation and proliferation of lymphoid precursor cells. Despite the lack of information in the literature, it is believed that leukemogenesis originates from a complex interaction between environmental and genetic factors, which combined lead to cellular modifications. Environmental factors have been evaluated as possible predisposing factors in the development of ALL but there are still conflicting results in the world literature. In this context, the aim of the present review is to discuss the major exogenous factors regarding ALL.

Keywords: Childhood; Environment; Infection; Leukemia.

Publication types

  • Review

MeSH terms

  • Adult
  • B-Lymphocytes / immunology
  • B-Lymphocytes / pathology
  • Carcinogenesis / genetics
  • Carcinogenesis / immunology*
  • Carcinogenesis / pathology
  • Cell Differentiation
  • Cell Proliferation
  • Child
  • Chromosome Aberrations
  • Cytokines / genetics
  • Cytokines / immunology
  • Gene Expression Regulation, Leukemic / immunology*
  • Gene-Environment Interaction*
  • Humans
  • Killer Cells, Natural / immunology
  • Killer Cells, Natural / pathology
  • Lymphoid Progenitor Cells / immunology*
  • Lymphoid Progenitor Cells / pathology
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / immunology
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology*
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • T-Lymphocytes / immunology
  • T-Lymphocytes / pathology

Substances

  • Cytokines
  • Neoplasm Proteins