Childhood acute lymphoblastic leukemia is triggered by the introduction of immunization against diphtheria

Med Hypotheses. 2007;68(2):324-7. doi: 10.1016/j.mehy.2006.07.019. Epub 2006 Sep 26.

Abstract

Background: Childhood acute lymphoblastic leukemia has prenatal origin. Leukemogenic translocations originating during fetal life are insufficient for overt leukemia. Transgenic TEL-AML1 mice have failed to develop leukemia. Additional postnatal events are required for full leukemogenesis. The significant peak-age (2-5 years) first appeared after 1940 in Great Britain. Since then, childhood leukemia has almost unchangeable incidence. In 1940 the introduction of immunization against diphtheria on a national scale was begun in Great Britain.

Hypothesis: Childhood acute lymphoblastic leukemia is triggered by vaccination against diphtheria.

Testing the hypothesis: Epidemiological survey for leukemia cases among "exemptors" and unvaccinated cases among ALL children should be done. Simultaneously, the transgenic TEL-AML1 mice should be vaccinated with the diphtheritic toxoid.

Implications of the hypothesis: If there is no leukemia among the "exemptors", no unvaccinated among ALL, and some mice develop leukemia upon vaccination childhood leukemia will be prevented by massive neonatal screening for leukemogenic genetics and/or with a new vaccination schedule.

MeSH terms

  • Animals
  • Child
  • Diphtheria Toxoid / adverse effects*
  • Disease Models, Animal
  • Humans
  • Incidence
  • Mice
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology*
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology*

Substances

  • Diphtheria Toxoid