| |
|
|
|
|
|
|
|||
|
LM Chelstrom, R Gunther, J Simon, SC Raimondi, R Krance, WM Crist and FM Uckun
Department of Therapeutic Radiology-Radiation Oncology, University of
Minnesota, Minneapolis.
Primary bone marrow blasts from 4 children with t(8;21) acute myeloid
leukemia (AML), 6 children with inv(16) AML, and 2 children with t(9;11)
AML were injected intravenously or transplanted under the kidney capsule of
sublethally irradiated mice with severe combined immunodeficiency (SCID).
Leukemic cells from all AML patients infiltrated the SCID mouse thymus,
suggesting that the thymic microenvironment supports the survival and
growth of human AML blasts. Blasts from 1 of 4 t(8;21) AML patients and 4
of 6 inv(16) AML patients caused histopathologically detectable
disseminated leukemia. Blasts from the remaining patients produced
disseminated occult leukemia that was only detected by polymerase chain
reaction. Occurrence of histopathologically detectable disseminated
leukemia was dependent on intravenous injection of leukemic cells; none of
the mice challenged with an inoculum transplanted under the kidney capsule
developed overt leukemia. No obvious association was noted between
occurrence of leukemia in SCID mice and clinical or laboratory features
presented by patients, including age, sex, or leukocyte count at diagnosis.
To our knowledge, this study is the first to show that leukemic blasts from
children with newly diagnosed AML, especially inv(16) AML, can cause
disseminated human leukemia in SCID mice without exogenous cytokine
support. The SCID mouse model system may prove particularly useful for
designing more effective treatment strategies against childhood AML.
This article has been cited by other articles:
| |||||||||||
| Copyright © 1994 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||