TY - JOUR
T1 - The expression pattern of the AML1 gene in non-Hodgkin's B-cell lymphomas and normal B lymphocytes
AU - Chimienti, Guglielmina
AU - Alaibac, Mauro
AU - Marzullo, Franco
AU - Carbone, Antonio
AU - Pepe, Gabriella
PY - 2000
Y1 - 2000
N2 - We have studied the expression of the three human acute myeloid leukemia (AML) genes in primary samples of non-Hodgkin's B-cell lymphomas in which translocations involving these loci were not present. We found a widespread expression of the three AML genes in all the lymphoma samples as well as in the purified normal B-lymphocytes. Thus, the presence of the three mRNAs 'per se' does not allow the identification of the pathological status. However, AML1 showed a different transcription pattern in the neoplastic tissues with respect to the normal B-cells. The AML1b isoform proved to be peculiar to this lymphoma. Our data support the idea that qualitative and quantitative alterations of AML1 gene expression deriving from deregulating mechanisms other than translocations may be involved in this malignancy. The usage of two differently regulated promoters driving the expression of the transcripts AML1b and AML1c may be one of these mechanisms. Finally, we report the presence of a new alternatively spliced transcript in normal B-cells. (C) 2000 Academic Press.
AB - We have studied the expression of the three human acute myeloid leukemia (AML) genes in primary samples of non-Hodgkin's B-cell lymphomas in which translocations involving these loci were not present. We found a widespread expression of the three AML genes in all the lymphoma samples as well as in the purified normal B-lymphocytes. Thus, the presence of the three mRNAs 'per se' does not allow the identification of the pathological status. However, AML1 showed a different transcription pattern in the neoplastic tissues with respect to the normal B-cells. The AML1b isoform proved to be peculiar to this lymphoma. Our data support the idea that qualitative and quantitative alterations of AML1 gene expression deriving from deregulating mechanisms other than translocations may be involved in this malignancy. The usage of two differently regulated promoters driving the expression of the transcripts AML1b and AML1c may be one of these mechanisms. Finally, we report the presence of a new alternatively spliced transcript in normal B-cells. (C) 2000 Academic Press.
KW - Alternative splicing
KW - B lymphocytes
KW - Lymphoid neoplasm
KW - RT-PCR
KW - Transcription pattern
UR - http://www.scopus.com/inward/record.url?scp=0033822313&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0033822313&partnerID=8YFLogxK
U2 - 10.1006/bcmd.2000.0295
DO - 10.1006/bcmd.2000.0295
M3 - Article
C2 - 10950938
AN - SCOPUS:0033822313
VL - 26
SP - 186
EP - 192
JO - Blood Cells, Molecules, and Diseases
JF - Blood Cells, Molecules, and Diseases
SN - 1079-9796
IS - 3
ER -