ABSTRACT
Human malignant melanomas, unlike normal melanocytes, can proliferate in the absence of exogenous basic fibroblast growth factor (bFGF). Exposure of primary melanomas in the vertical growth phase and metastatic melanomas to antisense oligodeoxynucleotides targeted against three different sites of human bFGF mRNA inhibited cell proliferation and colony formation in soft-agar. In contrast, exposure of human bFGF sense or antisense oligonucleotides complementary to human beta-nerve growth factor or insulin-like growth factor I mRNA had no such effects. These experiments indicate that activation of the bFGF gene may play an important role in the progression from melanocytic precursor lesions to malignant melanoma.
Subject(s)
Antineoplastic Agents/pharmacology , Fibroblast Growth Factors/genetics , Growth Inhibitors/pharmacology , Melanoma/pathology , Oligonucleotides/pharmacology , Base Sequence , Cell Division/drug effects , Cell Line , Colony-Forming Units Assay , Fibroblast Growth Factors/antagonists & inhibitors , Humans , Kinetics , Melanoma/genetics , Melanoma/metabolism , Molecular Sequence Data , Oligonucleotides/metabolism , Oligonucleotides, Antisense , Tumor Cells, CulturedABSTRACT
Two cases of acute myelocytic leukemia (AML) type M4 with trisomy 4 are presented. In one case trisomy 4 was associated with del(3). Both patients had no history of exposure to mutagenic events. In our material the frequency of trisomy 4-AML is not higher than 1%.