Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.1.26.9 (
ribonuclease
)
6,589
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Expression of the 93-kd tyrosine kinase encoded by the human
c-fes
proto-oncogene (also known as FES) is restricted to mature hematopoietic cells of the granulocytic and monocytic lineages, suggestive of a function essential to normal myeloid differentiation. However, recent studies have shown that
c-fes
can transform fibroblasts if sufficient levels of gene expression are achieved. These findings indicate that strict regulation of the
c-fes
gene is critical to normal myeloid development, whereas elevated
c-fes
expression may contribute to malignant transformation. In the present study, we compared the
c-fes
messenger RNA (mRNA) levels in leukemia blasts from patients with myeloid or lymphoid leukemia with those of peripheral monocytes from a normal donor with the use of a quantitative
ribonuclease
protection assay. The presence of
c-fes
mRNA was readily detected in both acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) cells, but
c-fes
mRNA was present in low levels or was absent in lymphoid leukemia cells. The leukemia cells of two of five AML patients and four of four CML patients expressed more
c-fes
mRNA than monocytes from a normal donor, with more than a threefold elevation in the cells of one CML patient. No evidence of amplification or rearrangement of the
c-fes
gene was detectable by Southern blot analysis of myeloid leukemia DNA, suggesting that the variation in
c-fes
mRNA levels are related to differences in transcriptional activity and/or message stability. These results indicate that elevated
c-fes
expression is a common feature of myeloid leukemia cells that could potentially contribute to the leukemia phenotype.
...
PMID:Elevated expression of the c-fes proto-oncogene in adult human myeloid leukemia cells in the absence of gene amplification. 198 16