Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The histogenesis of the Reed-Sternberg (R-S) cell in Hodgkin's disease is uncertain. Some have suggested that it is a derivative of the monocyte/macrophage lineage. To explore this possibility, we have searched for the presence of mRNA corresponding to the c-fms proto-oncogene, a marker for cells of the monocyte/macrophage lineage which encodes the colony-stimulating factor-1 receptor. In situ hybridization was performed using a single-stranded c-fms complementary RNA (cRNA) to probe R-S cells, lymphocytes, and eosinophils from touch imprints of a lymph node from a 12-year-old boy with mixed cellularity Hodgkin's disease in relapse. The probe was synthesized from a bacterial plasmid, pSM3, into which a portion of v-fms (a viral-derived oncogene) had been inserted. The plasmid was linearized with a restriction endonuclease, and 35S-labeled cRNA was synthesized from the DNA template using T3 RNA polymerase and the nucleotide analog [35S]UTP. Positive control hybridizations were obtained with the human acute promyelocytic cell line HL-60 induced to monocyte differentiation. R-S cells were clearly negative, supporting a cell of origin other than the monocyte. In situ hybridization is a potentially powerful method for exploring differentiation and assigning cell lineage in R-S cells.
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PMID:Lack of CSF-1 receptor message in Reed-Sternberg cells. 255 Apr 17

By using blot hybridization with a v-fms probe, a polymorphism for EcoRI, HindIII, and BamHI restriction endonuclease sites associated with the human c-fms locus was observed in a random adult population. This restriction fragment length polymorphism can be explained on the basis of the existence of two alleles, a and b, and is due to a short (congruent to 500 base pairs) deletion characteristic of allele a. The distribution in the analyzed population (48 unrelated individuals) is 23% heterozygotes ab, 75% homozygotes bb, and 2% homozygotes aa. Though the inheritance of this polymorphism follows a Mendelian pattern, the children from couples ab X bb are of the following genotype: 74% ab and 26% bb. These deviations from the expected frequencies of 50% suggest a selective pressure in favor of heterozygotes.
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PMID:Restriction fragment length polymorphism of the human c-fms gene. 298 42

A restriction fragment length polymorphism (RFLP) for the c-fms gene was identified in the human oral squamous cell carcinoma cell lines, Ca9-22, HSC-2 and -3. The RFLP was detected after EcoR I, BamH I and Hind III endonuclease digestion, indicating the presence of two alleles, a and b. The allele a deleted 426bp length of allele b. We determined the sequence of this deletion, that localized in intron 11 with an EcoR I site. The phenotype of Ca9-22 was aa, and the others were bb. Both phenotypes were equally expressed and the transcripts were phosphorylated in these cell lines. The distribution in the analyzed population (66 patients and normal individuals) was 3.1% homozygotic aa, 13.5% heterozygotic ab and 83.4% homozygotic bb.
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PMID:Restriction fragment length polymorphism of the c-fms gene in the human oral squamous cell carcinomas. 791 38

This study was aimed to investigate the frequency of FMS-like tyrosine kinase 3 (FLT3) mutations including internal tandem duplication (ITD) mutation of juxtamembrane region and point mutation of the second tyrosine kinase domain (TKD) in acute myeloid leukemia (AML) patients and its clinical significance. The ITD mutation in FLT3 exon 14, 15 of bone marrow mononuclear cells was detected by genomic DNA-PCR, the TKD point mutation in FLT3 exon 20 was detected by genomic DNA-PCR combined with restriction endonuclease digest. The results indicated that among 131 newly diagnosed AML patients, 21 patients (16.0%) showed FLT3-ITD positive, 3 patients (2.3%) showed FLT3-TKD positive. None was found harboring both mutations. The WBC and bone marrow blast counts in FLT3-ITD positive patients seemed both higher than those in patients with wild-type FLT3 (FLT3-wt), but there was significant difference only in WBC count (p<0.05). The complete remission (CR) rate in FLT3-ITD positive patients was 47.6%, which was significantly lower than that in FLT3-wt patients (88.1%, p<0.05). There was no statistical difference in CR rate between FLT3-ITD positive and negative patients in 20 cases of M3; the CR rate in FLT3-ITD positive patients with non M(3) was 37.5 (6/16) which was obviously lower than that in FLT3-wt patients with non M3 (90.6%, 48/53) (p<0.05). 3 FLT3-ITD positive patients with CR relapsed after CR for 14 (2-20) months with relapse rate 50% (3/6) which was higher than that in FLT3-wt patients (29.2%, 14/48). It is concluded that FLT3 mutation is common in AML patients, while FLT3-ITD mutation is more frequent than FLT3-TKD mutation. The AML patients with FLT3-ITD mutation have a poor prognosis, while FLT3-TKD point mutation does not significantly influences prognosis of the patients. Therefore early detection of FLT3 mutation may be important for targeting therapy and evaluating clinical prognosis of AML patients.
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PMID:[FMS-like tyrosine kinase 3 gene mutations in acute myeloid leukemia]. 1984 Apr 37