Myelodysplasia
|
0.050 |
AlteredExpression
|
disease |
BEFREE |
Accelerated exon skipping of IRF-1 mRNA in human myelodysplasia/leukemia; a possible mechanism of tumor suppressor inactivation.
|
7936656 |
1994 |
Childhood Leukemia
|
0.040 |
AlteredExpression
|
disease |
BEFREE |
Accelerated exon skipping of IRF-1 mRNA in human myelodysplasia/leukemia; a possible mechanism of tumor suppressor inactivation.
|
7936656 |
1994 |
Hematopoietic Neoplasms
|
0.010 |
PosttranslationalModification
|
group |
BEFREE |
Thus this accelerated exon skipping may cause the inactivation of IRF-1 and thereby contribute to the development of human hematopoietic malignancies.
|
7936656 |
1994 |
Leukemia, Myelocytic, Acute
|
0.380 |
GeneticVariation
|
disease |
BEFREE |
We have investigated the allelic loss of IRF1 in a group of 12 patients with MDS and a 5q deletion and 2 patients with AML and a 5q deletion.
|
8219215 |
1993 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Recently IRF1, a putative tumor suppressor gene localized to the long arm of chromosome 5, has been shown to be deleted from the 5q- chromosome in a group of patients with MDS and AML.
|
8219215 |
1993 |
MYELODYSPLASTIC SYNDROME
|
0.100 |
GeneticVariation
|
group |
BEFREE |
We have investigated the allelic loss of IRF1 in a group of 12 patients with MDS and a 5q deletion and 2 patients with AML and a 5q deletion.
|
8219215 |
1993 |
Myelodysplasia
|
0.050 |
Biomarker
|
disease |
BEFREE |
Allelic loss of IRF1 in myelodysplasia and acute myeloid leukemia: retention of IRF1 on the 5q- chromosome in some patients with the 5q- syndrome.
|
8219215 |
1993 |
5q-syndrome
|
0.010 |
Biomarker
|
disease |
BEFREE |
We conclude that IRF1 maps outside the commonly deleted segment of the 5q- chromosome and that loss of IRF1 is not solely responsible for the development of the 5q- syndrome.
|
8219215 |
1993 |
Myelodysplastic Syndrome with Isolated del(5q)
|
0.010 |
Biomarker
|
disease |
BEFREE |
We conclude that IRF1 maps outside the commonly deleted segment of the 5q- chromosome and that loss of IRF1 is not solely responsible for the development of the 5q- syndrome.
|
8219215 |
1993 |
Chromosome 5, trisomy 5q
|
0.010 |
Biomarker
|
disease |
BEFREE |
We conclude that IRF1 maps outside the commonly deleted segment of the 5q- chromosome and that loss of IRF1 is not solely responsible for the development of the 5q- syndrome.
|
8219215 |
1993 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Although more than 30 different 5q deletions are described, recent studies have demonstrated 5q31 as the common deleted region and have mapped a tumor suppressor (IRF-1) and a cluster of interleukin genes to 5q31.
|
8267400 |
1994 |
MYELODYSPLASTIC SYNDROME
|
0.100 |
Biomarker
|
group |
BEFREE |
Thus, IRF-1 may be a critically deleted gene in human leukemia and myelodysplasia.
|
8438156 |
1993 |
leukemia
|
0.060 |
Biomarker
|
disease |
BEFREE |
Thus, IRF-1 may be a critically deleted gene in human leukemia and myelodysplasia.
|
8438156 |
1993 |
Myelodysplasia
|
0.050 |
Biomarker
|
disease |
BEFREE |
Thus, IRF-1 may be a critically deleted gene in human leukemia and myelodysplasia.
|
8438156 |
1993 |
Childhood Leukemia
|
0.040 |
Biomarker
|
disease |
BEFREE |
Thus, IRF-1 may be a critically deleted gene in human leukemia and myelodysplasia.
|
8438156 |
1993 |
Acute leukemia
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Inactivating rearrangements of one IRF-1 allele, accompanied by deletion of the second allele, were also identified in one case of acute leukemia.
|
8438156 |
1993 |
Lipoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Using a chromosome walking approach combined with fluorescence in situ hybridization analysis, we were able to show that the chromosome 12 breakpoints involved in uterine leiomyoma, pleomorphic adenoma of the salivary gland, and lipoma cluster to the same chromosomal region, which we therefore designated MAR (multiple-aberration region).
|
8527387 |
1995 |
Lipomatosis, Multiple
|
0.010 |
Biomarker
|
disease |
BEFREE |
Using a chromosome walking approach combined with fluorescence in situ hybridization analysis, we were able to show that the chromosome 12 breakpoints involved in uterine leiomyoma, pleomorphic adenoma of the salivary gland, and lipoma cluster to the same chromosomal region, which we therefore designated MAR (multiple-aberration region).
|
8527387 |
1995 |
Carcinoma
|
0.020 |
Biomarker
|
group |
BEFREE |
Deletion at the APC gene locus may just be the result of large deletions on 5q and may not be important in esophageal carcinogenesis, and the IRF-1 gene or other gene(s) on 5q31.1 may be the true target of frequent deletions on 5q that may play an important role in the pathogenesis of the majority of esophageal carcinomas.
|
8536888 |
1996 |
Adenomatous Polyposis Coli
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Although many tumors exhibited large interstitial deletions on 5q that included the APC locus (5q21), we have identified minimum regions of deletion as the D5S428 locus and the interferon regulatory factor-1 (IRF-1) locus.
|
8564980 |
1996 |
Atrial Premature Complexes
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Although many tumors exhibited large interstitial deletions on 5q that included the APC locus (5q21), we have identified minimum regions of deletion as the D5S428 locus and the interferon regulatory factor-1 (IRF-1) locus.
|
8564980 |
1996 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
IRF-1 manifests tumor suppressor activity.
|
8622878 |
1996 |
leukemia
|
0.060 |
GeneticVariation
|
disease |
BEFREE |
This result predicts diminished expression of PKR as a potential consequence of deletion of the IRF-1 gene in human leukemias.
|
8622878 |
1996 |
Myelodysplasia
|
0.050 |
GeneticVariation
|
disease |
BEFREE |
Its overexpression results in inhibition of cell growth, and deletions of the IRF-1 gene were demonstrated in a number of human leukemias and myelodysplasias.
|
8622878 |
1996 |
Leukemia, Myelocytic, Acute
|
0.380 |
Biomarker
|
disease |
BEFREE |
Specific DNA protein complex formation was observed with the probes from the beta-casein and IRF-1 gene promoters, but not with the ISRE oligonucleotide probe, when cell extracts from acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) were investigated.
|
8634413 |
1996 |