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Results for “Somatic mutation”

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At least 919 records · Page 51Linked to original sources
PubMed1960

Induced somatic mutations affecting erythrocyte antigens.

The frequency of inagglutinable erythrocytes was increased in pigeons following total body irradiation and in human polycythemic patients treated with P(32). Persistence of the increased levels of inagglutinable cells was observed in pigeons retested at over 200 days after irradiation and in a polycythemic patient retested at 173 days posttreatment. These data provide additional evidence for the mutational origin of the antigen-lacking cells.

Antigens↗
PubMed1988

Identification of germline and somatic mutations affecting the retinoblastoma gene.

Retinoblastoma (RB) is a malignant tumor of developing retina that arises when abnormalities resulting in loss of function affect both alleles of the gene at the retinoblastoma locus (RB1) on chromosome 13q. The majority of RB tumors do not show gross alterations in a 4.7-kb fragment (4.7R), which is a candidate RB1 gene. To search for more subtle mutations, the ribonuclease protection method was used to analyze 4.7R messenger RNA from RB tumors. Five of 11 RB tumors, which exhibit normal 4.7R DNA and normal-sized RNA transcripts, showed abnormal ribonuclease cleavage patterns. Three of the five mutations affected the same region of the messenger RNA, consistent with an effect on splicing involving an as yet unidentified 5' exon. The high frequency of mutations in 4.7R supports the identification of 4.7R as the RB1 gene. However, the unusual nature of some of the abnormalities of 4.7 R alleles indicates that the accepted sequence of genetic events involved in the genesis of RB may require reevaluation.

Base Sequence↗
PubMed1984

Activation of a c-K-ras oncogene by somatic mutation in mouse lymphomas induced by gamma radiation.

Mouse tumors induced by gamma radiation are a useful model system for oncogenesis. DNA from such tumors contains an activated K-ras oncogene that can transform NIH 3T3 cells. This report describes the cloning of a fragment of the mouse K-ras oncogene containing the first exon from both a transformant in rat-2 cells and the brain of the same mouse that developed the tumor. Hybrid constructs containing one of the two pieces were made and only the plasmid including the first exon from the transformant gave rise to foci in NIH 3T3 cells. There was only a single base difference (G----A) in the exonic sequence, which changed glycine to aspartic acid in the transformant. By use of a synthetic oligonucleotide the presence of the mutation was demonstrated in the original tumor, ruling out modifications during DNA-mediated gene transfer and indicating that the alteration was present in the thymic lymphoma but absent from other nonmalignant tissue. The results are compatible with gamma radiation being a source of point mutations.

Animals↗
PubMed1989

Somatic mutation and transcriptional deregulation of myc in endemic Burkitt's lymphoma disease: heptamer-nonamer recognition mistakes?

We examined the structure and expression of the myc protooncogene in DNA extracted from a primary (uncultured) endemic Burkitt's lymphoma sample designated eBL3. Dot and Northern (RNA) blot analyses demonstrated extreme levels of myc RNA in the eBL3 sample. Nearly complete sequence data of the altered myc locus isolated from eBL3 DNA demonstrated extensive mutations (duplications, insertions, and deletions) in critical myc regulatory regions. Taken together, the data support the idea that myc transcriptional deregulation in Burkitt's lymphoma disease may be a consequence of the position and number of mutations produced within and around the myc locus. Furthermore, the myc exon-1-intron-1 hypermutable PvuII site is part of a potential heptamer-nonamer recognition sequence, suggesting a mechanism for mutation in endemic Burkitt's lymphoma disease.

Animals↗
PubMed1965

SOMATIC MUTATION.

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Biometry↗