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Results for “ERYTHROBLASTOSIS”

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At least 1,045 records · Page 58Linked to original sources
PubMed1978

Temperature-sensitive mutant of avian erythroblastosis virus suggests a block of differentiation as mechanism of leukaemogenesis.

A temperature sensitive mutant has been isolated for the first time from a replication defective acute leukaemia virus, AEV. In vivo, at 41 degrees C, the mutant shows a reduced leukaemogenic potential. In vitro, in erythroblasts transformed at 35 degrees C, haemoglobin synthesis can be induced by a shift to 41 degrees C. This indicates that the continuous expression of a viral gene product is necessary to maintain the undifferentiated state of the virus-transformed leukaemia cells.

Alpharetrovirus↗
PubMed1992

Erythroblastosis in birth asphyxia.

The pH and erythroblast count in umbilical venous blood were measured in 27 term neonates with normal birth weights. In seven cases, infants were admitted to the neonatal intensive care unit because of birth asphyxia, and the findings in these cases were compared to the values of the 20 non-asphyxiated neonates that were delivered either vaginally (n = 10) or by elective Cesarean section (n = 10). The umbilical venous blood pH in the asphyxiated group was significantly lower than that in the control group of infants that were delivered by Cesarean section, but not significantly different from the controls that were delivered vaginally. In contrast, the erythroblast count in the asphyxiated group was significantly higher than that in the controls, irrespective of the mode of delivery. These findings suggest that cord blood erythroblast count at delivery may provide a better measure of fetal tissue hypoxia than umbilical venous pH.

Journal Article↗
PubMed1985

The putative transforming protein of S13 avian erythroblastosis virus is a transmembrane glycoprotein with an associated protein kinase activity.

S13 is an avian retrovirus that transforms both fibroblasts and erythroblasts. The gene product responsible for the oncogenic effects of S13 is the env-related glycoprotein gp155. In this report we show that gp155 is a transmembrane protein with a 55-kDa cytoplasmic domain. Pulse-chase analysis shows that gp155 was cleaved posttranslationally into two glycosylated proteins, gp85 and gp70. In addition, we show that a tyrosine protein kinase activity is associated only with the gp70 protein in microsomes and in immune complexes.

Alpharetrovirus↗
PubMed1994

Avian erythroblastosis virus E26: only one (myb) of two cell-derived coding regions is necessary for oncogenicity.

The oncogene hypothesis postulates that mutated cellular genes, termed proto-onc genes, function as cancer genes because they are related to retroviral onc genes. However, in contrast to retroviral onc genes, mutated proto-onc genes from cancers are not sufficient for carcinogenesis. Therefore, it has been proposed that mutated proto-onc genes depend on other proto-onc genes for carcinogenesis. Since the oncogene of the avian leukemia virus E26 includes coding regions derived from two cellular proto-onc genes, proto-myb and proto-ets, this hybrid gene has been proposed to be a model for two-gene-carcinogenesis. Here we set out to test this proposal. For this purpose myb and ets deletion mutants of cloned E26 provirus were prepared, and the corresponding viruses, produced by transfected primary chicken embryo cells, were tested for leukemogenicity in newborn chickens. It was found that an ets deletion mutant was just as leukemogenic as the wild-type virus and that a myb deletion mutant lacked leukemogenicity completely. To eliminate the possibility that our E26 myb deletion mutant failed to be leukemogenic because it failed to replicate, the virus was titered by a quantitative polymerase chain reaction (PCR) method. By this method, E26 from the plasma of infected chickens was first allowed to reverse-transcribe viral RNA to cDNA in vitro, and then the cDNA concentration was determined from the lowest dilution that gave a positive signal after amplification of E26 cDNA by the PCR method. Virus titers of about 10(5) per ml were found for wild type and for myb and ets deletion mutants of E26. It is concluded that the ets region is not essential for carcinogenesis, and E26 derives transforming function from overexpression of its proto-myb coding region via the retroviral promoter. Thus, E26 is a single-hit carcinogen and, like all other oncogenic retroviruses, is not a model for two-gene-carcinogenesis. Viral ets probably reflects a genetic accident that transduced sequences of proto-ets together with proto-myb in generating E26.

Alpharetrovirus↗