William Atkins
Thursday, 14 May 2009 19:04
Science -
Health
Page 2 of 3
Their abstract states,
“The eukaryotic translation initiation factor eIF4E is elevated in 30% of malignancies including M4/M5 subtypes of acute myeloid leukemia (AML). The oncogenic potential of eIF4E arises from its ability to bind the 7-methyl guanosine (m7G) cap on mRNAs, thereby selectively enhancing eIF4E dependent nuclear mRNA export and translation.”
The study looked at patients with M4/M5 acute myeloid leukemia (AML).
M4 AML (acute myelomonocytic leukemia) and M5 AML (monocytic leukemia) are two subtypes of the AML cancer, based on the type of cell from which the leukemia is developed and how mature the cells are when looked at under a microscope.
Thirty percent of these patients had elevated amounts of the protein eukaryotic translation initiation factor (eIF4E). The patients had previously tried other treatments, which had failed to halt their cancer.
They stated,
“We tested the clinical efficacy of targeting eIF4E in M4/M5 AML patients with a physical mimic of the m7G cap, ribavirin. Among 11 evaluable patients there were: 1 complete remission(CR), 2 partial remissions(PR), 2 blast responses(BR), 4 stable diseases(SD) and 2 progressive diseases(PD).” [Abstract]
Their research shows that ribavirin restricts the activities of the eIF4E gene in the patients they tested. The team concluded this eIF4E gene is suppressed in 30% of the cancers including breast, colon and stomach, head and neck, and prostate.
They also stated,
“Ribavirin-induced re-localization of nuclear eIF4E to the cytoplasm, and reduction of eIF4E levels were associated with clinical response. Lack of response or relapse coincided with continued or renewed nuclear localization of eIF4E.” [Abstract]
Page three concludes with comments from the authors.
