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Analysis of five MDS/AML families harboring p.Thr354Met GATA2 mutations displayed significant intra- and interfamilial variations in disease latency, phenotype, and penetrance (Figure S1).
Coexpression of FLT3-ITD confers growth factor independent survival/proliferation, shortens disease latency, and results in an increase in the number of leukemic stem cells (LSC).
Furthermore, mice serially transplanted with Stat5 MOZ-TIF2 leukemic cells develop AML with longer disease latency and finally incomplete penetrance when compared with mice transplanted with Stat5 MOZ-TIF2 leukemic cells.
This BCR-ABL SH2 domain deletion mutant renders myeloid cells lines IL-3 independent [17], [18], [19], and induces a lymphoid leukemia or a CML-like disease in mice, but the disease latency is increased as compared to full length BCR-ABL [20].
We found significant spatial clusters of NHL after allowing for disease latency and residential mobility.
Here, we provide KRAS12V as a required secondary gene lesion, which significantly reduces disease latency time.
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Direct comparison of data without accounting for possible disease latencies may produce inconclusive results or erroneous effects.
Data with residential histories are preferable when causative exposures and disease latencies occur on a long enough time span that human mobility matters.
In assessing links between exposure and disease, epidemiologists must be particularly aware of: expected disease frequencies in relation to the size of populations studied, implications of long or varied disease latencies for study design and competing causes of disease and associated confounding variables.
The disease's latency period can last up to five years, making it difficult to detect.
At present these assays do not discriminate between disease and latency.
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