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Recent work challenges this view by providing evidence that luminal precursor cells are involved in the pathogenesis of basal breast cancers and has made new links between normal cell populations and molecular tumor phenotypes.
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Molecular similarities are also observed between other normal cell populations and cancer subtypes.
Studying and uncovering the interactions that take place between tumor and normal cell populations is essential for understanding cancer progression and for determining new ways to therapeutically inhibit pro-tumorigenic responses and enhance anti-tumorigenic behavior.
However, the technical limitations of the single parametric flow cytometry technique, including the inability to differentiate between DNA diploid tumour and normal cell populations (Hedley et al, 1983), does not allow accurate sub-grouping of breast tumours, thus limiting further statistical analysis.
Sampling and sequencing of distinct tumour cell populations as well as histologically normal cell populations allows the characterization of genetic changes occurring between these cell populations providing insight into cancer development and progression.
This strategy attempts to exploit the more rapid proliferation of malignant compared with normal cell populations.
These glial cells heavily infiltrate gliomas, and can constitute up to 30% of the infiltrating normal cell population (the stroma).
When this occurs between two non-allelic loci in a cell during mitosis, it gives rise to two cell populations with a deletion and a reciprocal duplication, respectively, along with an uninvolved normal cell population in an individual.
The primary aim of our coculture system is to harvest independently each side of cell population after coculture to study the cross talk between normal cell and cancer cell.
The difference between normal cells and persisters cannot be found in their DNA.
We used normal astrocytes to compare the cytotoxicity of AND between normal cells and glioma cells.
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