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With external validation this assumption is generally not appropriate.
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In future work, a validation of this assumption would be valuable.
While the general clinical lore suggests that early intervention benefits treatment outcome, the empirical validation of this assumption is inconclusive.
Further work will incorporate designs that formally include validation of this assumption.
However, testing or the validation of this assumption can be hampered by the small number of cycles a patient may undertake, and so violations are often undetected.
Furthermore, in the absence of empirical validation, the assumption that there is always a formula out there somewhere.
This assumption requires validation in appropriately constructed clinical trials.
This assumption requires validation, as genes on the Y chromosome may affect risk for cardiovascular disease [ 23- 25], and genes on the X chromosome may affect responses to hypoxia and apoptosis, processes involved in cardiac performance [ 9- 11, 26, 27].
However, this assumption lacks experimental validation, especially in the case of cancer cells.
We assumed that the surrounding nucleotide composition of these genes may be the genuine trigger, the upstream genome structure of these genes are more stable and avoid the insertion of non coding DNAs or other genes which leads to the shorter interval between adjacent gene; however this assumption requires further validation.
Whether this assumption is valid is an important but often neglected aspect of the validation of risk-adjustment methods.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com