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The identification of predictive markers for sensitivity to PARP inhibition is a priority area for research.
These results suggest the possibility that p16 and cyclin E might serve as predictive markers for sensitivity to pladienolide B derivative.
Recent reports have shown that there are differences between gefitinib responders and non-responders in the frequency of activating mutations in the EGFR gene, which suggests that such mutations might be predictive markers for sensitivity to gefitinib [ 7, 8].
Recently, differences in the frequency of activating mutations in the EGFR gene between gefitinib responders and nonresponders were reported and these EGFR mutations seem to be predictive markers for sensitivity to gefitinib (Lynch et al, 2004; Paez et al, 2004).
Recent reports showing differences in the frequency of activating mutations in the EGFR gene between gefitinib responders and nonresponders suggest that these EGFR mutations are predictive markers for sensitivity to gefitinib (Lynch et al, 2004; Paez et al, 2004).
Together with the identification of molecular and genetic markers for sensitivity and resistance to gefitinib, these trials will enable a more precise identification of which patients should receive gefitinib, when they should receive it for optimum benefit and if and how it should be sequenced with chemotherapy.
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The neuraminidase of all the Indian isolates possessed H275, the marker for sensitivity to the neuraminidase inhibitor Oseltamivir.
All the Indian isolates possessed residue H274 (position 275 in N1 numbering) a known marker for sensitivity to the neuraminidase inhibitor, Oseltamivir [17].
Furthermore, HJURP is a predictive marker for sensitivity of radiotherapy, indicating levels of HJURP mRNA and protein in breast cancer patients are clinically relevant.
All five SIVs possessed the NA H275 residue, a known marker for sensitivity to the neuraminidase inhibitor (oseltamivir) [ 25] and the genetic marker 31N in the M2 gene, confirming the amantadine resistance of A(H1N1 pdm09 viruses [ 26].
Recent reports have also implicated HER3 as having a critical role as a co-receptor for HER2 amplification as well as a marker for sensitivity to EGFR inhibition (Alimandi et al, 1995; Erjala et al, 2006; Engelman et al, 2007).
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