Irinotecan or taxane-based regimens could be the better alternative for patients with VEGF -634 G/G genotype.
Therefore, we cannot exclude the hypothesis that the observed higher efficacy of taxane-based regimens could be attributed to the effect of taxanes on HER2 CTCs.
In fact, PI-based regimens could be more cumbersome to follow, due to a higher number of pills and to dietary restrictions linked to drug assumption.
Fluoropyrimidine-based regimens could be used as the second-line chemotherapy in patients who failed in GEM alone or GEM plus nab-paclitaxel treatment, although their benefit has not been proven yet (Boeck et al, 2007; Gebbia et al, 2007; Kulke et al, 2007; Xiong et al, 2008; Morizane et al, 2009; Novarino et al, 2009).
However, the short survival attained in FOLFOX-treated patients with positive protein ERCC1 (HR, 1.91) (Kwon et al, 2007) or overexpression of ERCC1 mRNA (HR, 9.4) suggests that irinotecan or taxane-based regimens could be the better alternative for these patients.
NAC also allows for timely adjustment of administered drugs based on response, so ineffective regimens could be terminated early to spare patients from unnecessary toxicity while allowing other effective regimens to work sooner.
Furthermore, regimens could be defined based on other time-independent or time-dependent covariates (such as HIV viral load), although estimation may be hampered by the limited data available for each regimen if many factors are incorporated.
Using these costs and the mid-point estimates for ribavirin, daclatasvir, and sofosbuvir taken from a previous analysis, 5 the production costs of two-drug combination regimens could be estimated based on the combinations currently being studied in clinical trials (Table 1).
Thus, currently used sedative regimens could be considered to be predominantly hypnotic-based treatment regimens.
Individualized dosing regimens could be achieved by combining different capsules.
Based on the result, an MDR-selective regimen could be added to the next rounds of chemotherapy, to kill multidrug-resistant cells that express the transporter.
