The performance of all markers was poorer in the PLCO study when assayed in samples taken more than 6 months from diagnosis [26].
However, clinical and immunologic markers are poor predictors of virologic suppression [3], [4].
Despite their established use, standard inflammation markers are poor predictors of clinical outcome after MI.
This diagnostic criterion is questionable, because 1) E-cadherin expression is classically downregulated during EMT and absent in cells after complete EMT; and 2) as previously noted, the sensitivity of α-SMA and FSP1 as EMT markers is poor, because their late and/or rare expression during human EMT.
While HA has been shown to be accurate when used in combination with other parameters in HIV/HCV-coinfected patients (SHASTA index [ 24], HGM-3 [ 22]), its effectiveness at assessing liver fibrosis as an isolated marker is poorer.
Co-localization of dZIP13 with endosome markers, however, was poor.
Amplification rate of the 'ML' markers was the poorest (34%), less than half the rate of the 'MLG' and 'MP' groups (Table 1).
One of the bottlenecks in discovering appropriate cancer markers is a poor understanding of the pathophysiology of the disease [26], [27], [46].
Many call plots of the significant markers were of poor quality due to null alleles, cluster overlap, or more than three clusters.
Moesin is highly expressed in aggressive basal type breast carcinomas, it is transcriptionally upregulated upon EMT induction in breast cancer cell lines, and it is concomitant to the appearance of invasiveness markers, being a poor outcome prognostic marker [ 42 44].
