To minimize quantification errors, two transcript markers were utilized for each structure.
However, osteogenically and chondrogenically induced T-MPCs, respectively, expressed bone- and cartilage-associated mRNA transcript markers at a lower level compared with BM-MPCs.
In previous studies, we have analyzed selected transcript markers such as AMACR, EZH2, PSGR, PSMA and TRPM8 among others in PCa tissue specimens.
First, both high- and low-prevalent fusion genes/subtypes together provide improved clinical sensitivity through redundant transcript markers and mutually exclusive nature of some fusion genes [ 35].
Parallel and integrative analysis therefore revealed correlated modifications of ROS patterns, antioxidant biochemical defences, and corresponding transcript markers, under conditions of atrazine sensitivity and of sucrose-induced tolerance.
Key questions that we want to answer are: 1) Can previously reported transcript markers that are associated with clinical response be confirmed?; 2) What is the complexity of the transcript profile that is associated with responsiveness?; 3) Can we demonstrate the clinical utility of the transcript markers in an independent study?
In the present study we focus on further analysis of transcript biomarkers in predicting response to RTX in order to determine the value of the proclaimed transcript markers and extend the transcript profile associated with response outcome.
This fusion gene and its many subtypes not only allow stratification of clinically aggressive forms of cancer [ 10, 13], but also provide redundant and cancer-specific transcript markers for noninvasive cancer detection in bodily fluids.
The developmental incompetence (NSN) or competence (SN) of antral oocytes can be predicted using transcript markers expressed by their surrounding CCs (i.e., Has2, Ptx3, Tnfaip6, Ptgs2 and Amh).
