The pathogenesis of the sensorineural deafness in MWS is unclear although it is postulated that expression of mutated NALP3/ CinS1 in cartilage may have a causative role [ 3].
Thus, it is postulated that tight regulation of Ctgf expression is necessary to maintain healthy tissues and induce healthy, non-fibrotic healing [15].
Therefore, it has been postulated that the expression of hENT1 could serve as a predictive biomarker for gemcitabine in pancreatic cancer.
It has been postulated that AR protein expression is increased due to AR amplification by a gene dosage effect resulting in the development of androgen resistance.
It has been postulated that the increased expression of RTL1 is responsible for the clinical outcome, whereas a role of DLK1 can be neglected [ 42].
Upregulation of SDC1 has also been described in other tumors such as pancreatic, lung and brain cancer, and it has been postulated that this aberrant expression may play a key role in promoting growth factor signaling in cancer cells [ 13].
Upregulation of syndecan-1 has also been described in tumors other than those of the colon, and it has been postulated that this aberrant expression may play a key role in promoting growth factor signaling in cancer cells [ 30 ].
It has been postulated that the increased expression of dehydrogenases and oxidoreductases using NAD+ as a cofactor, could bind and capture triclosan, reducing its effective intracellular concentration [ 32, 45].
It has been postulated that DDC mRNA expression constitutes a biomarker for the detection of minimal residual disease (MRD) in neuroblastoma patients, as well as a useful biomarker for the discrimination of neuroblastoma from other small round-cell malignancies of childhood [ 29, 30].
It has been postulated that CHX induces gene expression via dual mechanisms; by preventing synthesis or activation of a short-lived transcriptional repressor or by removing specific labile transcript degrading enzymes [ 56].
