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These findings made us hypothesize that RUNX3 might be silenced by methylation in adult oral epithelial cells.
These findings made us hypothesize that disorder of PP2A may induce constitutive phosphorylation on Ser51 of Aur-A in cancer cells.
The highly differentiated cellular pattern in the synovium of the RA patients made us hypothesize that Flt3-L, with its ability to induce proliferation and differentiation, could be of importance in induction and/or progression of arthritis.
The highly significant and strikingly persistent chromosomal localization of the differentially expressed genes made us hypothesize about which transcriptional regulation mechanisms can underlie these gene expression patterns.
This difference made us hypothesize that the mechanisms of reovirus-induced innate immune responses differed between reovirus-susceptible and reovirus-refractory tumor cells.
The immune-suppressive effects of ongoing angiogenesis made us hypothesize those inhibitors of angiogenesis may revert endothelial cell anergy and increase leukocyte infiltration in tumors, thereby enhancing the vulnerability of tumors to the immune system.
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The fact that electronic symptom surveillance with clinician feedback using the Patient-Reported Outcomes version of Common Terminology Criteria for Adverse Events (PRO-CTCAE) in Danish prostate cancer patients was shown to be feasible in this study makes us hypothesize that the model is applicable to future research.
The fact that we could not detect Borrelia DNA in the AAA wall, even with sensitive PCR-based methods, makes us hypothesize that AAAs are not triggered by the direct infection of the aortic wall by Borrelia.
HPLC profile also showed few unidentified peaks, which made us to hypothesize that there might be some synergistic or cumulative effect of different phenolic compounds, resulting in high transformation efficiency.
The fact that HDACi cause a decrease in the expression levels of Wee1 and Chk1 made us to hypothesize that cell death may occur through mitotic catastrophe due to the accumulation of DNA damage that cannot be repaired before mitosis.
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