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In general, the wall polymer alteration could lead to a different cellulose CrI.
Of particular interest was the PIK3CA amlification was closely associated with elevated p-Akt, suggesting that this genetic alteration could lead to oncogenic activation of PI3K/Akt signaling pathway and thus contributed to the malignant progression of gastric cancer.
Finally, in situ RNA hybridisation (ISH) and reverse transcription PCR (RT PCR) were performed to assess whether the identified genetic alteration could lead to significant change in transcript level of the gene in question.
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In the future, such distinct alterations could lead to a better understanding and identification of potential thyroid-disrupting chemicals.
These structural and ultrastructural alterations could lead to transcriptional or posttranslational modifications of these proteins.
These alterations could lead to adverse birth outcomes and maternal pregnancy complications such as pregnancy-induced hypertension and preeclampsia.
Together these alterations could lead to the formation of pathological thrombi resulting in infarcts in the heart or brain.
Multiple pathways of genetic alterations could lead to development of ATC, as not all ATC have identical genetic profiles.
These alterations could lead to an abnormal MYC protein that is not recognized by either of the antibodies used in the present study.
These alterations could lead to interactions of these ions with membrane components, resulting in modifications of the lipid microenvironment that interacts with membrane transporters.
This aggregation of pathways, based largely on preexisting biological information, remains coarse-grained with many possible nodes in each of these TPs whose alterations could lead to toxicity.
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