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1 ro-inflammatory gene program of the organism is aberrantly activated.
2 nhibitor of the Wnt signaling pathway, which is aberrantly activated across a wide range of human tum
4 rase for branched-chain amino acids (BCAAs), is aberrantly activated and functionally required for ch
5 ion factor nuclear factor-kappaB (NF-kappaB) is aberrantly activated and that inhibition of NF-kappaB
7 T family of proteins, the ways in which they are aberrantly activated, and the molecular mechanisms b
8 ion, supporting the hypothesis that CaN-NFAT are aberrantly activated by Abeta and that CaN-NFAT acti
9 osphatidylinositol 3-kinase (PI3K) signaling is aberrantly activated by a mutant thyroid hormone beta
11 Fms-like tyrosine kinase 3 (FLT3) signaling are aberrantly activated in acute myelogenous leukemia (
12 -like growth factor-1 (IGF-1) signaling axes are aberrantly activated in both primary PCa and bone me
13 Rheb2 small GTPases and their effector mTOR are aberrantly activated in human cancer and are attract
14 ndicate that the RANK and NF-kappaB pathways are aberrantly activated in luminal progenitor cells res
15 ed that STAT3 and ras-ERK signaling pathways are aberrantly activated in Sle1ab B lymphocytes, consis
16 e and adaptive immune responses, is known to be aberrantly activated in a wide variety of cancers.
17 igenic axis, and suggest that Crtc genes may be aberrantly activated in a wider range of common adult
19 elopment and tissue regeneration, thought to be aberrantly activated in epithelial-derived cancer and
20 linositol-3 kinase (PI3K)/Akt pathway, which is aberrantly activated in >50% of carcinomas, inhibits
24 e formation, suggesting that the Wnt pathway is aberrantly activated in breast cancer mammospheres.
25 l growth, proliferation, and metabolism that is aberrantly activated in cancers and certain cancer-as
28 e same pathway as Tsc genes, the TOR pathway is aberrantly activated in ciliary mutants, resembling t
33 d endoplasmic reticulum (ER) stress response is aberrantly activated in Emu-TCL1 mouse and human CLL.
35 the insulin-like growth factor (IGF) pathway is aberrantly activated in HCC by IGF2 overexpression.
46 f the lymphoid enhancer factor-1 (LEF1) gene is aberrantly activated in sporadic colon cancer, wherea
47 y confined to germ cells of adult testes but is aberrantly activated in the vast majority of neoplast
48 ovide in vivo evidence that the mTOR pathway is aberrantly activated in TSC renal pathology and that
49 scade, a pathway regulating cell growth that is aberrantly activated in tuberous sclerosis complex (T
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