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mTOR inhibition induces upstream receptor tyrosine kinase signaling and activates Akt.
TLDR
The data suggest that feedback down-regulation of receptor tyrosine kinase signaling is a frequent event in tumor cells with constitutive mTOR activation, and reversal of this feedback loop by rapamycin may attenuate its therapeutic effects, whereas combination therapy that ablates mTOR function and prevents Akt activation may have improved antitumor activity.
Poor prognosis in carcinoma is associated with a gene expression signature of aberrant PTEN tumor suppressor pathway activity
TLDR
It is indicated that aberrant PI3K pathway signaling is strongly associated with metastasis and poor survival across carcinoma types, highlighting the enormous potential impact on patient survival that pathway inhibition could achieve.
ERKs and p38 Kinase Phosphorylate p53 Protein at Serine 15 in Response to UV Radiation*
TLDR
It is found that in a mouse JB6 epidermal cell line, ERKs and p38 kinase form a complex with p53 following UVB radiation, providing evidence that UVB-induced phosphorylation of p53 at serine 15 is mediated directly by ERKS and p 38 kinase.
Resistance to gefitinib in PTEN-null HER-overexpressing tumor cells can be overcome through restoration of PTEN function or pharmacologic modulation of constitutive phosphatidylinositol 3'-kinase/Akt
TLDR
Reconstitution of PTEN function through tet-inducible expression restores ZD1839 sensitivity to these cells and reestablishes EGFR-stimulated Akt signaling, and pharmacologic down-regulation of constitutive PI3K/Akt pathway signaling using the PI3k inhibitor LY294002 similarly restores EGFR -stimulatedAkt signaling and sensitizes MDA-468 cells to ZD 1839.
Resveratrol-induced activation of p53 and apoptosis is mediated by extracellular-signal-regulated protein kinases and p38 kinase.
TLDR
It is found that in a mouse JB6 epidermal cell line, resveratrol activated extracellular-signal-regulated protein kinases (ERKs), c-Jun NH2-terminal kinases, and p38 kinase and induced serine 15 phosphorylation of p53.
A simple HPLC method for the determination of S-adenosylmethionine and S-adenosylhomocysteine in rat tissues: the effect of vitamin B6 deficiency on these concentrations in rat liver.
TLDR
The marked reduction of the SAM/SAH ratios in vitamin B6-deficient rats were due to a drastic rise in SAH concentration with a concurrent striking decrease in SAM concentration.
Concurrent loss of the PTEN and RB1 tumor suppressors attenuates RAF dependence in melanomas harboring V600EBRAF
TLDR
Genetic alterations that co-occur with oncogenic BRAF in melanoma and abrogate cellular dependence upon this oncogene provide a genetic basis for the heterogeneity of clinical outcomes in patients treated with targeted inhibitors of the mitogen-activated protein kinase pathway.
Breast Tumor Cells with PI3K Mutation or HER2 Amplification Are Selectively Addicted to Akt Signaling
TLDR
Data demonstrate that breast cancers with PI3K mutation or HER2 amplification are selectively dependent on Akt signaling, and that effective inhibition of Akt in tumors is feasible and effective in vivo, and suggest that direct inhibition ofAkt may represent a therapeutic strategy for breast and other cancers that are addicted to the pathway.
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