MR images were analyzed qualitatively (location, shape, homogeneity, signal intensity, vascular involvement and extrapancreatic extent of ACC) and quantitatively (tumor size, apparent diffusion coefficient [ADC] and normalized ADC of ACC).
MR images were analyzed qualitatively (location, shape, homogeneity, signal intensity, vascular involvement and extrapancreatic extent of ACC) and quantitatively (tumor size, apparent diffusion coefficient [ADC] and normalized ADC of ACC).
Furthermore, the application of 1-aminocyclopropane-1-carboxylic acid (ACC) significantly enhanced the expression level of ZFP5 while the application of 2-aminoethoxyvinyl glycine (AVG) had the opposite effect when either Pi or potassium was deprived.
The beta-glucuronidase (GUS) activity driven by the promoter of <i>GmTIP2;6</i> was strongly induced in the heat- and ACC-treated transgenic plants and tended to be accumulated in the hypocotyls, vascular bundles, and leaf trichomes.
We show that PBK is regulated by FOXM1 and targeting PBK via shRNA decreased cell proliferation, clonogenicity, and anchorage independent growth in ACC cell lines.
Administration of NMDA receptor subunit NR2B antagonist Ro 25-6981 into the ACC significantly alleviated the potentiation of MT stimulation-evoked LFP in the ACC of EOI rats without affecting that in control rats.
SRC-1 expression in aggressive pheochromocytomas, may also be a potential diagnostic pitfall in view of the fact that these tumors may be misinterpreted as ACC in the primary or metastatic setting.
Furthermore, MALAT1 directly binds to SFPQ (Splicing Factor Proline and Glutamine Rich) protein, indicating its multifaceted roles in ACC pathophysiology.
GLP-1 suppressed lipid accumulation in primary hepatocytes with the involvement of (AMP)-activated protein kinase/Acetyl CoA carboxylase (AMPK/ACC) signaling.
We found recurrent somatic missense mutations in 22 genes (including PIK3CA, ERBB2, and GNAS) and a widespread APOBEC cytidine deaminase mutagenesis pattern (TCW motif) in both adenocarcinoma (ACC) and squamous cell carcinomas (SCCs).
The newly identified oncogenic driver gene set (ZFPM1, LRIG1, CRIPAK, ZNF517, GARS and DGKZ), specifically and most repeatedly mutated in ACC, is involved in tumor suppression and cellular proliferation and thus could be useful for the prognosis and development of therapeutic approaches for the treatment of ACC.
The protein expression level of IGF2, IGF1R and IGF2R was evaluated by immunohistochemistry in 17 human ACCs and the mRNA expression level of IGF1, IGF2, IGF1R, IR isoforms A and B, IGF2R, IGF-Binding-Proteins[IGFBP]-1, 2, 3 and 6 was evaluated by RT-qPCR in 12 samples.
Moreover, there seems to be activation of the immune inhibitory proteins/PD-L2 and HLA-G, a scenario that may favor tumor escape from the immune system and partially explain the poor prognosis of ACC.
Three days after cell injection, the cortisol-secreting ACC cell area in solvent-treated embryos was significantly higher than that in 1 µM AbiAC‒treated embryos, whereas no AbiAc effect was observed in SW13 cells, which lack the Abi target enzyme CYP17A1.Zebrafish embryos xenografted with ACC tumor cells could be a useful, fast, and reproducible experimental model to preclinically test the activity of new drugs in human ACC.
The effects of IGF2 (50, 100 ng/mL) in cell proliferation, viability, invasion, and metabolism, as well as in MAPK/ERK and mTOR pathways activation and N-cadherin expression, were evaluated in the ACC human cell line H295R.
We found recurrent somatic missense mutations in 22 genes (including PIK3CA, ERBB2, and GNAS) and a widespread APOBEC cytidine deaminase mutagenesis pattern (TCW motif) in both adenocarcinoma (ACC) and squamous cell carcinomas (SCCs).
This is the first study to identify the feedback axis of miR-497-MALAT1/eIF4E in ACC tumourigenesis, providing novel insights into the molecular functions of noncoding RNAs in ACC.
GLP-1 suppressed lipid accumulation in primary hepatocytes with the involvement of (AMP)-activated protein kinase/Acetyl CoA carboxylase (AMPK/ACC) signaling.
CONCLUSIONS ENST00000489707.5 is a preferred alternative splicing product of PTK7, with a significantly increased proportion in ACC compared with other cancers.