Publications by authors named "Ning Go"
Background: gene aberrations are found in several human cancers including gastric, ovarian and lung. In a large multinational cohort of patients with gastric/gastroesophageal junction/esophageal (G/GEJ/E) adenocarcinoma we assessed the MET status with respect to amplification and deletion and correlate the results with the phenotypical gene signal distribution pattern.
Methods: Tissue specimens from 1,580 patients were analyzed using a novel fluorescence in situ hybridization (FISH) assay employing a /CEN-7 IQFISH Probe Mix.
Article Synopsis
- Imetelstat effectively reduces the formation of CFU-MEG from mononuclear cells (MNCs) in patients with essential thrombocythemia (ET) and lowers the expression of the hTERT gene.
- In healthy donors, the same concentrations of imetelstat do not hinder the formation of CFU-MEG when stimulated by cytokines.
- This suggests that imetelstat's effects may be specific to certain conditions, particularly in ET patients, rather than having a universal inhibitory impact.
Purpose: gene amplification is associated with poor prognosis in gastric/gastroesophageal junction/esophageal (G/GEJ/E) cancers. We determined antitumor activity, safety, and pharmacokinetics of the small-molecule MET inhibitor AMG 337 in -amplified G/GEJ/E adenocarcinoma or other solid tumors. In this phase II, single-arm study, adults with -amplified G/GEJ/E adenocarcinoma (cohort 1) or other -amplified solid tumors (cohort 2) received AMG 337 300 mg/day orally in 28-day cycles.
View Article and Find Full Text PDFBackground: The gene mesenchymal epithelial transition factor () is a proto-oncogene that encodes a transmembrane receptor with intrinsic tyrosine kinase activity known as Met or cMet. is found to be amplified in several human cancers including gastroesophageal cancer.
Methods: Here we report the amplification prevalence data from 159 consecutive tumor specimens from patients with gastric (G), gastroesophageal junction (GEJ) and esophageal (E) adenocarcinoma, using a novel fluorescence in situ hybridization (FISH) assay, /CEN-7 IQFISH Probe Mix [an investigational use only (IUO) assay].
AMG 337, a selective small-molecule MET inhibitor, was evaluated in Asian patients with advanced solid tumors. Eligible patients orally self-administered AMG 337; the initial dose of 150 mg once daily (QD) was escalated to 300 mg QD (modified 3+3+3 design). Treatment continued until disease progression, intolerability, or death.
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- Cancer stem cells (CSCs) are rare but drug-resistant cancer cells linked to cancer recurrence and metastasis, making them a key target for treatment.
- Imetelstat (GRN163L) is a telomerase inhibitor that has shown efficacy in reducing telomerase activity in both bulk tumor cells and CSCs in breast and pancreatic cancer cell lines.
- The study found that imetelstat treatment not only decreased the CSC populations and their self-renewal capability but also hindered cancer growth in animal models, indicating its potential as an effective cancer therapy.
Article Synopsis
- Plasma cells are the main tumor cells in multiple myeloma but don’t grow indefinitely, while clonotypic B cells act like cancer stem cells and can regenerate the disease in mice.
- The study focused on using imetelstat, a telomerase inhibitor, to target these myeloma cancer stem cells, demonstrating that treatment reduced telomere length and inhibited tumor growth.
- Findings showed that both long and short-term telomerase inhibition affected cancer stem cell characteristics, indicating that telomerase plays a crucial role in their growth and could be a therapeutic target in treating multiple myeloma.
Most cancer cells have an immortal growth capacity as a consequence of telomerase reactivation. Inhibition of this enzyme leads to increased telomere dysfunction, which limits the proliferative capacity of tumor cells; thus, telomerase inhibition represents a potentially safe and universal target for cancer treatment. We evaluated the potential of two thio-phosphoramidate oligonucleotide inhibitors of telomerase, GRN163 and GRN163L, as drug candidates for the treatment of human hepatoma.
View Article and Find Full Text PDFA series of 1,3,5-triazine-based estrogen receptor (ER) modulators that are modestly selective for the ERbeta subtype are reported. Compound 1, which displayed modest potency and selectivity for ERbeta vs ERalpha, was identified via high-throughput screening utilizing an ERbeta SPA-based binding assay. Subsequent analogue preparation resulted in the identification of compounds such as 21 and 43 that display 25- to 30-fold selectivity for ERbeta with potencies in the 10-30 nM range.
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