Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

SIRT2 is involved in the development of a variety of cancers. Shikonin is a natural compound that is known to have antitumor effects. This study aims to assess the effects of shikonin on the development and metastatic progression of colorectal cancer (CRC) through regulation of SIRT2 expression and whether this effect is related to the phosphorylation of extracellular signal-regulated kinases (ERKs). The results demonstrated that SIRT2 is downregulated in CRC biopsy samples (n=31) compared with the adjacent non-cancerous tissues (ANCT, n=26). Furthermore, CRC metastases were positive for SIRT2 despite a lack of expression in the primary tumor. In addition, data from an in vitro assay revealed that overexpression of SIRT2 inhibited the proliferation and metastatic progression of SW480 cells while blocking of SIRT2 expression induced the proliferation and metastatic progression of HT29 cells. Shikonin inhibited the viability, migration and invasion of SW480 cells and it also inhibited the tumor growth in the nude mice model; while AGK2 (a specific inhibitor of SIRT2) reversed these effects. Epidermal growth factor (EGF, an activator of ERK) and ERK-overexpression inhibited the effects of shikonin on SIRT2 expression, proliferation and metastasis in SW480 cells. However, this proliferative effect of EGF was reversed by SIRT2 overexpression. In conclusion, these results suggest that SIRT2 is a new therapeutic target for the treatment of CRC. The antitumor effects of shikonin on CRC seem to be mediated by SIRT2 upregulation via phospho-ERK inhibition.
 ...
PMID:SIRT2 mediated antitumor effects of shikonin on metastatic colorectal cancer. 2808 87

Previously, a consolidated mathematical model of primary tumor (PT) growth and secondary distant metastasis (sdMTS) growth in breast cancer (BC) (CoMPaS) was presented. The aim was to detect the diagnostic periods for visible sdMTS via CoMPaS in patients with different subtypes ER/PR/HER2/Ki-67 (Estrogen Receptor/Progesterone Receptor/Human Epidermal growth factor Receptor 2/Ki-67 marker) of breast cancer. CoMPaS is based on an exponential growth model and complementing formulas, and the model corresponds to the tumor-node-metastasis (TNM) staging system and BC subtypes (ER/PR/HER2/Ki-67). The CoMPaS model reflects (1) the subtypes of BC, such as ER/PR/HER2/Ki-67, and (2) the growth processes of the PT and sdMTSs in BC patients without or with lymph node metastases (MTSs) in accordance with the eighth edition American Joint Committee on Cancer prognostic staging system for breast cancer. CoMPaS correctly describes the growth of the PT in the ER/PR/HER2/Ki-67 subtypes of BC patients and helps to calculate the different diagnostic periods, depending on the tumor volume doubling time of sdMTS, when sdMTSs might appear. CoMPaS and the corresponding software tool can help (1) to start the early treatment of small sdMTSs in BC patients with different tumor subtypes (ER/PR/HER2/Ki-67), and (2) to consider the patient almost healthy if sdMTSs do not appear during the different diagnostic periods.
 ...
PMID:A Mathematical Model to Predict Diagnostic Periods for Secondary Distant Metastases in Patients with ER/PR/HER2/Ki-67 Subtypes of Breast Cancer. 3282 78


<< Previous 1 2 3