Machine learning prediction model for gray-level co-occurrence matrix features of synchronous liver metastasis in colorectal cancer.

Background: Synchronous liver metastasis (SLM) is a significant contributor to morbidity in colorectal cancer (CRC). There are no effective predictive device integration algorithms to predict adverse SLM events during the diagnosis of CRC.

Aim: To explore the risk factors for SLM in CRC and construct a visual prediction model based on gray-level co-occurrence matrix (GLCM) features collected from magnetic resonance imaging (MRI).

Guanylate binding protein 5 accelerates gastric cancer progression via the positive feedback loop.

Guanylate binding protein 5 (GBP5) is a member of the interferon (IFN)-inducible large guanosine triphosphate hydrolases (GTPase) family that regulates cell-autonomous immunity and malignant tumor transformation. However, its specific roles and underlying mechanisms GBP5 in gastric cancer (GC) remain unknown. In this study, we aimed to determine the role GBP5 and underlying mechanism of in GC cell progression.

MicroRNA-328-3p facilitates the progression of gastric cancer via KEAP1/NRF2 axis.

Gastric cancer is a common lethal malignancy and causes great cancer-related mortality worldwide. MicroRNA (miR)-328-3p is implicated in the progression of various human cancers; however, its role and mechanism in the progression of gastric cancer remain unclear.Human gastric cancer cells were incubated with miR-328-3p mimic, inhibitor or the matched negative control.

miR-635 targets KIFC1 to inhibit the progression of gastric cancer.

Accumulating studies have shown that the dysregulation of microRNAs is related to the carcinogenesis and development of gastric cancer (GC), and the role of miR-635 in GC remains largely unknown. miR-635 and (KIFC1) mRNA expression in GC tissues and paracancerous tissues and cells were detected by quantitative real-time PCR. KIFC1 protein expression in GC tissues and paracancerous normal tissues and cells was detected by immunohistochemistry and western blot.

MicroRNA-103 promotes tumor growth and metastasis in colorectal cancer by directly targeting LATS2.

Colorectal cancer (CRC) has become the third most common cancer worldwide and leads to a high mortality rate. Although colorectal cancer has been studied widely, the underlying molecular mechanism remains unclear. Increasing evidence shows that the abnormal expression of microRNAs (miRNAs) is involved in tumorigenesis.

Paeoniflorin inhibits human gastric carcinoma cell proliferation through up-regulation of microRNA-124 and suppression of PI3K/Akt and STAT3 signaling.

Aim: To examine the potential anti-tumor activity of paeoniflorin in the human gastric carcinoma cell line MGC-803.

Methods: Cell viability and cytotoxic effects in MGC-803 cells were analyzed using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase assay, respectively. Cell apoptosis of MGC-803 cells was measured using flow cytometry, DAPI staining assay and caspase-3 activity assay.

miR-132 inhibits colorectal cancer invasion and metastasis via directly targeting ZEB2.

Aim: To investigate the biological role and underlying mechanism of miR-132 in colorectal cancer (CRC) progression and invasion.

Methods: Quantitative RT-PCR analysis was used to examine the expression levels of miR-132 in five CRC cell lines (SW480, SW620, HCT116, HT29 and LoVo) and a normal colonic cell line NCM460, as well as in tumor tissues with or without metastases. The Kaplan-Meier method was used to analyze the prognostic significance of miR-132 in CRC patients.

[Value of normalization window of tumor vasculature in neoadjuvant chemotherapy for patients with unresectable gastric cancer].

Objective: To evaluate the value of normalization window of tumor vasculature (NWTV) in patients with unresectable gastric cancer undergoing neoadjuvant chemotherapy.

Methods: From October 2010 to March 2011, 93 patients with unresectable advanced or locally advanced gastric carcinoma were prospectively collected and randomly divided to Group A(n=30), Group B(n=29), and Group C(n=34). Group A received FOLFOX4 as conventional neoadjuvant chemotherapy.