30 results about "Malignant phenotype" patented technology

Tryptophan degradation is a key metabolic pathway that controls immune responses, and evidence suggests that during cancer progression, the production of tryptophan metabolites may underlie immune evasion that promotes the malignant phenotype of cancer cells in an autocrine manner. The present invention relates to methods of measuring mass tag-labeled tryptophan and its metabolites, and the use of labeled molecules to monitor the effectiveness of a subject's treatment and disease recurrence following treatment, for stratifying patients and for diagnosing immunity in a subject method of response suppression.

The invention discloses the application of SLAMF8 in preparing preparations of tumor tissue markers or serum markers for evaluating the prognosis of human glioma, and as a marker for evaluating the prognosis of human glioma. The present invention also provides a method for evaluating the clinical prognosis of glioma by using immune co-stimulatory molecules. The present invention finds through research that SLAMF8 is highly expressed in the malignant phenotype of glioma and glioblastoma, and is closely related to the poor prognosis of glioma, and the high expression of SLAMF8 is an important sign of the poor prognosis of glioma. Moreover, high expression of SLAMF8 is associated with chemotherapy resistance. The present invention suggests that SLAMF8 mainly affects the glioma microenvironment through monocytes and dendritic cells, and is closely related to immune response. SLAMF8 can affect glioma immune function, inhibit glioma immune response and promote inflammatory response. In conclusion, SLAMF8 can be used as an important clinical prognostic marker for glioma.

The invention discloses the application of CEBPα as a detection reagent of RANBP2 target site in the preparation of glycosylation-related drugs for treating liver cancer. The study of the present invention shows that the high expression of RANBP2 in liver cancer cells is positively correlated with the malignant phenotype of liver cancer. RANBP2 down-regulates the expression of OGA, increases O-glycosylation modification, and then increases the proliferation and invasion ability of liver cancer cells. As a key transcription factor CEBPα that positively regulates OGA, RANBP2 can induce the SUMOylation of CEBPα, and experiments have confirmed that the K196 site of CEBPα is the key SUMO target site of RANBP2, and SUMOylation of this site can promote the degradation of CEBPα protein. Protecting the K196 site of CEBPα from SUMOylation or increasing the expression of CEBPα itself can slow down the OGA-mediated O-glycosylation pathway.

The invention relates applications of vitamin C derivatives in antitumor products. According to the present invention, with the continuous and long-time administration of the low-dose vitamin C derivatives, the differentiation of cancer cells can be inhibited, and the malignant phenotype of cancer cells can be effectively inhibited, such that the evidence can be provided for the application of thevitamin C derivatives in tumor differentiation therapy.

The invention discloses application of gap junction protein and coding gene thereof in preparing medicament for reversing malignant phenotype of a cancer stem cell, and investigates the functional state of gap junction communication in the tumor stem cell, expression condition of the gap junction protein and relation between the gap junction protein and special biological characteristics of tumor stem cells. Results prove that compared with differentiated tumor cells, gap junction communication obstacle exists in the tumor stem cell, no clear gap junction like structure is found among the cells, and expressions of various gap junction protein, particularly gap junction protein 43(Cx43), is down regulated; the down regulation of the expression of the Cx43 is related to promoter methylation of coding gene GJA1 thereof and expression of micro RNA; recovering of the expression of the Cx43 in the tumor stem cell can remarkably reduce the self-renew ability, tumor forming ability and invasion ability of the tumor stem cells, which is related to partial recovery of the gap junction communication function, up regulation of E-cadherin expression and inactivity of SDF-1 / CXCR4 downstream signal path (AKT and ERK1 / 2); and the gap junction protein and coding gene thereof can be used for preparing the medicament for reversing malignant phenotype of the cancer stem cell.