<i>Garcinia mangostana</i> Linn.(GME) may have chemopreventive property by reducing the tumor promoting growth factor and tumor necrosis factor-alpha levels in diethylnitrosamine (DEN)-induced hepatic cancerThe suppression in the levels of cancer biomarkers by GME due to the presence of anticancer phytoconstituentsThe histological studies proved the effective dose of GME against DEN-induced experimental hepatic cancer.
Tumors from Kras(G12D); IL-6(-/-) mice showed increased expression of TNFα and decreased expression of CCL-19, CCL-20 and phosphorylated STAT3(pSTAT3) than Kras(G12D) mice; however, these changes were not present between tumors from Kras(G12D); p53(flox/flox); IL-6(-/-) and Kras(G12D); p53(flox/flox) mice.
Tumor risk was associated with higher tumor necrosis factor-α and insulin and altered oxidative stress biomarkers in sera and with early changes in mammary expression of genes linked to tumor promotion [interleukin 6 (Il6)] or inhibition [phosphatase and tensin homolog deleted on chromosome 10 (Pten), B-cell lymphoma 2 (Bcl2)].
Tumor epithelial cells (TEpCs) and spindle-shaped stromal cells, not associated with the vasculature, of patients with early breast cancer express osteoprotegerin (OPG), tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), receptor activator of nuclear factor kappa B ligand, stromal cell derived factor-1, interleukin-6, macrophage colony stimulating factor, chemokine (C-C motif) ligand-2 (CCL-2) and their receptors at significantly higher levels compared with non-neoplastic breast tissues.
Tumor cell clones were analyzed for cytokine expression by reverse transcriptase-polymerase chain reaction (RT-PCR) and by cytokine-specific enzyme-linked immunosorbent assays (TNF-ELISA or IL-2-ELISA).
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), a novel member of the tumor necrosis factor family, induces apoptosis in TRAIL-sensitive tumors through the activation of the caspase pathway.
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL, APO2L) has been shown to induce apoptosis in a number of tumor cell lines as well as in some primary tumors whereas cells from most normal tissues are highly resistant to TRAIL-induced apoptosis.
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is expressed by immune cells and has been shown to play an important role in tumor surveillance due to its ability to induce apoptosis in various transformed cells.
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis in several human tumors both in vitro and in vivo, however, some tumors remain resistant for poorly understood reasons.
Tumor necrosis factor-alpha (TNF-alpha) was selected as the transgenic protein for its potent anti-tumor activity and synergistic interactions with ionizing radiation.
TNF secretion had no effect on tumor cell proliferation in vitro but caused a very impressive growth arrest in vivo that was dependent on both bone marrow- and non-bone marrow-derived host cells expressing TNFR.
Tumor necrosis factor related apoptosis-inducing ligand (TRAIL) receptors DR4 and DR5 have been mapped to chromosome 8p21-22, a region frequently deleted in different lymphoid neoplasms.
Tumour necrosis factor-related apoptosis inducing ligand (TRAIL) receptor 2 (TRAIL-R2) also known as TNFRSF10B (tumour necrosis factor receptor (TNFR) super family 10b) or KILLER/DR5, a member of the TNFR family, is a promising candidate tumour suppressor gene at 8p21-22.
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) preferentially induces apoptosis in transformed or malignant cells, thus exhibiting potential as a tumor-selective apoptosis-inducing cytokine for cancer treatment.
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) gene therapy and canstatin gene therapy have been investigated extensively in human xenograft tumor models established in immunocompromised nude mice.