After T-cell-depleted bone marrow transplantation (TD-BMT), these cells have an activated pattern of target cell killing; they also secrete lymphokines including gamma-interferon (gamma-IFN), interleukin-2 (IL-2), and tumor necrosis factor (TNF) and may have a significant role as a primary defense against viral reactivation and in the elimination of residual host malignancy.
In HNSCC, enhanced expression of TNF receptors on the cancer cells occurs and is likely to contribute to the regulation of TNF and its activation of tumor cells within the tumor microenvironment; targeting these receptors in cancer cells may provide a new approach to controlling tumor growth and metastasis.
Gene therapy for cancer is being tested in clinical trials using tumor-infiltrating lymphocytes (TIL) or tumor cells modified by the insertion of genes coding for interleukin 2 or tumor necrosis factor alpha.
The most common type of approved clinical trial for cancer gene therapy involves the ex vivo gene transfer of cytokine genes (e.g., tumor necrosis factor, interleukin-2, granulocyte-macrophage colony-stimulating factor) into tumor cells.
Rather, the presence of LT, TNF and IL-6 transcripts appeared to characterize Hodgkin and Reed-Sternberg cells in general, supporting concepts which suggest that HD represents a malignancy of cytokine secreting activated cells, and that many of the features distinguishing HD from other malignant lymphomas may ultimately be due to expression of cytokines.
To define if alterations of tumor necrosis factor alpha (TNF alpha), interleukin 1 alpha (IL-1 alpha), IL-1 beta and IL-6 gene expression are present in this malignancy, samples from 19 tumors as well as samples from seven paired normal renal tissue were examined using Northern blot and immunohistochemical analysis.
Functional and molecular characterization of tumor-infiltrating lymphocytes transduced with tumor necrosis factor-alpha cDNA for the gene therapy of cancer in humans.
Thus, overall results demonstrate that oligonucleotides directed to the specific regions of TNF can be designed, which may have a potential in cancer therapy.
The progress in the field of TNF is focussed on gene organization and transcription, gene polymorphism, biochemistry of TNF, TNF receptors and the biological role of TNF in autoimmune diseases, infectious diseases, transplantation, cancer and TNF functions on endothelial cells.
TNF levels vary with different TNF microsatellite alleles, and associations of these microsatellite markers with autoimmune diseases and different types of cancer have been shown.
This molecule binds to LeY antigen on cancer cells with the same affinity as B1(scFv) and B1(scFv) immunotoxins but with significantly lower affinity to the TNF receptor compared to the TNF trimer.
The link between NF-kappaB and cancer stems, in part, from the fact that this transcription factor is capable of inducing gene products that control proliferative responses and that suppress apoptotic cascades, such as those induced by tumor necrosis factor (TNF), expression of oncoproteins, and genotoxic stress.
Tumor necrosis factor-alpha (TNF), which was initially supposed to be a promising cancer therapeutic reagent, does not kill most types of cancer cells partly due to the activation of an anti-apoptotic gene, NF-kappaB.
In the second part, we report a promising screening method for cancer preventive agents, based on evidence that pretreatment with agents such as tamoxifen, sulindac, 1alpha, 25-(OH)2 vitamin D3, quercetin, caffeic acid phenethyl ester, and (-)-epigallocatechin gallate (EGCG) commonly inhibited TNF-alpha release from BALB/3T3 cells induced by okadaic acid.
Inhibition of NF-kappaB in the presence of tumor necrosis factor-alpha (TNF) is supposed to be a promising cancer therapeutic approach, since it disrupts the protective mechanism of NF-kappaB activated by TNF.