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Topic Review
Tumor Suppressor
A tumor suppressor gene, or anti-oncogene, is a gene that regulates a cell during cell division and replication. If the cell grows uncontrollably, it will result in cancer. When a tumor suppressor gene is mutated, it results in a loss or reduction in its function; in combination with other genetic mutations this could allow the cell to grow abnormally. The loss of function for these genes may be even more significant in the development of human cancers, compared to the activation of oncogenes. Tumor suppressor genes can be grouped into the following categories caretaker genes, gatekeeper genes, and more recently landscaper genes. Caretaker genes ensure stability of the genome via DNA repair and subsequently when mutated allow mutations to accumulate. Meanwhile gatekeeper genes directly regulate cell growth by either inhibiting cell cycle progression or inducing apoptosis. Lastly landscaper genes regulate growth by contributing to the surrounding environment, when mutated can cause an environment that promotes unregulated proliferation. The classification schemes are evolving as medical advances are being made from fields including molecular biology, genetics, and epigenetics.
  • 902
  • 25 Oct 2022
Topic Review
Tumor Necrosis Factor-α
Tumor necrosis factor-α (TNF-α) is a pleiotropic cytokine expressed by macrophages, monocytes, and T cells, and its expression is triggered by the immune system in response to pathogens and their products, such as endotoxins. TNF-α plays an important role in host defense by inducing inflammatory reactions such as phagocytes and cytocidal systems activation. TNF-α also plays an important role in bone metabolism and is associated with inflammatory bone diseases. TNF-α binds to two cell surface receptors, the 55kDa TNF receptor-1 (TNFR1) and the 75kDa TNF receptor-2 (TNFR2).
  • 621
  • 11 Mar 2022
Topic Review
Tumor Necrosis Factor-Alpha (TNF-α) in COVID-19
The coronavirus disease 2019 (COVID-19) became a worldwide concern at the beginning of 2020 and has affected millions. High levels of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukins are produced readily by innate immune cells to fight Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) infections. The presented work describes the potential of TNF-α in the prognosis, therapeutic and management of COVID-19.
  • 428
  • 06 Apr 2023
Topic Review
Tumor Necrosis Factor-Alpha
Tumor necrosis factor-alpha (TNF-α) is a multifunctional Th1 cytokine and one of the most important inflammatory cytokines.
  • 650
  • 22 Jun 2021
Topic Review
Tumor Necrosis Factor Receptor 2 in Colorectal Cancer
Colorectal cancer (CRC) represents one of the most common causes of death among cancers worldwide. Its incidence has been increasing among the young population. Many risk factors contribute to the development and progression of CRC and about 70% of them are sporadic. The CRC microenvironment is highly heterogeneous and represents a very complex immunosuppressive platform. Many cytokines and their receptors are vital participants in this immunosuppressive microenvironment. Tumor necrosis factors (TNFs) and TNF receptor 2 (TNFR2) are critical players in the development of CRC. TNFR2 was observed to have increased the immunosuppressive activity of CRC cells via regulatory T cells (T regs) and myeloid-derived suppressor cells (MDSC) in the CRC microenvironment.
  • 458
  • 07 Feb 2023
Topic Review
Tumor Necrosis Factor Receptor 2 in Cancer Therapy
Tumor necrosis factor (TNF) receptor 2 (TNFR2) is a type I transmembrane protein and a prototypic member of the TNF receptor superfamily (TNFRSF). TNFR2 belongs to the TRAF (TNF-receptor-associated factor)-interacting subgroup of the TNFRSF and mediates pro-inflammatory effects, but can also stimulate strong anti-inflammatory activities. TNFR2 is  stimulated by the membrane-bound form of TNF (memTNF). TNFR2 expression is typically high in myeloid cells but is also found in certain T- and B-cell subsets and a few non-immune cells such as endothelial cells, glial cells and cardiomyocytes.
  • 537
  • 09 Jun 2022
Topic Review
Tumor Necrosis Factor in Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a complex and heterogenous disease; what differentiates patients with RA are the number of affected joints, antibodies and serum cytokines levels, and the severity of joint destruction. TNF (tumor necrosis factor) is a proinflammatory cytokine which exerts multiple biological activities in RA. Blocking TNF with antibodies became a standard of modern RA therapy in patients not responding to conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), e.g., methotrexate.
  • 1.3K
  • 15 Mar 2022
Topic Review
Tumor Necrosis Factor Alpha
Tumor necrosis factor (TNF, cachexin, or cachectin; once named as tumor necrosis factor alpha or TNFα) is a cell signaling protein (cytokine) involved in systemic inflammation and is one of the cytokines that make up the acute phase reaction. It is produced chiefly by activated macrophages, although it can be produced by many other cell types such as CD4+ lymphocytes, NK cells, neutrophils, mast cells, eosinophils, and neurons. TNF is a member of the TNF superfamily, consisting of various transmembrane proteins with a homologous TNF domain. The primary role of TNF is in the regulation of immune cells. TNF, being an endogenous pyrogen, is able to induce fever, apoptotic cell death, cachexia, inflammation and to inhibit tumorigenesis and viral replication and respond to sepsis via IL1- & IL6-producing cells. Dysregulation of TNF production has been implicated in a variety of human diseases including Alzheimer's disease, cancer, major depression, psoriasis and inflammatory bowel disease (IBD). Though controversial, studies of depression and IBD are currently being linked to increased levels of TNF. Recombinant TNF is used as an immunostimulant under the INN tasonermin. TNF can be produced ectopically in the setting of malignancy and parallels parathyroid hormone both in causing secondary hypercalcemia and in the cancers with which excessive production is associated.
  • 728
  • 10 Oct 2022
Topic Review
Tumor Necrosis Factor -Related Apoptosis-Inducing Ligand Signaling Pathways
The tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a type II transmembrane protein that undergoes proteolytic cleavage to produce an extracellular ligand. TRAIL can bind to decoy receptor 1 (DcR1) which lacks a death domain (DD) altogether, and DcR2 which has a truncated DD. These decoy receptors are unable to induce DISC (death-inducing signaling complex) formation and act as negative regulators of the apoptotic signaling by competitively binding TRAIL. The canonical TRAIL-induced apoptotic signaling pathway is an example of apoptosis mediated through the extrinsic death pathway, which entails activation of cell-surface receptors by a ligand to induce activation of downstream caspases.
  • 953
  • 30 Nov 2022
Topic Review
Tumor Microenvironment of Squamous Cell Carcinomas
Squamous cell carcinomas arise from stratified squamous epithelia. Here, a comparative analysis based on recent studies defining the genetic alterations and composition of the stroma of oral and cutaneous squamous cell carcinomas (OSCC and CSCC, respectively) was performed. Both carcinomas share some but not all histological and genetic features. 
  • 231
  • 03 Jul 2023
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