Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite the ability of cancer vaccines to induce tumor-specific T-cells in the blood of patients with cancer, and early, promising data indicating their ability to delay cancer progression, their ability to induce cancer regression remains low. The use of ex vivo-generated dendritic cells (DCs) in such vaccines can help to sidestep the cancer-associated dysfunction of endogenous DCs and to deliver the key instructive signals needed for effective antitumor responses. Effective ways of loading DCs with tumor-related antigens, while retaining the high costimulatory function required for T-cell expansion (ie, effective delivery of 'signal one' and 'signal two'), have been previously identified. More recently, different DC populations have been found to deliver a specialized third signal, able to regulate the acquisition of desirable T-cell effector functions, as well as an additional fourth signal that regulates the homing properties of T-cells. Moreover, ex vivo instruction of DCs can be used to preferentially activate CTLs, T-helper 1 and NK cells, while limiting the undesirable activation of regulatory T-cells. These developments can result in the induction of T-cells with desirable effector functions and tumor-relevant homing properties, even in the absence of proinflammatory signals (typically present in recall infections, but not in advanced cancer), thus helping to bridge the gap between the effectiveness of therapeutic and preventive cancer vaccines.
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PMID:Dendritic cells in immunotherapy of established cancer: Roles of signals 1, 2, 3 and 4. 1951 41

Metastasis is the leading cause of cancer-associated death in most tumor types. Metastatic dissemination of cancer cells from the primary tumor is believed to be initiated by the reactivation of an embryonic development program referred to as epithelial-mesenchymal transition (EMT), whereby epithelial cells lose apicobasal polarity and cell-cell contacts, and gain mesenchymal phenotypes with increased migratory and invasive capabilities. EMT has also been implicated in the regulation of cancer stem cell property, immune suppression and cancer regression. Several transcription factors have been identified as master regulators of EMT, including the Snail, Zeb and Twist families, and their expression is tightly regulated at different steps of transcription, translation and protein stability control by a variety of cell-intrinsic pathways as well as extracellular cues. Here, we review the recent literature on the signaling pathways and mechanisms that control the expression of these master transcription factors during EMT and cancer progression.
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PMID:Multilayer control of the EMT master regulators. 2360 23

Macrophages are the most abundant cells within the tumor stroma displaying noticeable plasticity, which allows them to perform several functions within the tumor microenvironment. Tumor-associated macrophages commonly refer to an alternative M2 phenotype, exhibiting anti-inflammatory and pro-tumoral effects. M2 cells are highly versatile and multi-tasking cells that directly influence multiple steps in tumor development, including cancer cell survival, proliferation, stemness, and invasiveness along with angiogenesis and immunosuppression. M2 cells perform these functions through critical interactions with cells related to tumor progression, including Th2 cells, cancer-associated fibroblasts, cancer cells, regulatory T cells (Tregs), and myeloid-derived suppressor cells. M2 cells also have negative cross-talks with tumor suppressor cells, including cytotoxic T cells and natural killer cells. Programed death-1 (PD-1) is one of the key receptors expressed in M2 cells that, upon interaction with its ligand PD-L1, plays cardinal roles for induction of immune evasion in cancer cells. In addition, M2 cells can neutralize the effects of the pro-inflammatory and anti-tumor M1 phenotype. Classically activated M1 cells express high levels of major histocompatibility complex molecules, and the cells are strong killers of cancer cells. Therefore, orchestrating M2 reprogramming toward an M1 phenotype would offer a promising approach for reversing the fate of tumor and promoting cancer regression. Macrophage switching toward an anti-inflammatory M1 phenotype could be used as an adjuvant with other approaches, including radiotherapy and immune checkpoint blockades, such as anti-PD-L1/PD-1 strategies.
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PMID:Macrophage polarity in cancer: A review. 3027 Apr 58