Cancer target cells

The primary function of the B lymphocytes is to produce antibodies, which are molecules that identify and lead to the destruction of foreign substances such as bacteria. The B lymphocytes and the antibodies they produce are responsible for humoral immunity. T lymphocytes provide immunity against viruses and cancer cells. These lymphocytes directly attack and destroy their targets by forming holes in the target cell membrane, causing cell lysis. The T lymphocytes are responsible for cell-mediated immunity. 

Fig. 9 Utility of de-PEGylation technology in liposomes, (a) PEG derivative possessing a lipid moiety. The covalent bond between PEG and the lipid moiety can be cleaved by stimuli such as those within the acid environment of cancer and inflammation, (b) After binding the target cell via specific recognition of the receptor by the ligand, PEG molecules on the surface of the liposome are cleaved. The release of PEG facilitates membrane fusion of the liposome and liposome decomposition, resulting in efficient drug delivery...

Camero A. (2002) British J. Cancer, Targeting the cell cycle for cancer therapy, 87, 129-133. 

HDAC inhibitors can also operate independent of p53. HDAC inhibitors are able to upregulate p21, a cyclin-dependent kinase. They can also target TOB-l,i< p27 P ," GADDTS. CYCLIN Bl, CYCLIN Dl, and CYCLIN A genes. Downregulation of genes such as can also be achieved by HDAC inhibitors. All of these contribute to cell cycle progression and apoptosis of the cancer/tumor cells. 

In general, when the cells of the endothelium in the lungs are the target cells of interest (see Chapters 7 and 9 on aspects of targeting drugs to endothelium in inflammatory diseases and cancer, respectively), systemic administration seems the route of choice. Bronchial epithelium on the other hand can more easily be reached via the pulmonary route. The accessibility of other cells in the lungs is most hkely governed by disease conditions, factors that can affect epithehal permeability and vascular permeability, and others as described earher. 

The reason for the selective toxicity of 6-mercaptopuiine remains to be established, but two factors may be of primary importance. 6-Mercaptopurine is anabolized primarily, if not exclusively, to the monophosphate level, and it is readily catabolized by xanthine oxidase, an enzyme that is low in most cancer cells compared to normal cells. Another factor that must be considered is the metabolic state of the target cells. Actively proliferating leukaemia cells are more sensitive to 6-mercaptopurine, as they are to all antimetabolites, than cells in the so-called Gq or stationary phase. Although this does not explain the difference between 6-mercaptopurine and other purine analogues, it may explain the ineffectiveness of 6-mercaptopurine against solid tumours, most of the cells of which are in the non-dividing state. 

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