Tumour cells

Dimeric complexes like [Cl(NH3)Pt H2N(CH2)4NH2 Pt(NH3)Cl]Cl2 are also being investigated as they bind to DNA in a different way to that involved in cisplatin binding and are active in cisplatin-resistant human tumour cells. They are more potent than cisplatin in lung cancer models in vivo and are likely to go on clinical trials in the near future [204],... 

The ability of cisplatin to be toxic to tumour cells is believed to relate to its binding to DNA, but since trans- [Pt (NH3) 2 Cl2 ] also binds to DNA, the reason for the inactivity of the trans-form is more complex. 

Since COX-2 is overexpressed in tumour cells, such as those of colorectal cancer, it was anticipated that selective COX-2 inhibitors may inhibit tumour growth. 

At present, the use of microarrays in pharmacology is especially established in the field of oncology by gene expression analysis with either tumour cell... 

S100A14/S100A16 Detection of circulating tumour cells in peripheral blood... 

Type I interferons induce a vims-resistant state in human cells, whereas Type II are more active in inhibiting growth of tumour cells. 

In oncology, to study the relationship between the normal and the tumour cell, to detect tumour-associated antigens (CEA, carcino-embryonic antigen, and AFP, a-fetoprotein) and subsequently to enable cancer therapy to be monitored, to locate tumour metastases, and to deliver cytotoxic drugs, toxins, radionuclides, or liposomes to tumour cells. 

Neuraminidase Vibrio cholerae Possible increase immuno-genicity of tumour cells 2.4.3... 

L-Asparaginase, an enzyme derived from E. coli or Erwinia carotovora, has been employed in cancer chemotherapy where its selectivity depends upon the essential requirement of some tumours for the amino acid L-asparagine. Normal tissues do not require this amino acid and thus the enzyme is administered with the intention of depleting tumour cells of asparagine by converting it to aspartic acid and ammonia. Whilst L-asparaginase showed promise in a variety of experimentally induced tumours, it is only useful in humans for the treatment of acute lymphoblastic leukaemia, although it is sometimes used for myeloid leukaemia. 

NOWELL p c (1976) The clonal evolution of tumour cell populations . Science, 194, 23-8. 

Table 4.2 Summary of smdies comparing the anti-proliferative effects against tumour cell lines of glucosinolate metabolites in vitro. The comparisons do not distinguish between increased cell death and reduced rate of cell division...

CONSTANTINOU A, HUBERMAN E (1995) Genistein as an inducer of tumour cell differentiation possible mechanisms of action. Proc Soc Exp Biol Med. 208 109-15. 

HAGUE A, MANNING A M, HANLON K A, HUSCHTSCHA L I, HART D, PARASKEVA C (1993) Sodium butyrate induces apoptosis in human colonic tumour cell lines in a p53-independent pathway impUcations for the possible role of dietary fibre in the prevention of large-bowel cancer. /ni J Cancer. 55 498-505. 

Except for its narrow specificity, the ATRI gene product shares a number of properties with the higher eukaryotic MDR proteins responsible for multidrug resistance in tumour cells. The MDR gene products are also transmembrane proteins which seem to function as ATP-dependent drug-efflux pumps pumping out a variety of structurally unrelated compounds (see [25,26]). 

Polymorphonuclear leucocytes (PMNs) employ a system comprising myeloperoxidase, hydrogen peroxide, and a halide factor to kill microorganisms and tumour cells. This process is sometimes loosely called the respiratory burst , which refers to the sudden rise in oxygen consumption by the phagocytosing neutrophils that is independent of the mitochondrial electron transport chain. 

Zimmerman, RJ., Chan, A. and Leadon, S.A. (1989). Oxidative damage in murine tumour cells treated in vitro by recombinant human tumour necrosis factor. Cancer Res. 49, 1644-1648. 

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