Anti-cancer drugs 2

===Lecture Details===
Shane Bullock; Week 10 MED1011; Pharmacology
===Lecture Content===
Novel agents are monoclonal antibodies, biological response modifiers, cytokine treatment of sampled immune cells, tyrosine kinase inhibitors, sensitising agent. Tumour cells are grown in culture and fused with antibody forming cells in mice, form antibodies to tumours (hybridomas). Monoclonal antibodies are hybridised for cultivation.
Rutiximab is directed towards CD20 surface antigen expressed on B cells, triggers B cell lysis.
Trastuzumab (Herceptin) binds to HER2 overexpressed in some forms of breast cancer. 
Interferons augment the cytotoxicity of immune cells, high doses inhibit cell proliferation and facilitate cytotoxicity, alter antigen expression on tumour cells and immune cells. IL-2 stimulates lymphocyte proliferation and cellular immunity. Remove patients lymphocytes, grow in culture, sensitise against tumour cell antigens, more aggressive immune response against tumour.
Antisense oligonucleotides create synthetic segments of single strand DNA, bind to complementary portion of mRNA and prevents expression of oncogene
Tyrosine kinase inhibitors end with -inib. Some also inhibit angiogenesis. Small molecule drugs bind to enzyme's ATP binding site and inactivate enzyme. Tyrosine kinase inhibitors are a model for inhibition of proliferation signals associated with other cancers.
Sensitising agents such as BCG used to immunise people against TB, mycobacterium bovis preparation to make cells more immunoreactive and induce an inflammatory reaction, superficial cancer cells more likely to be attacked by immune cells.
Drug resistance, spontaneous mutations and acquired adaptations that afford protection are often encountered. Tumour cell sanctuaries are when cells grow in compartments that are inaccessible to drugs and can create sites of relapse. Dose exhaustion is where maximum dose is not enough to attack remaining cells, and any higher pushes dose into toxic range.
===Readings===
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