7. Mohamed Bahr; MD, PhD
I. ALKYLATING
AGENTS (CCNS)
Cyclophosphamide, Busulphan – Nitrosoureas – Cisplatin.
They are chemical substances containing highly reactive
groups (alkyl). They transfer these active groups to various
cellular constituents, mainly DNA, proteins and enzymes
decreasing their synthesis and/ or function.
9. Mohamed Bahr; MD, PhD
II. ANTIMETABOLITES
(S PHASE)
They are structural analogs of naturally occurring metabolites
competing with them for enzyme systems → ↓ DNA and RNA
synthesis.
A. 6- Mercaptopurine (purine antagonist)
Decreases purine synthesis → ↓ DNA and RNA synthesis.
B. Methotrexate (folic acid antagonist)
Inhibits DHFR → ↓ H4F synthesis → ↓ DNA and RNA synthesis.
15. Mohamed Bahr; MD, PhD
B. Antibiotics
Bind to DNA → fragmentation of its strands → ↓ DNA
synthesis.
Bleomycin (G2 - M)
Dactinomycin - Adriamycin - Mitomycin - Doxorubicin (CCNS)
28. Mohamed Bahr; MD, PhD
F. Enzymes (L- asparaginase)
↓ Blood asparagine → deprives tumor cells of this amino acid
which is essential for protein synthesis.
32. Mohamed Bahr; MD, PhD
IV. HORMONES AND
ANTAGONISTS
Corticosteroids in leukemia and lymphomas.
Testosterone in cancer breast.
Estrogen in cancer prostate.
Hormone receptors agonists and antagonists:
(estrogen/tamoxifen), (testosterone/cyproterone, flutamide).
GnRH agonists (leuprolide and goserelin) for prostate and
breast tumors.
36. Mohamed Bahr; MD, PhD
V. MISC
Protein tyrosine kinase inhibitors: Imatinib
Immunomodulators: Thalidomide
37. Mohamed Bahr; MD, PhD
ADVERSE EFFECTS
A. GENERAL
Bone marrow depression: leucopenia, thrombocytopenia or pancytopenia.
Hair loss.
GIT disturbances: vomiting, diarrhea and GIT ulcers.
Hyperuricemia (due to destruction of ↑number of tumor cells).
Immunosuppression: liability to infections and delayed healing of wounds.
Gonadal damage: sterility, amenorrhea and azospermia.
Teratogenicity and mutagenicity.
Secondary malignancy.