Mcc - Chemo Weeks 3&4

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Curative chemotherapy

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Elimination of all known tumor mass

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Palliation

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Treatment aimed at improving symptoms and controlling tumor growth

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Adjuvant

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Chemotherapy which attempt to eliminate micrometastatic disease following primary treatment

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Neoadjuvant

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Chemotherapy offered prior to other primary potentially curable therapy

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Log-Killl hypothesis

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Most anticancer drugs are thought to work by First Order Kinetics

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S Phase specific chemotherapy drugs

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cytosine arabinoside
hydroxyurea
6-mercaptopurine
methotrexate

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M Phase specific chemotherapy drugs

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vincristine
vinblastine
paclitaxel

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Phase Nonspecific chemotherapy drugs

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alkylating agents
nitrosoureas
antitumor antibiotics
procarbazine
cis-platinum
dacarbazine

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Basic mechanisms of Chemotherapy resistance

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Increase/ decrease in cellular efflux/uptake
Increased proficiency of DNA repair
Increase in levels of target enzyme
Alterations in target enzyme
Decrease in drug activation

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Mechlorethamine

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Alkylating Agent/Nitrogen Mustard
Forms carbonium ion that attacks nucleophiles
DLT: BMS, recovery around 42 days
Increase inactivation/decrease uptake

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Cyclophosphamide

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Alkylating Agent/Nitrogen Mustard
Generates phosphoramide mustard and acrolein
DLT: BMS, Max 10-12 days recovery by 21days
Cells express aldehyde oxidase

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Bendamustine

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Alkylating Agent/Nitrogen Mustard
Alkylator with purine like properties
DLT: hematopoietic, GI, CNS
N/A

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Carmustine

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Alkylating Agent/Nitrosoureas
Forms interstrand crosslinks - guanine
DLT: BMS, stored in liver/adipose
Increased DNA repair

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Lomustine

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Alkylating Agent/Nitrosoureas

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Streptozocin

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Alkylating Agent/Nitrosoureas

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Cisplatin

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Alkylating Agent/Platinum Compunds
Generates DNA crosslinks
DLT: nephro, neuro, oto, nausea/vomiting
Increased efflux, DNA repair and inactivation

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Carboplatin

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Alkylating Agent/Platinum Compunds
Analog is that is less toxic than cisplatin but less active.

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Oxaliplatin

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Alkylating Agent/Platinum Compunds
Lacks cross resistance with other platinum compounds
No nephro, oto toxicity

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Procarbazine

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Alkylating Agent/Other
DLT: pneumonitis

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Dacarbazine

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Alkylating Agent/Other
DLT: BMS

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Temozolomide

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Alkylating Agent/Other
DLT: myelosuppression

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Busulfan

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Alkylating Agent/Other
Forms DNA crosslinks
DLT: pulmonary fibrosis, hepatic necrosis, hepatic veno-occlusive disease

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Methotrexate, Amethopterin; Aminopterin

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Antimetabolite/Folate anatagonist
Dihydrofolate reductase - thymine synthesis
DLT: renal, immunosuppresive, BM, GI
Increased activity of enzyme, decreased influx, binding, formation of MTX-PG

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5-Fluorouracil; 5-FU

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Antimetabolite/Nucleotide analog
Pyrimidine analog - thymidine synthesis
DLT: BMS, N&V, GI
Decreased activation, cofactors; increased catalysis

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Capecitabine

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Oral analog of 5-FU

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Cytosine arabinoside

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Antimetabolite/Nucleotide analog
Inhibits DNA polymerase alpha
DLT: myelosuppresive, neuro, renal
Detoxification from Ara-C to Ara-U

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6-mercaptopurine

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Antimetabolite/Purine analog
Negative feedback to PRPPase; incorporated into DNA/RNA
DLT: BMS, hepatic, N&V
Decreased activation

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Hydroxyurea

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Antimetabolite
Blocks dNTP formation
DLT: BMS, neoplasia, teratogen
Increased synthesis of target enzyme

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Leucovorin

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reduced form of folic acid used to rescue cells exposed to folate antagonists

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Alkylating Agents

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largest class of antineoplastic drugs
Electrophilic compunds that react with DNA
Toxicities vary

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Alkylating Agents
Subclasses

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Nitrogen Mustards
Nitrosoureas
Platinum Compounds

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Alkylating Agents
Bifunctional

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Inhibit repication and transcription by crosslinking DNA
Nitrogen mustards and platinums

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Alkylating Agents
Monofunctional

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Cause single strand DNA breaks
Many nitrosoureas

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Alkylating Agents
Toxicities

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Severe BMS
Platinum show more renal

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Antimetabolites

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Cell cycle dependent agents
Require bioactivation
Inhibit enzymes for DNA; precursors; DNA synthesis
Toxicities affect all cells with high turnover

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Antimetabolite
Classes

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Antifolates
Antinucleotide analogs

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Mesna

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traps acrolein, protects against bladder toxicities