Chapter 8 anticancer drugs - general info

Question 1

Four ways anticancer drugs work?

Answer 1

1) crosslinking DNA — prevents separation of DNA strands
2) Linking alkyl groups to DNA bases // inhibit DNA repair
3) Mimick DNA bases l/t — 1) incorporate drug into DNA or RNA preventing repair or terminates chain or 2) induce neg feedback on enzymes that synthesize or recycle purines
4) intercalating between base pairs of DNA, disrupting triplicate codons or producing o2 free radical that damage DNA

Hormonal anticancer durgs — antagonize receptors, preventing endogenous growth promoting hormones; while others, are agonist that inhibit tumor growth

Question 2

alkylating agents

Answer 2

• generally more effectve against slow growing tumors than other classes of antineoplastics b/c these drugs are cell-cycle nonspecific
• toxic to hematologic cells => myelosuppression expected (decrease in bone marrow activity that results in reduced production of blood cells. Some blood cell disorders include: fewer red blood cells (anemia) fewer white blood cells (neutropenia))
• can cause secondary tumors

Question 3

antimetabolites

Answer 3

• cell cycle specific agents which prevent synthesis of nucleotides or inhibit enzymes by mimicking nucleotides

Question 4

Cancer cells how they become resistant?

Answer 4

1) reduced uptake of drug
2) enchaned production of enzymes that repair damanged DNA
3) produce checmially altered enzymes
4) reduced transformation of prodrugs
5) enhanced transform of drugs into inactive metabolites

become resistant to several classes of antitumor even if not exposed before =>
* antibiotics
* colchicine (gout attacks)
* vinca alkaloids or vincristine + vinblastine (chemotherapy drug that belongs to a group of drugs called vinca alkaloids.)
* epidophylloxtoxins (cancer)

cross-resistance happens despite no common mechanism of action