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128 Cards in this Set

  • Front
  • Back
what term means new growth
neoplasia
what is a neoplasm and what are its characteristics
tumor; benign or malignant
malignant tumors are characterized by what
local invasion and distant metastasis
what shows evidence of dedifferentiation
malignant cells
malignant cells show evidence of what
dedifferentiation
Cells that have undergone malignant transformation express signs of what
immaturity such as the expression of fetal antigens
what might show chromosomal abnormalities, and have altered metabolic pathways
neoplasia
A normal cell turns into a cancer cell because of ?
one or more mutations in its DNA which can be inherited or acquired
what happens during the formation of cancer cells
Activation of proto-oncogenes to oncogenes; Inactivation of tumor suppressor genes
what are the characteristics of cancer cells
Dedifferentiation
Uncontrolled proliferation
Invasiveness
The ability to metastasize
similar to normal cells/difficult to find areas of selective toxicity
what is significant about the proliferation of cancer cells
not that it proliferates faster than normal cells but that it is unregulated
what is apoptosis
programmed cell death
what is a hallmark of cancer cells
resistance to apoptosis
true or false cancer cells show telomerase expression
true
what is the significance of telomerase expression in cancer cells
it repairs telomeres; allows cancer cells to continue to proliferate
The multiplication of normal cells involves what
division of the stem cells in a particular tissue to give rise to daughter cells
daughter cells differentiate to become what
mature cells
what cells show a reverse process
cancer cells
what cancers have faster growth and a worse prognosis
poorly differentiated cancers
Normal cells are not found where
outside designated tissues of origin
Cancer cells will proliferate where and how
wherever they reside and secrete enzymes that break down the extracellular matrix
what are Metastases
secondary tumors that are released from the primary tumor
what are the principle cause of morbidity and mortality
metastases
what is a carcinogen
any physical, chemical, or biological factor that causes or promotes cancer.
what are examples of carcinogens
Chemicals, radiation, and viruses
what are oncogenes
genes that are responsible for the conversion of normal cells into cancer cells.
what are tumor suppressor genes
genes that inhibit the transformation of normal cells into malignant cells
Damage to the p53 tumor suppressor gene is associated with what
cancers of the breast, lung, brain, colon, and bone
what is associated with cancers of the breast, lung, brain, colon, and bone
Damage to the p53 tumor suppressor gene
Cancer chemotherapy is based on what
principle of selective toxicity
when treating cancer what is cell cycle specific
anticancer agent that acts selectively on tumor stem cells when they are traversing the cell cycle and not when they are in the G-0 or resting phase
when treating cancer what is cell cycle nonspecific
anticancer agent that acts on tumor stem cells when they are traversing the cell cycle and when they are in the resting phase
what is the log kill hypothesis
concept used in cancer chemotherapy to mean that anticancer drugs kill a fixed proportion of a tumor cell population, not a fixed number of tumor cells
what is an example of the log kill hypothesis
a 1-log-kill will decrease a tumor cell population by one order of magnitude
i.e. 90% of the cells will be eradicated
what is growth fraction
proportion of cells in a tumor population that are actively dividing
what is the rescue therapy
administration of endogenous metabolites to counteract the effects of anti-cancer drugs on normal cells
what is the mech. of action of CCNS drugs (alkylating agents)
They form reactive molecular species that alkylate nucleophillic groups on DNA bases, particularly the N-7 position of guanine.
This leads to cross-linking of bases, abnormal base pairing, and strand breakage
Tumor resistance to alkylating agents occurs through ?
increased DNA repair, decreased drug permeability, or the production of trapping agents such as thiols
thiols containt what
a sulfur-hydrogen bond and are very nucleophillic
what contains a sulfur-hydrogen bond and are very nucleophillic
thiols
what are the pharmacokinetics of Cyclophosphamide
Hepatic transformation is needed for antitumor activity
what is the clinical use of cyclophosphamide
Non-Hodgkin’s lymphoma, breast and ovarian cancer, and neuroblastoma
what toxicity is associated with cyclophosphamide
GI distress, myelosuppression, alopecia, hemorrhagic cystitis, cardiac dysfunction, lung toxicity, and SIADH
what are the pharmacokinetics of Carmustine (BCNU)
High lipophilicity that facilitates CNS entry, used intravenously
what is the clinical use of Carmustine (BCNU)
Hodgkin’s disease, melanoma, multiple myeloma, brain cancer, mycosis fungoides
what is the toxicity associated with Carmustine (BCNU)
GI distress, myelosuppression, CNS dysfunction
what are the pharmacokinetics of Cisplatin (Platinol)
Used intravenously, widely distributed and cleared unchanged by the kidneys
what is the clinical use of Cisplatin (Platinol)
Testicular, bladder, ovary, uterine, head and neck cancers
what is the toxicity associated with of Cisplatin (Platinol)
GI distress, myelosuppression, neurotoxicity (peripheral neuropathy and acoustic nerve), renal damage
what is the mech. of action of platinum analogs
unclear but are thought to act in a similar fashion to the alkylating agents.
are platinum analogs cell cycle specific or nonspecific
nonspecific
antimetabolites are structurally similar to what
endogenous compounds
antimetabolites are antagonists of what
folic acid (methotrexate), purines (mercaptopurine), or pyrimidines (fluorouracil).
are antimetabolites cell cycle specific or nonspecific
specific
when do antimetabolites primarily act
in the S phase
true or false: antimetabolites have immunosuppressant action
true
what drugs are the antimeabolites
methotrexate, Mercaptopurine (6-MP), Fluorouracil (5-FU),
what class of drug is methotrexate
antimetabolite
what is the mech of action of methotrexate
Substrate for and inhibitor of dihydrofolate reductase.
This interferes with nucleic acid and protein synthesis.
Tumor cell resistance mechanisms include decreased drug accumulation, changes in dihydrofolate reductase, and decreased formation of cytotoxic metabolites of methotrexate
what are the pharmacokinetics of methotrexate
Both oral and IV administration afford good tissue distribution except to the CNS.
Excreted unchanged by the kidneys.
Adequate hydration is required to prevent crystallization in renal tubules
what is the clinical use of methotrexate
Acute lymphoblastic leukemia, choriocarcinoma, head and neck cancer, testicular cancer, osteogenic sarcoma, rheumatoid arthritis, psoriasis, and it is also used as an abortifacient
what is the mech. of action of Mercaptopurine (6-MP)
Purine antimetabolite which is activated by hypoxanthine-guanine phospho-ribosyltranferases (HGPRTases) to toxic nucleotides that inhibit several enzymes involved in purine metabolism.
A Prodrug
what is the resistance associated with mercaptopurine
decreased activity of HGPRTase, or increased inactivation of the toxic nucleotide
what are the pharmacokinetics of mercaptopurine
Low oral bioavailability due to first pass metabolism.
The metabolism of mercaptopurine is inhibited by allopurinol
what is the clinical use of mercaptopurine
Childhood acute leukemia
what is the toxicity associated with mercaptopurine
Bone marrow suppression, and hepatic dysfunction
what is the mech of action of flurouracil
Transformed to 5-FdUMP which inhibits thymidylate synthase and leads to “thymineless” death of cells
what is the resistance associated with fluorouracil
Decreased activation of 5-FU, increased thymidylate synthase activity, and reduced drug sensitivity of this enzyme
what are the pharmacokinetics of fluorouracil
Given IV and widely distributed including the CSF. Elimination is by metabolism
what is the clinical use of fluorouracil
Breast, colon, rectum, stomach, and pancreas, topically used for skin cancer
what is the toxicity associated with lfuorouracil
GI distress, myelosuppression, and alopecia
what drugs are the antitumor antibioltics
Doxorubicin (Adriamycin),
Bleomycin
what class is doxorubicin
antitumor anitbiotics
what class is bleomycin
antitumor antibiotics
what class is mercaptopurine
antimetabolite
what class is fluorouracil
antimetabolite
what is the mech of action of doxorubicin
An anthracycline which can intercalate between base pairs, inhibit topoisomerase II, and generate free radicals.
Blocks the synthesis of RNA and DNA and causes DNA strand scission
is doxorubicin cell cycle secific or nonspecific
nonspecific
what are the pharmacokinetics of doxorubicin
Must be given IV.
Metabolized in the liver and excreted in the urine, imparting to it a red color
wjhat is the clinical use of doxorubicin
Lymphoma, sarcoma, acute leukemia, breast, lung, testes, thyroid, and ovary
what is the toxicity associated with doxorubicin
Myelosuppression, GI distress, and alopecia.
Unique side effect is cardiotoxicity
how does bleomycin act
by binding to DNA, which results in single-strand and double-strand breaks following free radical formation, and inhibition of DNA biosynthesis
is bleomycin cell cycle specific or nonspecific
specific
what drug causes accumulation of cells in the G2 phase of the cell cycle
bleomycin
what does bleomycin cause
accumulation of cells in the G2 phase of the cell cycle
what is the clinical use of bleomycin
Hodgkin's and non-Hodgkin's lymphomas, germ cell tumor, head and neck cancer, and squamous cell cancer of the skin, cervix, and vulva
what is the toxicity associated with bleomycin
Pulmonary toxicity
true or false: pulmonary toxicity is dose limiting
true
pulmonary toxicity usually presents as what
pneumonitis with cough, dyspnea, dry inspiratory crackles on physical examination, and infiltrates on chest x-ray
when is the incidence of pulmonary toxicity increased
in patients older than 70 years of age, in those who receive cumulative doses greater than 400 units, in those with underlying pulmonary disease, and in those who have received prior mediastinal or chest irradiation
are plant alkaloids cell cycle specific or nonspecific
specific
what are the plant alkaloids
the vinca alkaloids, the podophyllotoxins, and the taxenes
what class is Vincristine (Oncovin)
plant alkaloid
what is the mech of action of Vincristine (Oncovin)
A spindle poison derived from the periwinkle plant.
Prevents the assembly of tubulin dimers into microtubules, and blocks the formation of the mitotic spindle.
Acts on the M phase of the cell cycle
what is the resistance associated with Vincristine (Oncovin)
occurs as a result of increased efflux from the cell by a transporter molecule
what are the pharmacokintecis of Vincristine (Oncovin)
Given IV. Good tissue penetration except into the CSF.
Cleared mainly by biliary excretion
what is the clinical use of Vincristine (Oncovin)
Lymphoma, Hodgkin’s disease, Wilm’s tumor, childhood acute leukemia
what is the toxicity associated with Vincristine (Oncovin)
GI distress, alopecia, and myelosuppression.
Also causes peripheral neuropathy
what class of etoposide
plant alkaloid
what is etoposide
podophyllotoxin derived from the May apple plant
what is the mech of action of etoposide
Interacts with Topoisomerase II to increase the degradation of DNA. Most active in the late S and early G2 phases
what are the pharmacokinetics of etoposide
Good oral absorption, eliminated via the kidney
what is the toxicity associated with etoposide
GI, alopecia, and myelosuppression
what is the clinical use of etoposide
germ cell cancers, small cell and non-small cell lung cancers, Hodgkin’s and non-Hodgkin’s lymphomas, and gastric cancer
what class is Paclitaxel (Taxol)
plant alkaloid
what is Paclitaxel (Taxol)
A taxane derived from the Pacific yew tree
what is the mech of action of Paclitaxel (Taxol)
A spindle poison which prevents microtubule disassembly into tubulin monomers
what are the pharmacokinetics of Paclitaxel (Taxol)
given IV
what is the clinical use of Paclitaxel (Taxol)
Breast and ovarian cancer
what is the toxicity associated with Paclitaxel (Taxol)
Myelosuppression, neuropathy, and hypersensitivity reactions
what is prednisone used to treat
acute leukemia, Hodgkin’s disease, and lymphoma
what class is prednisone
hormone
what class is Diethylstilbestrol (DES)
hormone
what is Diethylstilbestrol (DES) used to treat
prostate and breast cancer
what are SERM’s
mixed estrogen agonists that act as antagonists in certain tissues
what class isTamoxifen
hormone
how does Tamoxifen act
as an antagonist in hormone-responsive breast cancers where it prevents receptor activation by endogenous estrogen
what drug has more agonist than antagonist action on bone and thus helps to prevent osteoporosis.
tamoxifen
what drug is a Selective Estrogen Receptor Modifier (SERM) which blocks the binding of estrogen to receptors of estrogen-sensitive cancer cells in breast tissue
Tamoxifen (Nolvadex
what is the mech of action of Tamoxifen (Nolvadex
a Selective Estrogen Receptor Modifier (SERM) which blocks the binding of estrogen to receptors of estrogen-sensitive cancer cells in breast tissue
what is the clinical use of Tamoxifen (Nolvadex
treatment of receptor-positive breast cancers and may help prevent cancer in high risk women
what toxicity is seen with tamoxifen
nausea, vomiting, hot flushes, vaginal bleeding, hypercalcemia, and peripheral edema
what drugs are biologic response modifiers
interferon alfa-2,
interferon alfa-2 is made by what
lymphocytes
what is the mech of action of interferon alfa-2
inhibits cell proliferation
what is clinical use of interferon alfa-2
treatment of hairy cell leukemia, Kaposi’s sarcoma, and hepatitis
what is the toxicity associated with interferon alfa-2
Causes flu-like symptoms, fatigue, depression, nausea, vomiting, and diarrhea
what are the miscellaneous anticancer drugs
imatinib, Cetuximab, vascular endothelial growth factor (VEGF), epidermal growth factor receptor (EGFR), Bevacizumab, Asparaginase (L-asparagine amidohydrolase)