Final Exam - Cancer (Intro) Flashcards
noeplasm
new growth, benign or malignant
tumor
nonspecific term meaning lump or swelling
cancer
malignant neoplasm
types of -plasias
hyperplasia
metaplasia
dysplasia
anaplasia
hyperplasia
increase in organ or tissue size due to increase in the number of cells
metaplasia
a substitution of one type of adult tissue for another
dysplasia
abnormal proliferation in which there is loss of normal architecture
anaplasia
Loss of structural differentiation. Cells dedifferentiate.
types of -omas
carcinoma
adenocarcinoma
sarcoma
lymphoma/leukemia
melanoma
blastoma
teratoma
carcinoma
malignant neoplasm, squamous epithelial cells
adenocarcinoma
malignant neoplasm, glandular tissue
sarcoma
malignant neoplasm, mesenchymal tissue
lymphoma/leukamia
malignant neoplasm, hematopoietic tissue
melanoma
cancer of pigment cells (skin or eye)
blastoma
malignancy in precursor cells (blasts)
-more common in children
teratoma
germ cell neoplasm of several different types of tissues
numerical staging
worse prognosis with increasing stage #
TNM staging
more involvement and higher numbers mean worse prognosis and worse outcomes in general
hallmarks of cancer
- sustaining proliferative signaling
- avoid immune destruction
- enable replicative immortality
- invasion and metastasis
- accessing vasculature
- resisting cell death
oncogenes
promote tumor growth
-v-Src
-EGFR
-Ras or Kras
-PI3K
tumor supporessors
suppress tumor growth
-RB1
-BRCA1 and BRCA2
-p16
-p53
all CML have this
bcr-abl translocation
15-30% of NSCLC have this mutation
EGFR
EGFR is a ______ mutation
activating (cells begin to grow unchecked)
drugs used to target EGFR mutation
tyrosine kinase inhibitors
BRCA mutations in breast cancer are susceptible to what therapy
PARP inhibitors
-olaparib
-any other -paribs
olaparib MOA
Binds PARP to DNA so that it cannot go to other DNA strand breaks. This leads to more and more DNA damage until eventually the cell dies.
drug class and area of cell cycle it targets
-5 categories
-9 drug classes
DNA damaging agents (non-specific)
-alkylators
-intercalaters
DNA replication (S phase)
-anti-metabolites
-anti-folates
-topo1 inhibitors
sister chromatid separation (G2 phase)
-topo 2 inhibitors
chromosome segregation (M phase)
-microtubule inhibitors
mitogenic signaling (G1 phase)
-kinase inhibitors
-hormone inhibitors
regulators of cell cycle steps
CDC2 - M phase/G2 phase
CDK4/6 - G1 phase
CDK2 - G1 phase at replication point/S phase
CDK4/6 inhibtors
ribociclib
palbociclib
abemaciclib
palbociclib AE
neutropenia
N/V/D
fatigue
palbociclib MOA
approved for BRCA1/2 mutations
are alkylating agents dependent on the cell cycle stage
no, they can damage DNA in G0 resting phase and cells that are progressing through the cell cycle
cell cycle non-specific drugs
alkylating agents and DNA intercalating agents
majority of SE from chemo occur to what cells in the body
rapidly dividing cells
-GI tract (N/V, loss of appetite)
-WBCs (infections)
-RBCs (anemia)
major dose limiting toxicity in chemo drugs
myelosuppression
most common SE in chemo drugs
N/V
drugs that work at G1 stage
asparaginase
steroids (prednisone)
drugs that work at S stage
folic acid analogs
methotrexate
cytarabine
gemcitabine
capecitabine
fluorouracil
mercaptopurine
irinotecan
topotecan
drugs that work at G2 stage
bleomycin
etoposide
drugs that work at M stage
docetaxel
paclitaxel
vinblastine
vincristine
vinorelbine
drugs in CHOP
cyclophosphamide
doxorubicin
vincristine
prednisone
mechanisms of drug resistance
- altered drug metabolism
- changes in drug target or fxn
- physiological changes that promote resistance
- cell survival mechanisms
altered drug metabolism examples
- increased transport of drugs out of the cell through efflux pumps
-PgP
-MRP: multidrug resistant proteins - reduced transport into the cell
-loss of drug importer, decreased membrane permeability - decreased activation of prodrug
- increased detoxification of drug molecule
changes in drug target or fxn examples
- increased expression of drug target through gene amplification or expression
-upregulation of target makes it harder to inhibit - emergence of mutant, structurally altered target
cell survival mechanisms examples
- activation of anti-apoptotic regulators
- increased repair of damage caused by chemotherapies
microtubule inhibitors
vincristine
paclitaxel
docetaxel
topoisomerase inhibitors
etoposide (topo 2)
irinotecan (topo 1)
doxorubicin (topo 2, DNA damage)
bleomycin (topo 2, DNA damage)
alkylators/platinum compounds
chlorambucil
cyclophosphamide
mitomycin C
cisplatin
anti-metabolites
6-mercaptopurine
methotrexate
5-fluorouracil
cytarabine
