Oncology Flashcards
How does the cell cycle catch mistakes in DNA?
has checkpoints
Order of cell cycle
G0, G1, S, G2, M
G0 phase
rest phase
G1 phase
enter cell cycle and prep for DNA replication–proto-oncogenes are activated
S phase
synthesis of chr and chr move to opp poles to prep for division into 2 cells (23 chr at end each with nuclear mem around each)
G2 phase
cells prep to divide
Mitosis phase
2 daughter cells develop
Immune surveillance
- our immune sys surveys bod for foreign subs or “no-self” antigens to attach
- with age, system worsens and reaction declines–mutated cells escape easier
Patho of cancer cells
- rapid rep w/o G0 and checkpoints
- altered DNA keeps reproducing; no apoptosis
- constant move thru cycle
- ignore growth inhibitors released by neighboring cells so nothing stops them from going where they want
Differentiation
how neoplastic cells resemble normal cells with structure and function
anaplasia
lack differentiation
- often malignant cells
- total cell disorganization, abnormal appearance, cell dysfxn
Which tumors are more well-differentation?
Benign
Rules that cancer cells BREAK
- contact inhibition–push others aside
- not cohesive (mets)
- little communication
- proliferation w/o apoptosis
- avoid “non-self” markers so the sys doesn’t attach
Cancer cells are…
UNORGANIZED
VARIABLE SHAPE
MAY DIVIDE
VARIABLE NUCLEUS
Benign tumor characteristics
- well-differentiated
- local
- cohesive
- no mets
- no necrotic core–living
Malignant tumor char
- poor diff or anaplastic
- break free easily
- slow or rapid growth
- neurotic core esp with age–harder to tx bc can’t get tx in
Tumor markers
- hor, enzymes, genes, or antigens in blood, urine, or CSF
- let us follow the clinical course (dec w/ tx)
- can also be present w/o cancer (ex: PSA)
Phases of cancer cell grwoth
- initiation–alt of genes (spon) or induced by contract with (carcinogen)
- promotion–cells accum
- progression–more mutate with met potential
- metastasis
Cancer genetics
gene mutations are sporadic or hereditary (BRCA)
tumor suppressor genes
genes that normally “brake” cell division but can mutate and become inactive, inhibiting the brake
Oncogenes
Proto-oncogenes that normally tell the cell to grow and mutate to be permanently “on”–prolif
Carcinogens
Substances that cause the development of cancer–start mutations
- can alter DNA
- damage accums
3 classes of carcinogens
- known–HPV, HIV, alcohol, virus, tobacco
- probable–nightshift
- possible–insuff evidence; exhaust engine
promoting agents
help genes proliferate and encourage further mutation
- hi fat diet
- alc
- tobacco
- hor (estrogen)
Reversible
viral-induced cancer
- malignancies assoc with virus–HIV, HPV, Hep B and C
- insert gene into host cell and host cell begins manufacturing virus
- activate growth - promo paths or inhibit tumor supp in infected cells
3 ways cancer can spread
- seeding - tumor erodes and sheds into body cavity
- implantation - exposure to adjoining tissue
- mets - travel thru lymph or vasc
Primary tumor
origin tumor
Secondary tumor
metastasis; loos like cells from original site
- site depends on location of primary tumor
- can make own blood supply and secrete vascular endo Grwoth factor
most common sites of secondary tumors
lung, bone, liver, brain
Where does colon cancer often met to
liver
Where does lung cancer often met to
bone and brain
Where does breast cancer met to
everywhere
Where does prostate cancer met to
vertebrae
Where does melanoma met to
the brain
Why is the liver a common site for mets?
all blood flow thru the liver
intraperitoneal seeding
Spreads thru the peritoneum to other ab organs
lymph spread of cancer
cells can get trapped and die, go dormant, or flourish
vasc spread of cancer
penetrate BVs and drain local veins; first stop often liver
Classifications of malignancy
1 - well diff
2 - mod diff
3 - poor dif
Layman class of tumors
1 - confined to organ of origin
2 - locally invasive
3 - regional spread
4 - spread to distal sites
TNM classifications
T - tumor size, location, involvement
N - lymph node involvement
M - metastasis (N0 none, M1 yes)
P53
a tumor suppressor gene that triggers apoptosis
