ch10: biology of cancer and tumor spread Flashcards
mutated cells
cells affected by genetic or environmental factors
cancerous cells
have the ability to blow past cell cycle checkpoint
tumor
mutated cells growing rapidly with no control from checkpoints or neighboring cells
_____ precedes the growth of a neoplasm
cellular dysplasia
dysplasia
abnormal cell growth in number, shape, size
when cells are dysplastic, they have a higher __________
higher mitotic index: higher ability and rate at which cells go through mitosis (therefore get more access to nutrients to fuel growth)
what natural body cells have the highest mitotic index (that are targeted by chemotherapy)
hair cells, skin cells, stem cells of bone marrow
neoplasm
tumor
in situ
neoplasm hasn’t extended to the basement membrane or surrounding tissues (yet)
invasive neoplasm
tumor extends past basement membrane and into other types of tissues
benign tumor
- encapsulated (keeps it from metastasizing and extravasating)
- lower mitotic index
malignant tumor
- not encapsulated
- metastasize and extravasate
- higher mitotic index
what are the three places you can commonly find metastasis and why?
liver, lungs, lymph
- lots of narrow capillaries and small spaces
carcinoma
epitelial tissue derived tumor
carcinoma in situ
carcinoma that has not passed basement membrane
adenocarcinoma
clinical manifestation?
gland/duct tissue derived
- swings in hormone balance
sarcoma
connective tissue derived
lymphoma
lymphatic tissue derived
leukemia
do you see tumors forming?
blood forming tissue derived
- don’t see tumors forming
teratoma
germ cell derived
clinical staging of tumors (4 stages)
0 - no evidence of tumor/cancer 1 - there but confined to organ of origin 2 - locally invasive 3 - spread to "regional" structures 4 - spread to distant sites
what is the only way for a tumor to reach stage 4?
to metastasize and extravasate
explain the TNM system
T = degree of tumor spread N = lymph node involvement M = presence of distant metastasis
clinical staging of tumors depend on how _____ the tumor is and how ______ it is.
obvious, contained
what are tumor markers
abnormal concentration of normal molecules indicate possible cancerous growth
what can you use tumor markers for?
- screen high risk individuals
- diagnose tumors
- follow treatment –> provide prognosis
t/f: cancer prevalence increases with age
true
what is the multi-hit hypothesis
older cells = more likely to get mutations bc of time
spontaneous mutation
DNA polymerase makes a mistake and won’t correct
induced mutation
outside force came in and caused mutation to happen =MUTAGEN
why do cancer cells have a competitive advantage?
“clonal expansion/proliferation”
- cancer cells divide more rapidly –> more access to nutrients vs normal tissues
why are cancerous tumors “jerks”
- autonomy
- inappropriate autocrine signaling
- lose density dependent inhibition
- lose anchorage dependence
- disable apoptosis
- Warburg effect
- angiogenic factors
- fibronectin synthesis
- telomerase enzyme
cancer cell autonomy
cares only about self disregarding other cells
inappropriate autocrine signaling
secrete hormones to stimulate themselves
loss of density dependent inhibition
cancerous tissues don’t stop dividing when a certain density is reached
lose anchorage dependence
cancer cells do not have to be anchored to another tissue/basement membrane in order to function
- makes metastasis easier
disable apoptosis
cancerous tumors don’t go through preprogrammed cell suicide
warburg effect
cancerous cells use pyruvate to make into molecules they can use for growth (building blocks, amino acids) instead of ATP
angiogenic factors
molecule that encourages development of blood vessels (tumor gets nutrients for itself)
down regulate fibronectin synthesis
allows cells to stick to each other/other things, if down regulated, EXTRAVASATION happen (squeeze extensions out to other tissues)
telomerase enzyme
lengthens telomeres and prevents wear down of chormosome = increase lifespan = increase likelihood of mutations
oncogene
gene that can lead to the development of cancerous tumor proliferation
proto-oncogene
inactive oncogene
what is the theory about oncogenes?
used to be genes that we’re used in embryonic development (rapid growth) that are turned off and don’t need anymore, but are turned on again
how can oncogenes be activated?
- point mutations
- chromosomal alterations/amplifications
- loss of herterozygosity
- gene silencing (DNA methylation)
- external pathogens
point mutations
when a single base pair is added, deleted or changed
chromosomal alterations/amplifications
one section of a chromosome gets copied and replicated over and over again
loss of heterozygosity
one copy of good gene and one bad gene –> if something happens to good gene, bad gene dominates
gene silencing (dna methylation)
turning off genes by adding molecules (wrong gene gets turned off at the wrong time = trouble)
external pathogens (what virus is known as a link to cancer)
HPV –> can indirectly trigger oncogenes
- other pathogens trigger chronic inflammation –> trigger dev of cancer
what does COX-2 have to do with cancer
COX-2 = inflammation promoting chemical that can trigger cancer dev
what genes make hereditary risks for cancer?
BRCA1, BRCA2 = breast cancer gene
what are some of our body’s internal protectors from cancer?
- tumor suppressor genes
- caretaker genes
- t-cells
tumor suppressor genes
antioncogenes that negatively regulate cell growth; help body control several types of cancer when it develops
what is an example of a tumor supressor gene
retinoblastoma gene
caretaker genes
function all the time; repair damage to genes/chromosome
t-cell
able to recognize cancerous cells; can be flagged down when cells present cancerous molecules
metastasis
spread to distant sites via fragmenting
5 parts of metastasis?
- direct spread to adjacent tissues (down regulation of fibronectin)
- penetration into blood/lymph system
- fragmentation into blood/lymph
- transport to secondary sites (the three Ls)
- entry, attachment, and growth in secondary sites
organ tropism
certain cancers that originate in certain tissues DO have a preference for spreading to certain places for a secondary site
