Cancer (E1) Flashcards
neoplasia
process of a tumor forming
in situ neoplasia
localized to one site
invasive neoplasm
non-localized, spread
cellular dysplasia
irregular, abnormal nuclei numbers or shape.
cells have higher mitotoc index than original tissue
benign tumor
has a capsule that contain the tumor
mailgnant tumor
spreads through the body
metastasis
fragment of tumor breaks off and travels via bloodstream or lymph to take over second site
what are the most commons sites that get metastasized
lungs, lymph nodes, and live, have small blood vessels and lots of capillaries
extravasation
branches into surrounding tissue
malignant
high mitotic index, cell are les differentiated
carcinoma
epithelial tissue derived, like skin cancer
adenocarcinoma
gland/duct derived
sarcoma
connective tissue derived
lymphoma
lymphatic tissue
leukemia
blood-forming tissue
teratoma
germ cell, can grow teeth, fingernail, hair
5 clinical stages of tumors
0- no evidence of tumor/cancer
1- confined to organ of origin
2- locally invasive
3- spread to regional structures
4- spread to more distant sites
TNM system
T- degree of tumor spread
N- lymph node involvement
M- presence of distant metastasis
Tumor marks
made in high amounts by cancer cells
can be used to screen high risk individuals
found on cancer cell membranes/ body fluids
multi- hit hypothesis
as cells get older the occurrence of genetic mutations increase
what does the multi-hit hypothesis explain
cancer prevalence increasing with age as older DNA has had more time to accumulate damage
clonal proliferation
cancer cells have a competitive advantage, outcompete normal cells and use more nutrition
autonomy with cancer cells
ignore bodies signals
Why are cancer cells able to metastisize
they have lost anchorage dependence and are able to survive even while not attached to a basement membrane
Why are cancer cells able to stimulate themselves
‘inapprpriate’ autocrine signaling
density-dependent inhibition
controls cell growth, but something cancer cells do not have so they grow unihibited
apoptosis pathways
trigger cells to self destruct, something cancer cells disable
warburg effect
cancer cells take pyruvate to make amino acids and nucleotides for their own growth, rather than allowing it to go to the ETC. Takes nutrition from surrounding cells
angiogenic factors
cancer cells able to secrete this that helps make new blood vessels
how do cancer cells effect fibronectin synthesis
lessen its effect, fibronectin keeps tissue together and by lowering it synthesis, cells are able to better slip through tissue
cell imortality
with cancer cells able to divide even with mutationa, result in increase of telomerase enzymes
what can cause proto- oncogenes to be turned on
point mutations
chromosomal alteration/ amplifications
homozygosity
gene silencing (DNA methylation)
External pathogens (HPV w/ cervical cancer)
Inflammation-promoting chemicals
genetic predisposition
Tumor- suppressor genes
antioncogenes,negatively regulate cell growth
caretakes gene
repair damage to genes/ chromosomes, can help protect from cancer
How do T-cells protect against cancer
are often able to recognize cancerous cells
primary tumor
the primary source of metastasis
organ tropism
a preference to metastasis in certain organs
ecogenetics
study between environment and development of cancer
xenobiotics
alien/foreign compounds that can exasperate compounds
carcinogen
substance that can cause cancer
common carcinogens (7)
tobacco use, radiation, electromagnetic fields, air pollution, obesity, alcohol, unsafe sexual behaviors
cachexia
wasting syndrome, gaunt, manifestation of cancer
how do cancer drugs cause anemia
they are often antimitotic, which lower the amount of cell division
leukopenia (low on white blood cells) or thrombocytopenia (low on platelets)
paraneoplastic syndromes
specific clinical manifestations of cancer
where do paraneoplastic syndromes develop/ what do they effect/cause
nervous system- physical sensation, numbness
central nervous system- cognitive/personality changes
chemotherapy
any drug used to work against cancer
single agent chemotherapy
uses single chemotherapautic agent
combination chemotherapy
uses multiple agents
principle of dose intensity
the more you take, the more profound of an effect it will have
therapeutic index
the range of how much of a drug you can take that will be non toxic/harmful
why dont cancer drugs have a poor therepautic index
the amount needed to have an effect is the same as the amount that become harmful.
anti mitotic drugs
inhibits mitosis, but will effect all other highly mitotic cells like skin, hair, and blood
anti angiogenic drugs
inhibit growth of new blood vessels and starve cancer of blood supply
radiation
blasts cancer cells, but also damage surrounding cells
surgeical removal of tumor
needs analysis of margins to see if cancer spread to surrounding tissues.
immunotherapy
stimulating t-cells, supplementing immune system
iatrogenic metastasis
with surgical removal of tumor, cancerous cells enter into blood stream
side effects of cancer treatment
GI tract disruption
bone marrow suppression
alopecia
damage to gametes
dry skin
