Neoplasms Flashcards
neoplasm
new tissue, tumor, mainly cancers
neoplasia
new growth
cancer
malignant tumor
where do neoplasms come from?
normal tissue that can proliferate
how many mutations have to occur in a cell for a change to occur?
two
fibroma
from fibroblasts
lipoma
adipose
adenoma
exhibits gland patterns or from adrenal glands
chondroma
cartilaginous
leiomyoma
smooth muscle
myoma
regular skeletal muscle
papilloma
epithelial growth on surface, finger like fronds
how are benign neoplasms named?
beginning of word tells you where its coming from, and always ends in ‘oma’
sarcomas, carcinomas, adenocarcinomas, teratoma, melanoma, hematopoietic invade adjacent tissue metastasize wide range of differentiation kills host not encapsulated goes from one tissue to another does not look like the tissue that is supposed to be there
malignant neoplasms
from mesenchymal tissue (liposarcoma, fibrosarcoma, osteosarcoma); mesoderm (middle layer)
sarcomas
from epithelial cells; ectoderm (surface)
carcinomas
glandular growth/gland association
adenocarcinomas
made of cells from more than one germ layer; come from the stem cells and can grow into anything
teratoma
coming from melanocytes (cells in your skin that give color or freckles) start to grow out of control and end up with patchy tumors
melanoma
blood cells; leukemia
hematopoietic
remain localized, don't metastasize grows as a cohesive unit tend to become encapsulated well differentiated not deadly looks like the tissue cell that is supposed to be there
benign neoplasms
we have this wide arrange of differentiation or no differentiation at all
anaplasia
increase in size but not in number
still the correct type of cell
ex: pregnant, cardiovascular disease
hyperplasia
replacement of one cell type with another
better adapted to altered environment
ex. ppl w acid reflux
metaplasia
disordered growth loss of uniformity loss of architectural orientation metastasize many different cells type show up
dysplasia
any sort of chemical that can cause cancer
can be called mutagen
but not all of _____ are mutagen and vice versa
carcinogen
what must happen for cancer to occur?
mutate DNA twice
what two types of cancers are associated with viruses?
cervical carcinomas (HPV) and hepatomas (liver cancers, hep C)
any sort of gene that’s in the DNA that will lead to the development of a cancer
oncogene
how do tumor viruses cause cancer?
by the interaction between carcinogen and endogenous viruses
#1 on the outside, you have this extracellular domain and that's where the signal binds #2 domain that goes through the membrane - transmembrane domain #3 on the inside, there's kinase
growth factors - start of the signal cascade
enzyme that phosphorylates and activates the protein and changes its shape
kinase
what happens to mutated receptors?
changes kinase domain of growth factor so it no longer needs the signal and can activate itself
how many cells produce and stimulate growth factors and how are they related?
two cells (epithelian and mesenchymal) one will produce some of the growth factors and go to the other cell to be activated and/or vice versa
what happens to these cells in a cancer cell?
a cancer cell that produces the signal will also produce the receptor thus it can activate itself
autocrine signaling
self signaling
what is G1 preparing for?
S phase
S phase
synthesizes (makes two copies of) DNA
after S phase
G2
what is G2 preparing for?
mitosis (inphase)
how much time in G1?
12-15 hrs
how much time in S phase?
6-8 hrs
how much time in G2?
3-5 hrs
how much time inphase (Mitosis)?
1 hour for cell to divide into two
how long does it take for a cell to divide?
1 day
why do we need checkpoints?
stops cell from going through cycles and makes sure we have all the enzymes and proteins to go through with
what does the check point in S phase used for?
it checks for DNA damage and stops everything and causes cell to kill itself if damaged
what does the check point in G2 used for?
it makes sure that the DNA is replicated
what is the R point?
restrictive point will determine whether cell cycle will go all the way through or not
what do CDKs depend on?
presence of kinase
why are cyclins important and how many are there?
this is how the cell knows it should be in a specific cycle; 4 (DEAB)
around G1 then it goes away
D
at the end of G1 and beginning of S phase after that it goes away
E
middle of S phase and goes away towards beginning of G2
A
is around in G2
B
CDK 4/6
D and G1
CDK 2
E
CDK 1
A and B
where is the R point?
at the end of CDK 4/6 and D and this is the point that will determine whether the DNA will be synthesized
what is the protein that controls the R point?
retinoblastoma, Rb
what does Rb do?
it causes CDK 4/6 to go away and process continues
guardian of the genome - makes sure that there are no other mutations in the DNA
initiates cell death
p53
a cell that is cancerous we say that the cell has been ______
transformed
contact inhibition loss foci development altered shape ability to grow in low serum immortal anchorage independence tumorigenicity
transformed characteristics
how can cancer make new blood vessels form?
through angiogenesis)
first line of defense
second line of defense
defenses against any pathogen
not specific
innate immunity
third line of defense
immunity or resistance to a specific pathogen
specific response –> going to be a lot stronger
has memory
slower to respond
adaptive immunity
intact skin
mucous membranes and their secretions
normal microbiota
first line of defense
phagocytes (neutrophils, eosinophils, dendritic cells, macrophages)
inflammation
fever
antimicrobial substances
second line of defense
specialized lymphocytes: T cells and B cells
antibodies
third line of defense
ability to ward off disease
immunity
keratinized epidermis (consists of tightly packed cells)
replaced every 4-5 days
dry environment
no blood vessels
skin
sebum (oil)
sweat (viscous)
organic acids (lowers pH)
glands
transports microbes trapped in mucus away from lungs
ciliary escalator
washes eye
lacrimal apparatus
dilutes and washes microbes off
saliva
flows out
urine
flow out and low pH
vaginal secretions
in perspiration, tears, saliva, and urine
an enzyme that breaks down bacterial cell wall
lysozyme
microbial competition (competing w pathogens)
normal microbiota
one organism (microbe) benefits, the other (host) is unharmed may be opportunistic pathogens
commensal microbiota
part of the immune system, a series of proteins made to fight bacteria/infections
complement system
increased in numbers at start of infection, most abundant
neutrophils
present in all tissues, important in presenting antigen to adaptive immune
dendritic cells
10-15% of lymphocytes in peripheral blood
lack antigen specific receptors
attack whatever but kill tumor cells and virally infected cells
natural killer cell
10-15% of lymphocytes in peripheral blood
lack antigen specific receptors
attack whatever but kill tumor cells and virally infected cells
natural killer cell
redness, swelling, pain, heat, loss of function
inflammation
- destroy injurious/infecting agent, remove it and its products - vasodilation
- limit the effect of agent by confining - not letting it spread - phagocytose
- repair or replace damage tissue - start the repair process - repair
inflammation steps
in fever, which endotoxin does gram negative bacteria cause phagocytes to release ?
IL-1 and TNF a ; they instruct the hypothalamus to increase internal temperature
what does the hypothalamus release that resets the hypothalamus to a high temperature
prostaglandins
increases transferrin
increases IL1
produces interferon
advantages of fever
tachycardia
acidosis (pH of blood goes down)
dehydration
106 dg C
disadvantages of fever
cause cell to produce antiviral proteins that inhibit viral replication
IFNa and IFN b
causes neutrophils and macrophages to phagocytize bacteria; puts a little tag on bacteria
IFNy
IFNa IFNb IFNy
interferons
binds iron
transferrin
inhibits microbial growth by inhibiting cell wall, forms pores in membranes and destroys DNA and RNA
non-antibody proteins that attack and destroy bacteria
antimicrobial peptides (pt of complement system)
what are the two complement proteins?
C3 and C5
what causes pores to be formed in the membrane, part of the flagging mechanism so that macrophages and neutrophils find the offending agent
C3B
activates other sorts of neutrophils and WBC to hunt down microbes present in the area; need to be cut in half
C3
is activated via C3 in order to bring those macrophages and neutrophils to kill offending agent
C5
coats microbes for phagocytosis and complement activation
elevated plasma levels
beginning of an infection
tagging mechanism
c-reactive proteins
releases antibodies in order to do something; pathogens outside of the cell
humoral; B cells
specifically use cells to attack things with antibodies; trying to control antibodies by attacking cell; pathogens inside the cell
cellular; T cells
where do B and T cells mature?
B in bone marrow, T in thymus
a substance that causes the body to produce specific antibodies or sensitized T cells
antigen
what do antibodies interact with?
epitopes
globular proteins called immunoglobulins
number of antigen-binding sites determines valence (how many epitopes present)
nature of antibodies
protein with 2 heavy chains and 2 light chains
constant region
variable region
antibody structure
how many immunoglobulins are there?
5 )GAMED)
monomer 2 epitope binding site 80% of serum antibodies neutralize toxins 23 days
IgG
dimer 4 epitope binding sites 10-15% of serum antibodies secretions, mucosal protection 6 days
IgA
pentamer 10 epitope binding sites 5-10% of serum antibodies agglutinate microbes 5 days first to show up in adaptive immune response
IgM
monomer 2 epitope binding site 0.2% of serum antibodies B cells, innate immune response 3 days
IgD
monomer
0.002% of serum antibodies
allergic rxn, lysis of parasitic worms
2 days
IgE
where are B cells sitting?
lymph nodes
antigen presented Th cell
Th cell produces cytokines
T dependent antigens
stimulate the B cell to make antibodies
antigen/epitope randomly bumps into a cell and causes activation to occur
T independent antigens
what do B cells differentiate into?
plasma cells and memory cells
what eliminates harmful B cells?
clonal deletion
what do B cells do?
agglutination opsonization activation of complement neutralization antibody dependent cell mediated cytotoxicity
macrophages, Tc Cells, natural killer cells
T Helper (1) cell
eosinophils, IgM and IgE
T helper (2) cell
destroys target cell on contact
cytotoxic T lymphocyte
regulates immune response and helps maintain tolerance
T regulatory cell
attacks cancer cells
activated macrophage
destroys target cells (virus infected, tumor cells)
participates in antibody dependence
cell mediated cytotoxicity
granular leukocytes destroy cells that don’t express MHC I
natural killer cells
what are the three antigen presenting cells ?
dendritic
macrophage
B cell
viral pathogens and allergens; all throughout the body
dendritic
intracellular and extracellular pathogens; mainly bacteria
macrophage
recognize viruses and pathogens
B cell
what is the pedestal where the bacteria is presented?
MHC II
CD4+
TCR recognize antigens and MHC II
produce cytokines and differentiate
T Helper Cells
CD8+
endogenous antigens
releases perforin and granzymes
carry their own antigens
T cytotoxic cells
stops autoimmune responses
T regulatory cells
situation where we have a foreign thing inside of us that is too big to be phagocytosed - coat it with antibodies
antibody dependent cell mediated cytotoxicity (ADCC)
amount of antibody in the serum
antibody titre
occurs after initial contact with the antigen
primary response
occurs after second exposure
secondary (memory or anamnestic) response
adaptive immunity resulting from infection
naturally acquired active immunity
adaptive immunity resulting from transplacental or via colostrum
naturally acquired passive immunity
adaptive immunity resulting from injection of antigen (vaccination) itself
artificially acquired active immunity
adaptive immunity resulting from injection of antibody to take care of something
artificially acquired passive immunity
