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292 Cards in this Set

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Name the basic amino acids.
Arginine, histidine and lysine
Name the acidic amino acids.
Aspartic acid and glutamic acid
Name the essential amino acids.
Histidine, leucine, isoleucine, lysine, methionine, phenylalanine, valine
List the prion diseases.
Bovine spongiform encephalopathy, creutzfeldt-jacob diseasae, scrapie, deer-elk wasting disease and kuru
What stabilizes the relaxed conformer of hemoglobin?
Carbon monoxide - makes it harder for hemoglobin to release oxygen
What stabilizes the taut conformer of hemoglobin?
2,3-BPG - makes it harder for oxygen to bind oxygen (encourages hemoglobin to release oxygen where it is needed - shifts dissociation curve to the right)
What is scurvy?
Vitamin C deficiency - prolyl hydroxylase needes vitamin c to convert proline to hydroxyproline and lysine to hydroxylysine.
Michaelis-Menton equation
Vo = k2[ES]
Vmax?
Vmax = k2[E]t
Key parts of Lineweaver-Burke plot
y-axis = 1/Vo, x-axis = 1/[S], y-intercept = 1/Vmax, x-intercept = -1/Km
How do competitive inhibitors change the plot?
increase Km, no change on Vmax
How do non-competitive inhibitors change the plot?
decrease Vmax, no change on Km
How do competitive inhibitors rotate the L-B plot?
rotate up and left around the Y-intercept
How do non-competitive inhibitors rotate the L-B plot?
rotate up and left around X-intercept
What tissues are GLUT4 receptors found in?
muscle and adpiose (insulin dependent)
Normal blood glucose level.
80mg/dL (5mM)
Steps of glycolysis.
Glucose, G6P, F6P, F1,6bisP, GA3P, 1,3bPG, 3PG, 2PG, PEP, Pyruvate
Irreversible (regulatory) steps in glycolysis.
Hexokinase, Phosphofructokinase, Pyruvatekinase (encouraged by insulin, discouraged by glucagon)
Extra step in gluconeogenesis.
pyruvate => oxaloacetate => PEP
Steps of glycogenesis
G6P, G1P, UDP-G, Glycogen (a1-4 bonds make chain, a1-6 bonds make branches)
Main steps of pentose phosphate pathway.
G6P => Ribose5P and Erythrose4P
Steps in beta oxidation.
Fatty acyl CoA, Enoyl CoA, 3-hydroxyacyl CoA, 3-ketoacyl CoA, Fatty Acyl CoA + acetyl CoA (goes until 2 acetyl CoAs)
How many ATP from 16 carbon fatty acid?
131 (FADH2, NADH and acetyl CoA goes through TCA)
Where do the 131 ATP come from?
Every two carbons = 1 FADH2 and 1 NADH (5 ATP) and 1 acetyl CoA (12 ATP) = 17 ATP per 2 carbons
Steps in TCA cycle.
Acetyl CoA, Citrate, Isocitrate, a-Ketoglutarate, Succinyl CoA, Succinate, Fumarate, Malate, Oxaloacetate, Repeat (12 ATP per Acetyl CoA)
What are the ketone bodies?
acetoacetate, acetone, D3Hydroxybutyrate
What tissues can use ketone bodies?
brain and muscles
What does ALT do?
Alanine + a-ketoglutarate <-> Glutamate + Pyruvate
What does AST do?
Aspartate + a-ketoblugarate <-> Glutamate + oxaloacetate
Coenzyme for AST and ALT?
pyridoxyl phosphate
Allosteric inhibitory of glutamate dehydrogenase?
GTP (when energy is low, amin acid degradation is increased)
Defects in the conversion of methionine to Cys cause?
met => homocysteine => cys (requires VitB6) causes homocystineuria -
What is the rate limiting step in the urea cycle?
attachment of amonia (from amino acids) to phosphate via carbamoyl phosphate (uses biotin)
Symptoms of phenylketonuria?
defect in phenylalanine hydroxylase, elevated Phe, hypopigmentation, mental retardation and mousy odor (phenylpyruvic acid)
Symptoms of maple syrup urine disease?
error in catabolsim of branched chain amino acids, build-up of amino acids and alpha-ketoacids, neurological symptoms
What are the purines?
adenine and guanine
What are the pyrimidines?
cytosine, thymine and uracil
What is the role of dihydrofolate reductase?
convert DHF to THF
Deficiency in Adesonine deaminase causes?
SCID, build up of dATP, inhibitis ribonucleotide reductase, decreased lymphocyte production
What does xanthine oxidase do?
converts hypoxanthine => xanthine => uric acid (allopurinol targets this to treat gout)
Symptoms of Lesch Nyhan syndrome?
100% loss of HGPRT activity (needed to salvage purines)
What is the only importatn pyrimidine salvage?
thymidine - salvaged from free thymine and dRP, needs thymidine phosphorylase and thymidine kinase, inhibiting may be useful in cancer therapy (gancyclovir and zidovudine are analogs that thymidine kinase can use)
Requirements for DNA polymerase to work.
dNTPs, DNA template, Zn, Mg, primer (RNA or DNA with a free 3'-OH end)
Job of DNA Polymerase I
removes, replaces RNA primer, DNA repair, (YES proofreading, YES repair) synthesis on lagging strand
Job of DNA polymerase III
DNA replication, leading strand (YES proofreading, NO repair)
Job of DNA helicase
unzips annealed nucleotides
Job of DNA ligase
complete strand synthesis (phosphage linkage)
How is condensed DNA produced?
methylation
When does telomerase stop?
when RAP1 proteins bind
What is a transition?
A to G / T to C
What is a transversion?
A to T / G to C
Deaminatino of cytosine forms?
uracil - can result on a G-C pair being converted to A-T
Job of RNA polymerase I
produce rRNA
Job of RNA polymerase II
produce mRNA
Job of RNA polymerase III
produce tRNA and 5s rRNA
Job of RNA mito
produce mitochondrial RNAs
What is a ribozyme?
enzyme caused by folding of RNA molecule - Peptidyl transferase - primary enzymatic functino of the ribosome
secondary structure of tRNA
cloverleaf
tertiary structure of tRNA
leg of lamb
Steps in mRNA formation.
transcription, 5' cap, poly-A tail, excision of introns, splicing to add different tails
What is the start codon?
AUG - codes methionine
Wobble base pairs for G anticodon?
C or U
Wobble base pairs for U anticodon?
A or G
Wobble base pairs for I anticodon?
A, C or U
Example of insulin as secretory protein.
Insulin maked as preproinsulin - cleaved in ER to proinsulin - cleaved in golgi to insulin + c-peptide - secreted
How are misfolded proteins handled?
attached to ubiquitin and sent to proteasome
What causes cystic fibrosis?
incorrectly folded CFTR protein (has many B-sheets that lead to misfoldign) - improper regulation of ocmponents of sweat and mucus
What is inactive X chromosome covered with?
XIST gene transcript
Where is the basal promoter located?
40bp upstream of start site (contains tata box)
Where is the upstream promoter located?
200bp upstream - many transcription factors - turn gene on
What are siRNA?
small interfering RNA - dsRNA is cleaved by DICER into siRNA, siRNA binds to protein complex to form RISC, allows RISC to seek out complementary mRNA and destroy it
Negative feedback example?
increase in arterial pressure, stimulates stretch receptors, stimulates afferent autonomic nerves, stimulates autonomic efferent nerves, INHIBITS increase in arterial pressure
Positive feedback example?
pituitary gland secretes LH, LH stimulates ovary, ovary secretes estradiol, estradiol stimulates pituitary
Total body water?
60% of body weight
ECF?
1/3 of TBW (plasma + ISF)
ICF
2/3 of TBW (total - ISF - plasma)
Plasma?
1/4 of ECF
What separates plasma from ISF?
blood vessel wall
What separates the ECF from the ICF?
cell membrane
Mostly intracellular ions?
potassium
Mostly extracellular ions?
sodium, calcium
Excretion formula to determine ECF
Volume(ECF) = [(Amount Injected) - (Amount Excreted)] / (Concentration) ALWAYS CONVERT TO mg/L FIRST
Define osmoles
number of mols of a chemical compound that contribute to a solution's osmotic pressure ex: 1 mol/L of NaCL = 2 osmol/L (1 for Na and 1 for Cl)
Define osmolarity
the measure of solute concentration: number of osmoles of solute / Liter of solution
Define molar equivalent
the amount of substance that will react with one mole of electrons in a redox reaction
Rank molecules from high to low permeability
O2, H2O, Urea, Glucose, K+, Na+
Endogenous ligand
produced within the bodiy
Exogenous ligand
produced outside the body (ex: drug)
Ligand with high specifity
only binds to one receptor
Ligand with high promiscuity
binds to many receptors
Synaptic signaling facts
short distance, fast onset, high precision, can be delivered from far soma, FedEx
Paracrine signaling facts
short distance, fast onset, not as selective as synaptic, Loudspeaker
Endocrine signaling facts
long distance, slow onset, very non-specific, radio broadcast
Autocrine signaling facts
single cell gets weak autocrine signal, aplifies the signal, listserv
Ionotropic receptor
open or close when directly bound by a ligand (the receptor IS the pore)
Metabotropic receptor
indirectly linked to ion channels through coupling (G protein)
Receptor sequestration
pull receptor back into an endosome
Receptor down-regulation
pull receptor back into a lysosome
Receptor inactivation
remove a phosphate
Steps of the 2nd messenger cascade
Activate G protein, activate adenylyl cyclase, produce cAMP, activate Protein kinase A
Activation of phospholipase C causes?
cleavage of PIP2 into DAG and IP3, DAG activates protein kinase C, IP3 releases Ca2+ from ER
Job of phosphodiesterase?
degrades cAMP into AMP
Job of protein phosphatase?
remove phosphate from active PKA
Job of Calmodulin?
Ca2+ activates it and it activates protein kinases
What does tyrosine kinase respond to?
insulin, EGF and PDGF
What does serine kinase respond to?
TGF-b
Job of mitogen-activated protein kinases (MAPKs)?
activate Ras protiens (Ras proteins activate MAP kinase-kinase-kinase)
Characteristics of gap junctions
direct between cells, connexons, pass electrical current, ATP and second messengers, fast, bidirectional
Characteristics of chemical synapse
slow, unidirectional, action potential + neurotransmitter release
Job of synapsin
binds vesicles together as they more from endosome toward cell membrane
Job of SNARE complex
composed of synatobrevin, syntaxin and SNAP-25 - anchors vesicle to cell membrane
Job of synaptotagmin
when Ca2+ enters the cell, it binds to synaptotagmin and causes the vesicle membrane to fuse with the cell membrane
Job of clathrin
vesicles that are formed by membrane invagination are coated with clathrin and sent back to the endosome
5 criteria to classify a neurotransmitter
persent in the nerve terminal, released by electrical stimulation of neuron, specific receptors exist, direct application of substance mimics neuronal stimulation, there is a mechanism for terminating the action
Otto Loewi experiment
heart solution
time constant =
(resistance)(capacitance)
size of time constant
small = fast, large = slow
nernst equation
Ex = 26.73 ln [K+ out] / [K+in]
Nernst potential for Na?
67
Nernst potential for K?
-98
Nernst potential for Cl-?
-90
Driving force = ?
Em - Ex (x=ion)
time constant again =
(membrane resistance) x (membrane capacitance)
How is the sign of a post synaptic potential determined?
positive ion flowing in = positive, negative ion flowing in or positive ion flowing out = negative
Absolute refractory period?
time from beginning of depolarization to return to polarized (everything before relative refractory period)
Relative refractory period?
sodium channels begin to reactivate - NaKATPase brings back to resting potential
Length constant?
(membrane resistance) / (cytoplasmic resistance)
size of length constant?
small = fast, large = slow
Increased axon diameter?
increased velocity
Increased myelination?
increased velocity
Isotonic contraction
muscle contraction under a load (apply load, measure velocity of shortening muscle, repeat)
Isometric contraction
muscle does not change length (set muscle length, measure force, set new length, measure new force, repeat)
total tension = ?
passive tension + active tension
lengthening contraction
muscle length is increased while the muscle is contracting (quadriceps while going down stairs)
Torque = ?
force x distance
define tetanus
frequency summation
purpose of t-tubules?
propagate action potential into muscle
haplotype
snps that are close together (over 10 million have been identified)
hemizygous
used to describe males with a mutation in x chromosome (or females with loss of one x chromosomal locus)
heterogeneity
when a phenotype is caused by multiple alleles or loci
uniparental disomy
when an individual receives two copies of a chromosome from one parent and none from the other
autosomal recessive pedigree pattern
75:25 phenotype
autosomal dominant pedigree pattern
50:50 inheritance pattern (from heterozygous parent)
x linked pedigree pattern
absence of father-son inheritances - all daughters of affected male are carriers
mitochondrial inheritance
maternal inheritance - affects all children from affected mother - mitochondrial functions affected only
equations for gene frequency
p = frequency of allele A, q = frequency of allele a, p+q=1, p^2 + 2pq + q^2 = 1, p^2 = AA frequency, 2pq = Aa frequency, p^2 = aa frequency
isochromosome
formed when the centromere divides horizontally rather than vertically
polyploidy vs aneuploidy
polyploid = multiple copies of ALL chromosomes, aneuploid = multiple copies of a particular chromosome
robertsonian translocation
when the long arms of two acrocentric chromosomes join together
philadelphia chromosome
t(9;22)(q34;q11)
types of down syndrome
47,XX,+21 46,XX,rob(14;21)(q10;q10),+21 Mosaic 21q211 and partial
trisomy 18
edwards syndrome, clenched hands, crossed legs, feet with rounded bottom, interferes with normal development
trisomy 13
patau syndrome, cleft lip, clenched hands, close set eyes, severe mental retardation
cri du chat syndrome
deletion of part of chromosome 5, high pitched cry like a cat, downward slanted eyes, low birth weight
22q11.2 deletion syndrome
DiGeorge syndrome - thymic hypoplasia with diminished T-cell immunity and parathyroid hypoplasia with hypocalcemia
Klinefelter syndrome
XXY, male hypogonadism, large breasts, cells have barr body = results from random x inactivation
47, XYY syndrome
no major physical abnormalities, possible slow learning/speech development
Turner syndrome
45XO, hypogonadism in females, some are mosaic
Trisomy X
XXX, x inactivation in females will cause most to be asymptomatic
Multifactorial disorder
genes + environment + other factors
concordance
rate of both twins showing a particular phenotype
heritability
(variance in DZ - Variance in MZ) / (Variance in DZ)
Causes of congenitial abnormalities
50% = complex inheritance, 25% = chromosomal imbalance, 20% = single-gene mutation, 5% = environmental teratogen
Noninvasive prenatal testing
prenatal risk assessment screening, obstetrical ultrasonography
Invasive prenatal testing
amniocentesis, chroionic villus sampling
genetic intervention strategies
gene transfer, siRNA, mutant protein trapping, protein/enzyme replacement
southern blot
DNA - hybridized with probes
northern blot
RNA
western blot
protein
Blot Acronym
SNoW DRoP
Marfan Syndrome
basic defect in connective tissue. All symptoms stem from mutation in fibrillin, defect in fibrillin 1, dominant trait
Ehlers-Danlos syndrome
extremely loose joints, hyperelastic skin, easy bruising, defect in collagen synthesis, dominant
Familial Hypercholesterolemia
high cholesterol levels, mutations of LDL receptor gene, heterozygous - respons to therapy, homozygous - needs other treatments
Phenylketonuria
missing phenylalanine hydroxylase, autosomal recessive, chromosome 12
cystic fibrosis
mutatin in CFTR, recessive, chromosome 7
Neurofibromatosis
excessive production of neural crest cells - leads to melanocytes, autosomal dominant
sickle cell disease
autosomal recessive, chromosome 11
changes in reversible cell injury
cell swelling, vacuole formation, decreased function of NaKATPase, fatty change, blebbing, swelling of mitochondria, clumping of chromatin, dilation of ER, increased pallor, increased turgor, increased weight
changes in irreversible injury
mitochondrial damage, severe membrane damage, massive calcium influx, pyknosis, karyorrhexis, karyolysis, rupture of lysosomes
ATP depletion causes:
Na-K pump failure, Na-Ca pump failure, cell swelling
Loss of calcium homeostasis causes:
massive calcium influx
What are the reactive oxygen species?
hydrogen peroxide, superoxide anion, hydroxyl radicals
enzymes that remove ROS
superoxide dismutase, glutathione peroxidase and catalase
coagulative necrosis
denaturation of cellular proteins. Tissue appears as solid mass, ghosted cell outline. Firm texture. Affects solid organs: heart, intestine, kidney, liver. Characteristic of ischemic injury
liquifactive necrosis
tissue digestion by phagocytes and hydrolytic enzymes. In the CNS, infarction results in liquifactive necrosis. Cavity filled with clear watery fluid. Hypoxic cell death of brain cell.
Dry gangrenous necrosis
widespread coagulative necrosis with NO infection
Wet gangrenous necrosis
widespread coagulative necrosis WITH infection
Caseous necrosis
combination of coagulative and liquifactive necrosis. Found in tuberculosis infection and fungal infection. Associated with granuloma formation - tissue architecture is COMPLETELY destroyed
fatty necrosis
typically occurs as a result of a release of pancreatic lipase - when mixed with calcium, it causes fat saponification
fibrinoid
occurs in the blood vessel, associated with immunological injury
what happens during apoptosis?
protein cleavage by Caspases, genetic activation, only affects single cells, no inflammatory response
what does bcl-2 do?
inhibits apoptosis
what does p52 do?
stimulates apoptosis
Pyknosis, karyorrhexis, karyolysis
darkening, fragmentation, disappearance
hyperplasia
increase in the number of cells - increased rate of division
metaplasia
reversible replacement of one mature cell by another mature cell type which is better able to tolerate the stress
dysplasia
not a true adaptive change - abnormal proliferation characterized by changeds in size, shape and organization of cells - not cancer, but may progress to cancer
vessel proteins involved in rolling
e-selectin, p-selectin
vessel proteins involved in tight binding
ICAM-1
vessel proteins involved in diapedesis
PECAM-1
vessel proteins involved in migration
bacterial products, C5a, IL-8, LTB4
transudate
hypocellular, protein poor
exudate
cellular and protein ritch
labile cell
multiply constantly throughout life - epithelial cells
stable cell
only multiply when receiving external stimulus - muscle cells
permanent cell
do not have the ability to multiply - RBCs
function of IL-1 and TNF
mediate fever
left shift
leukocytosis - 15,000-20,000 cells/ml
highESR
increased erythrocyte sedimentation rate
oxygen independent killing
release of lysosomal hydrolases
granuloma
central area of macrophages, epitheloid cells and multinucleated cells - surrouned by lymphocytes and plasmal cells - outer rim = fibroblasts and connective tissue, very center can have caseous necrosis
leukocyte adhesion deficiency
nonfunctioning CD18 - unable to extravasate
myeloperoxidase deficiency
lack myeloperoxidase (still have NADPH oxidase) = poor respiratory burst
chronic granulomatous disease
certain cells have difficulty forming ROS. Extremely defective respiratory burst
macrophage activation
differentiation of monocytes - express CD14 and CD11b
innate immune system
epithelial barriers, phagocytes, complement, NK cells (non-specific, non memory, fast, constant)
adaptive immune system
B-lymphocytes, antibodies, T-lymphocytes, effector T-cells (highly specific, has memory, slow, improves)
primary lymphoid organs
bone marrow and thymus
secondary lymphoid organs
spleen and lymph nodes
good antigens
large proteins (protein>carb>>>>lipid) (large>small)
how phagocytes kill pathogens
complement activation - CR1 on macrophage binds C3b on bacterium, endocytosis, phagolysosome formation
C3a and C5a
potent anaphylotoxins, allow proteins to extravasate, allows migration of monocytes and neutrophils from blood into tissue
THF-a
activates vascular endothelium and increases vascular permeability. Fever, mobilization of metabolites, shock (secreted locally or systemically)
IL-1beta
activates vascular endothelium, activates lymphocytes, local tissue destruction increases access of effector cells, fever, production of IL-6
IL-1, IL-6, TNF-a effect on Liver
acute phase protein release, mannose-binding lectin release, starts complement and opsonization
IL-1, IL-6, TNF-a effect on Bone marrow
neutrophil mobilization - phagocytosis
IL-1, IL-6, TNF-a effect on hypothalamus
increased body temperature, leads to decreased viral and bacterial replication
IL-1, IL-6, TNF-a effect on fat/muscle
protein and energy mobilization to generate increased body temp - decreased viral and bacterial replication
Acute phase proteins
c-reactive protein, fibrinogen, MBL, alpha1-antitrypsin, serum amyloid A
C-reactive protein
can activate the classical C' pathway (C4 -> C4a + C4b)
Type I interferons
inhibit viral replication and activate host-defense responses - induce resistance to viral replicaiton, increase expression of ligands for receptors on NK cells, activate NK cells to kill virus-infected cells
MHC molecule
present antigen after it has been processed - control T cell mediated immune responses - MHC class I binds to CD8 and TcR, MHC class II binds to CD4 and TcR
CD8 T cell
when it comes in contact with a virus infected cell that is expressing viral protein in its MHC, it will trigger death of tha tcell
CD4 T cell (Th1)
when it comes in contact with a macrophage that is presenting bacterial protein, it secretes cytokines and activates the macrophage. The activated macrophage secretes more cytokines and begins digesting its phagosomes.
CD4 T cell (Th2)
when it comes in contact with a B-cell expressing protein, it releases cytokines that activate the B cell into a plasma cell. The B cell releases its antibodies
Regulatory T cell
maintain tolerance to self-antigens and down-regulate autoimmune disease
FcR
cell surface receptors for the Fc regions of antibodies - found on phagocytes, APCs, mast cells and eosinophils - CRUCIAL for antibody mediated opsonization
Avidity
over strength of the combined binding sites (2x for IgG, 10x for IgM)
VDJ recombinase
catalyzes recombination of gene segments in B cells
Affinity maturation
affinity of antibodies for antigen increases with prolonged or repeated exposure to that antigen (occurs in germinal centers, B cells with the highest affinity have a selective advantage, only the best antibodies are produced)
4 processes for antibody diversity
multiple VDJ gene segments, multiple heavy and light chains, junctional diversity, somatic hypermutation
how many possible combinations are there for antibodies?
10^14
features of IgG
crosses placenta, neutralization
features of IgM
activation of complement
features of IgA
found in body secretions
features of IgE
sensitization of mast cells
complement fixation
when C3b is bound in conjunction with antibodies
Live attenuated vaccines
smallpox, measles, mumps, rubella
Killed (whole organism) vaccines
influenza, polio, rabies
Subunit or recombinant vaccines
Hep. A and b, H. influenza type b and S. pneumonia
Toxoid vaccine
tetanus, pertussis, diptheria
passive immunization
no new response, immediate protection, no memory, temporary, OCCURS NATURALLY WITH MATERNAL ANTIBODIES
active immunization
new immune response, delayed protection, memory, occurs naturally with infection
benign tumor
generally slow growing, remain localized, do not recur, do not become malignant
malignant neoplasms
anaplastic, rapidly growing, invasive, metastatic
how to name a benign tumor
add -oma at the end
how to name malignant tumor of epithelium
add -carcinoma
how to name malignant tumors of mesenchymal origin
add - sarcoma at the end
adenoma
benign tumor of glandular epithelium
polyploidy vs aneuploidy
any growth that projects out from the surface of a mucosal epithelium
papilloma
benign microscopic finger-like projections growing on any surface
sarcoma
malignant tumor of connective tissue
carcinoma
malignant tumor of the epithelial tissue
teratoma
arise from gem cell layer - can differentiate into many forms
choristoma
normal tissue, but present in an abnormal area
hamartoma
normal tissue in the right area, but in abnormal quantity or arrangement
pleomorphism
variability in size and shape of cells
seeding
invasion of the body cavity - typical of ovarian cancer
blood spread
veins are mostly penetrated, liver and lung are the common destinations, renal cell carcinoma, hepatocellular carcinoma
lymphatic spread
more typical of carcinoma, follow lymphatic drainage, lung cancer to bronchial lymph node, breast cancer to axillary lymph node,
sentinal node
first node in the line of drainage
tumor invasion of ECM
detachment (loss of e-cadherin function), ECM degradation by proteases (MMPs, cathepsin D, uPA), attachment to novel EcM components, migration
xeroderma pigmentosa
hyperpigmented skin lesion - autosomal recessive
oncogenes
cause cancer when activated
tumor suppressor genes
cause cancer when suppressed
cachexia
loss of body fat/lean body mass, weakness, anemia, anorexia - caused by cytokines produced by tumor cells (TNF-a, IFN-gamma, IL-6) or by proteolysis inducing factor
paraneoplastic syndrome
a disease or symptom that is the consequence of cancer but is not caused by the presence of cancer cells
staging of cancer
used to evaluate the extent and the spread of the tumor - clinical, radiological or surgical examination - better than grading in clinically evaluating the tumor - based on size, extent of spread to LN and presence of metastasis, 0-IV
grading of cancer
measure of how aggressive the tumors is - cytological examination - based on differention and number of mitosis, I-IV (higher - poorly differentiated, low = well differentiated)
cytologic diagnosis
used for cancer of the cervix, uterus, lung, bladder, prostate and stomach
fine needle aspiration
used in palpable lesions - breast, thyroid, lymph nodes
immunohistochemistry
confirms the tissue of origin of metastatic or poorly differentiated tumor - uses monoclonal antibodies
PSA
marker for prostate cancer
CEA
marker for GI cancer
a-feto protein
marker for hepatoceullular carcinoma
Erb-2/HER2/Neu
receptor tyrosine kinase, inhibits apoptosis, gene amplificaiton of ErbB-2/HER2/Neu is found in breast cancer
Bcr-Abl
oncogene encoded on the philadelphia chromosome t(9;22), found in chronic myeloid leukemia, potent tyrosine kinase activity
Bcl-2
found in B-cell lymphoma, govern apoptosis (mitochondrial outer membrane permeability), caspase activity is no longer inhibited
Rb
retinoblastoma gene - deletions or mutations lead to retinoblastoma - eye cancer - cell cycle (G1-S) is no longer controlled
p53
endoes a transcription factor, mediates cell cycle, DNA repair, cell death, mutations or inactivations of p53 are found in 50% of all human cancers, p53 is a major suppressor that guards genome integrity
Wnt/B-catenin
wnt secretion results in the inactivation of APC, stabilization of b-catenin levels, transcription, and ultimately in "familial adenomatous polyposis)
HPV oncogenes
E6 - binds to and promotes degradation of p53 tumor suppressor. E7 binds to and inactivates Rb tumor suppressor