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177 Cards in this Set

  • Front
  • Back
what does neoplasia result from?
hereditable genetic alterations that are passed down to progeny of the tumor cells. genetic changes allow excessive and unregulatd proliferation that becomes autonomous (indepenent) of physiologic growth stimuli
what is a synonym for neoplasia?
what does clonal mean?
entire population of neoplasm arises from a single cell that has incurred genetic change
why have absolute numbers of malignancies incrased?
b/c of an aging population
def of cancer?
all malignant neoplasms
def of malignant?
tend to become progressively worse and ending in death
**potential to metastasize and kill patient
size of malignant vs benign?
malignant: gross-big
micro- always bigger/huge
benign: gross-small
micro-cells normal to mild increase
symmetry of malignant vs benign?
malignant: asymmetric*
benign: symmetric
margins of malignant vs benign?
malignant: indistinct, infiltrative*
benign: circumscirbed
necrosis of of malignant vs benign?
malignant: common*
benign: uncommon
age of onset of malignant vs benign?
malignant: old**
benign: young
ex of benign tumor that is small, symmetrical and circumscribed?
fibroadenoma of breast
pushing margin =
benign and malignant neoplasm nomenclature for mesenchyme origin
benign: lipoma
m: liposarcoma
benign and malignant neoplasm nomenclature for endothelial origin?
b: hemangioma
m: angiosarcoma
benign and malignant neoplasm nomenclature for lymphocyte origin?
m: lymphoma
benign and malignant neoplasm nomenclature for muscle origin
b: leiomyoma
m: leiomyosarcoma
benign and malignant neoplasm nomenclature for squamous epithelial origin
b: papilloma
m: carcinoma
benign and malignant neoplasm nomenclature for glandular epithelial origin
b: adenoma
m: adenocarcinoma
benign and malignant neoplasm nomenclature for melanocyte origin
b: nevus
m: melanoma
what is a papilloma?
benign squamous epithelial neoplasm that has fingerlike projections
what is a teratoma?
a teratoma is a tumor with tissue or organ components resembling normal derivatives of all three germ layers. Rarely, not all three germ layers are identifiable.
benign=mature teratoma
malingnat=immature teratoma
what are the 2 basic types of cellular components w/n neoplasms? (both benign and malignant?
parenchyma: proliferating neoplastic cellular component
stroma: supportive non-neoplastic cellular component that consists of CT and blood vessels
what is desmoplasia?
incrsaed fibrous tissue stimulated by neoplasm
what is angiogenesis?
increased blood vssls stimulated by neoplasm
what type of tumor is this describing:tumor is infiltrating the surrounding breast substance
assymetrical, retracts the adjacent fat, stony hard on palpation (scirrous)
invasive malignant
what is grade of neoplasm? how do benign grade?
degree of differentiation
benign=well differentiatied and are not graded
what does well differentiated mean? moderatley ifferentiated?
closely resemebles the parent tissue
moderately: features of original present but not the dominant pattern or appearance
what does term poorly differentiated mean? undifferentiated?
poorly differentiated: small minority of cellular components allow identification of the parent tissue
undifferentiated: tissue of origin cannot be determined
how will well differentiated SCC of skin appear?
tumor cells are similar to normal squamous epi cells
have intercellular bridges
nests of keratin pearls
what are 2 overall cellular (cytologic) features of neoplastic cells?
pleomorphism: variability in size and appearance
presence of distinctive cells as markers of malignancy such as Reed-Sternberg cell in Hodgkin disease and "orphan annie" nucleus in papillary carcinoma thryroid
the Reed-Sternberg cell is a distinctive cell used ad marker for what disesae?
hodgkin disease
what are the 4 nuclear features of neoplastic cells?
1. enlarged size: 2-5x normal
2. mitotic rate and atypical mitotic features
3. pleomorphism
4. hyperchromaticity: incrase in DNA content per nucleus
what is dysplasia?
cytologic changes in neoplastic cells indicative of "pre-malignant" change, but all cells are not involved
consists of an increased population of immature (basal-like) cells which are restricted to the mucosal surface, and have not invaded through the basement membrane to the deeper soft tissues
what do the borders of neoplasm tell us?
pushing or circumscribed = benign
infiltrative or invasive = malignant
what is this describing: represents the transformation of a neoplastic lesion to one in which cells undergo essentially no maturation, and thus may be considered cancer-like. In this state, cells have lost their tissue identity and have reverted back to a primitive cell form that grows rapidly and without regulation. However, this form of cancer remains localized, and has not invaded into tissues below the surface.
carcinoma in situ: failure of normal differentiation, marker nuclearand cellular pleomorphism and numerous mitotic figures extending toward the surface
what type of tumors grow as a cohesive, expansile mass that remains localized to tissue of origin
benign tumor
what type of tumors expand by infiltration and destrxn of adjacent tissue
malignant tumor
*are invasive NOT cohesive b/c they detach from one another
compare benign and malignant tumors in terms of cohesivness?
malignat: not cohesive, invasive
benign: cohesive
why does metastasis mark as tumor as malignant?
b/c benign tumors DO NOT metastasize
which metastatic spread is the primary and most impt spread for carcinomas?
lymphatic spread
(hematogenous spread is major route for malignant tumors that are lethal)
which metastatic spread is used to stage cancer?
lymphatic spread
what is the major route for malignant tumors that are lethal?
hematogenous spread
what are the 3 pathways of spread?
seeding of body cavities and surfaces ex: lung cancer, ovarian carcinoma
lymphatic spread
hematogenous spread ex: breast cancer, renal cell carcinoma
liver metastisis is mostly from what origin?
from colon b/c it sends blood to liver to filter
>80% of liver involved before symptomatic
population for benign tumors? malignant?
benign: younger
malignant: older >30
why is screening unselected populations a failure?
if screen everyone, get more FP less TP ex: PSA for prostate, X ray for lung cancer
this is more expensive
need to screen those that have an increased prevlance based on epidemiology
what is prevalance?
overal # of cases in a defined population at a certain time (2003)
*new and pre-existing cases in contrast to incidence which is new cases during a given time period
is incidence of lung cancer more common, staying the same or decreasing?
decline in black and white male
incresae in black and white female but plateau
what is expected of the mean age in 2030?
higher mean age because decrease young ppl and increase older population
why is lung cancer have higher incidence in men?
b/c they had a higher rate of smoking
what is the incidence trend in lung cancer?
decline in men
what is the peak age of onset of lung cancer?
disease of older ppl
peaks 75-79
highest in black male
what is mortality?
death rate
# of deaths caused by a type of malignancy during a specified time/ unit population
in gall bladder adenocarcinoma, what is the incidence analogous to?
mortality b/c very fatal
what race/gender has the highest incidence and mortality of lung cancer?
black males
what is the most impt variable in malignancy?
malignancy is a problem in older ppl:all cancers peak at age 70-79
what are the 2 most prevalant cancers in males?
colon/ rectum
what are the 2 most prevalant cancers in females?
lung and bronchus*
lung cancer is #1 killer
what is the peak age of Hodgkin Lymphoma?
peak age 30 then 2nd peak age 65+
what is the age of onset for Non-Hodgkin Lymphoma?
older ppl: 75-79
as opposed to Hodgkin whcih peaks at 30 and 65
what is the peak age of testis cancer?
age 35-59 mostly in white males then American Indian/Alaska Native
sharp increase in late adolescence
what ethnicity is most affected by testis cancer?
white males
then American Indian/Alaska native
do men or women have more malignancies?
what are the female (4) and male (2) specific malignancies?
female: uterine cervix, uterine corpus, ovary, breast
male: testis, prostate
in 1990, what cancer peaked in men and what cancer progressively declined?
peaked: lung b/c cigarretes designed to let smoke particles be smaller so they burn longer thus they get past mucociliary escalator and reach alveoli
Stomach cancer went away b/c of better hygeine and less helicobactor pylori ifxns
which cancer has progressively increased in womean from 1950-2000? which has decreased and why?
lung cancer
prior to 1950 it was unacceptable for women to smoke
uterine cancer has decline b/c more hysterectomies were performed
malignant melanoma is most often in what ethnicity?
caucasians: both male and female (male highest)
less likely to see skin melanoma in blacks
multiple myeloma is most often in waht ethnicity?
A. Americans
B cell lymphomas more common in blacks and mostly in older ppl
what geographic location is bladder cancer and Schistosomiasis more common?
where is gastric carcinoma more common? what causes it?
**90% due to helicobactor pylori
we are now better at tx it so it is declining
as the japanese migrate to California, see less incidence of gastric carcinoma in those japanese
what percent of individuals have an inherited mutation that predisposes to the development of a malignant neoplasm? if they do, what age does it present?
less than 10% (more like 5%)
occur at younger age**
inheritedd predisposition for mutated Rb?
inherited predispostiion for mutated APC?
familial adenomatous polyposis/colon cancer
what environmental factor is the most common cause of malignancies?
chronic mid-UV radiation that causes SCC and BCC
what 2 environmental factors lead to developement of Hepatocellular carcinoma?
ethanol dependence + cirrhosis
(need cirrhosis to be present)
what does Helicobactor pylorii cause?
lymphoma and gastric carcinoma
99% of carcinoma of uterine cervix is caused by what?
HPV subtypes 16,18
how is a tumor formed?
by the clonal expansion of a single precursor cell that has incurred genetic damage
what enzyme is coded on the X chromosme? what are the different forms of this enzyme?
maternal X(XA) codes G6PD isoenzyme A
paternal X(Xa) codes G6PD isoenzyme B
when neoplasms arise in women who are heterozygous for X linked markers such as G6PD, what enzyme will the neoplastic cells contain?
contain only one G6PD isoenzyme-single precursor cell
AKA: monoclonal neoplasm
all individual neoplasmas arise from what?
one genetically altered cell (clonality)
what is the field effect?
numerous cells in a particular tissue will each have individual genetic alterations
waht is synchrnous neooplasma?
more than one cell may undergo a final genetic change into a cancer clone at roughly the same time in approx the same location
what type of tumors usually show field effect with multiple synchronous neoplasmas?
malignant tumors of urniary bladder
what are the 4 principal targets of genetic damage?
1. growth promoting protooncogenes
2. growth inhibiting TSG
3. apoptosis regulating genes
4. DNA repair genes
what fundamental change in neoplasia makes a malignant phenotype?
ability to invade and metastasize
what cell types are susceptible to genetic alteration and developemnt of progeny that propogate the altered genetic material?
rapidly turning over cell populations that continually enter G1 phase
G0 nonproliferating such as CNS and cardiac myocytes DO NOT become malignant
what are cellular oncogenes (c-onc)?
transformed protooncogenes that are involved in tumor development
what is the most common oncogene?
what isthe problem when Ras is mutated?
acts as oncogene that permanenly activates transcription leading to constant cell growth
how does Chronic Myelogenous Leukemia arise?
translocation of chrom 9 to 22
get abl-bcr hybrid gene that leads to chronic incrase in tyrosine kinase activity which is impt in cell proliferation
(c-abl is oncogene_
what does C-myc do? what about c-myc?
C-myc: gene responsible for protein Myc that simulates nuclear dNA transcription
c-myc: oncogene in Burkitt Lymphoma that leads to chronic incresae in Myc protein
what happens when you have a mutation in TSG?
lose the break that normally regulates cell growth
with mutation tumor is not suppressed and leads to proliferation (less controlled cellular prolif)
what isthe most common TSG? what is it a marker for?
APC present in colon adenocarcinomas
*marker for development of colon adenocarcinoma
what is the role of APC?
regulates stability of Beta catenin to bind and prevent beta catenin from entering nucleus
when mutated it can't block beta catenin, therefore it enters the nucleus and turns on several genes in the cell cycle
50% of human tumors contain mutations in what gene?
p53 the guardian of the genome
what is required for transformation into a continously replicating clone?
many combinations of oncogenes: no single oncogene can cause transformation into a contniously replicating clone *require multiple genetic alterations
waht are the 2 type of gatekeeper genes that affect tumor growth?
oncogenes that acclerate cell proliferation
TSG that inhibit or "brake" cell proliferation
the development of malignant neoplasma requires waht?
years, sometimes decades
what is the adenom-adenocarcinoma sequence?
normal epithelium
then loss or mutation of APC at 5q (first hit)
early adenoma
second hit: loss of normal copy of the APC (other allele)
late adenoma: increse # polyps = incresae risk
loss of p53
*accumulation of mutations
what is a marker for the adenoma-adenocarcinoma seq?
when the muscularis mucosa has been crossed
normally acts as a BM surrogate therefore if polyps invade muscularis mucosa there is an incresed risk of carcinoma
why do an increase # of polyps indicate incrsaed risk of carcinoma?
b/c polyps grow upward b/c no barrier exists
as grow up, pull adjacent tissue w/ it
lose cohesiveness and infiltrate subjacent tissue
waht is the dysplasia-carcinoma seq?
transition from normal squamous epi through a series of transitional morphologic states to invaseive squamous cell carcinoma
**only applies to epithelial cancers*
where does dysplasia-carcinoma seq occur?
uterine cervix, vulva, oral cavity, skin
in skin, dysplasia = actinic keratosis
completion of the progression from normal to invasive carcinoma in the dysplasia-carcinoma seq takes at minumum how long?
10 years
the dysplasia-carcinoma seq serves as the basis for what?
pap smear
detection of early "premalignant" changes before lesion is far advanced
what are the abnormal characteristics associated with dysplasia?
incraesed proliferation at greater rate
mititotic cells above BM
atypical mitotic cells
big cells
what do OB/GYNs refert to dysplasia-carcinoma as?
Cervical Intraepithelial Neoplasia (CIN)
in dysplasia, instead of cells filling with keratin, how do they appear?
darker b/c more nuclie and tighly packed
nuclei larger
I: low grade dysplasia
III: Carcinoma in situ
CIN normally occurs due to?
multiple sex partners at early age
occurs b/c HPV
what does CIN III look like?
carcinoma in situ
full thickness
hyperchromatic: increase blue b/c incrase nuclei
when does CIN I-III peak?
early 20's then 25 years later early 50's
why is the 2nd round of chemo no as effective as the 1st?
b/c a growing tumor is enriched with clones that "beat the odds-survival of the fittest" therefore they are the cells that will regrow after the 1st round of chemo no chemo won't work
what are promoters?
can induce tumors in initiated cells (exposed to carcinogens) but are NOT tumorigenic by themselves
DO NOT affect DNA directly
ex: hormones or alcohol
do promotors or initiators introduce permanent DNA damage?
promotors are NOT tumorigenic by themselves
what are the 2 categories of initiators?
1. direct acting: do not require chemical transformation
2. indirect acting: Procarcinogen: require metabolic conversion
what is the molecular target of initiator chemical carcinogens?
DNA is primary target
*if doesn't target DNA won't causes cancer
ex of endogenous promotors? exogenous?
endo: hormones like estrogen in breast cancer, androgens in prostate cancer
exo: ethanol in esophageal and laryngeal carcinoma
what UV region is impt agent in development of malignancies in skin?
UVB b/c causes formation of pyrimidine dimers that damage DNA
waht is the most common carcinogen that affects humans?
UVB: actinic keratosis, SCC, BCC
who has a 2,000x increased incidence of all types of skin cancer in sun exposed areas of skin?
waht are 3 major carcinogens after UVB that involve oncogenic DNA?
Hep B and C
waht are the 2 impt oncogenic HPV subtypes? what is unique about HPV growth?
16 and 18
wont grow on tissue culture therefore use PCR
HPV ongogenic subtypes are now causitive agents in waht?
SCC of uterine cervix
Adenocarcinoma of uterine cervix
the rapidly dividing cells of malignant neoplasms have markedly increased demand for what?
oxygen and other nutrients
malignant neoplasma cannot enlarge beyond ___ millimeters until they stimulate _____
1-2 millimeters
stimulate neovascularization-angiogenesis
to effect local tissue, tumors must have what/ big and solid
ex: carcinomas and sarcomas
leukemias circulate in blood tehrefore don't have solid mass
why do tumors stimulate a capsule?
to stimulate injury in adjacent tissue by fibrosis
acts as a perimeter
ex of tumor distortion of adjacent structures?
tumor displaces and disrupts normal tissue such as in obstruction of bile duct by tumor in head of pancreas causeing jaundice
what are the steps in invasion of ECM
1. tumor cells first disassociate as individual cells or small cell aggregates
2. these cells then migrate or infitrate through the ECM
what are the 2 basic barriers for epithelial malignancies?
1. BM
2. Interstitial CT
steps in invasion of BM?
1. loosening of intercellular jxns: dissolve desmosomes
2. tumor cell attaches to ingrins and laminin Rs
3. secrete proteolytic enzymes including Type IV collagenase and plasminogen activator
4. migration thru BM now termed invasive carcinoma
grade =
stage =
grade = penetration
stage = size
what does metastasis indicate?
original malignant tumor has moved as individual cells or cellular aggregates to a body site distant or separate from the original location
what are the 4 diff mechxns of maligancies?
1. nonmetastatic primary tumor has mets variants
2. mets caused by gene expression of primary tumor = mets signature ex: small cell carcinoma of lung
3. mets variants appear in tumor with a mets gene signature (combo 1 and 2)
4. stromal response allows primary tumor to become mets
what body caviites, spaces and channels do we see malignant spread?
1. pleural, peritoneal, and pericardial cavities ex: ovarian carcinoma
2. subarachnoid space and CSF
3. ureters
4. medullary cavity of long bones ex: epiphyses cause osteosarcoma
5. Nerve sheaths -prostatic adenocarcinoma
**these sits have no barriers therfore great site of mets
lymphatic dissemination of maligancy is associated with what type of cancers? hematogenous?
lymphatic: carcinomas and adenocarcinomas
hematogenous: sarcomas
**but, most fatal carcinomas have both lymphatic and hematogenous spread and it is the hematogenous route that kills you
what is cancer cachexia?
muscle wasting
progressive loss of body fat and lean body mass
wt loss of 50-100lbs
tumors consume many calories
what type of malignant tumor effect is not the result of mets or hormones INTRINSIC to tissue?
paraneoplastic syndromes
cannot be accounted for by local tumor effects or distant spread of tumor or hormone production intrinsic to cell of origin
ex: hypercalcemia in SCC of lung
what is the interval of time b/n mild dysplasia to cancer in pap smear results?
17 year interval thus if found "early" decrease deaths
what are the most impt factors in predicting biologic behavior of malignant tumors?
specific histiopathological type (identity)
what are the 5 measures or indicators used to predict biologic behavior and clinical outcome of malignancy/
in this order of importance
1. specific type of malignancy and location
2. stage (size, spread)-differnt for diff classes of tumors: TNM for cacinomas and adenocarcinomas
3. grade (differentiation)
4. pt factors (age, health, concurrent disease)
5. Tx efficacy
what is the central requirment for all autoimmune diseases?
have to have stimulated CD4 T cell
what is the normal situation for immune complexes?
they are formed every time antibody meets antigen
normally they are effectivly removed in liver and spleen
what happens when immune complexes are not properly removed from the circulation?
they trigger large increases in vascular permeability
what is happening in EBV?
th virus induces polyclonal B cell proliferation and antibodies to viral protein are produced which cross react w/ ribonuclear proteins
how doe IC activate dendritic cells and macrophages?
by binding to FcgammaR's causing these cells to upregulate CD40 and CD80/86
what are the pro-inflammatory cytokines?
TNF-alpha, IL-1, IL-6
what is the most impt trigger for tissue depositiong of immune complexes? where does it most likely occur?
increase in vascular permeability cuased by inflamm cytokines and mediators released by mast cells
occur where there is high BP
what are the 3 autoimmune diseases caused by continously produced large quantities of immune complexes?
Sjogren's syndrome
onset of SLE?
acute, insidous
gender and age associated with SLE?
more severe in Afican Amercian womean
clinical manifestatations of SLE are due to?
trapping of IC in capillaries of visceral structures or to antibody mediated destrxn of host cells
what is epitope spreading?
imune system starts to react tho things it didn't react to originally
criteria for SLe?
malar rash
discoid rash
oral ulcers
renal disorder
neurologic disorder
hematologic disorder
immunologic disorder
ANA Ab: Anti ds DNA, anti Sm
any 4/11 must be present
common environment trigger involved in SLE?
UV light
what is a key event in the pathogenesis of SLE?
Fcgamma R-mediated delivery of nucleic acid containing IC's to TLR-7and 9 in plasmacytoid dendritic cells, which causes copious secretion of IFN-alpha
what complement proteins are deficient in SLE?
C2 and C4 therefore can't do classical or alternative pathways
what Ab are highly antibodies are highly specific for SLE
anti-dsDNA and anti-Smith
what does an immunofluorscent stain of SLE show?
deposition of IgG and C along dermo-epidermal jxn
what is the more appropriate name for scleroderma?
systemic sclerosis
what is happening in scleroderma?
abnormal accumulation of fibrous tissue in the skin and multiple organs
turn on fibroblasts in abnormal way
how doe diffuse and limited scleroderma differ?
diffuse: extensive skin involvment
limited: limited skin involvment
diffus: anti-scl70Ab
limited: anti-centromere Ab
what impairs the normal organ fxn in scleroderma with death resulting from renal faiure, resp failure, cardiac?
macrophages stimulating fibroblasts to deposit abnormally high amts of collagen
S/s of scleroderma?
shortened frenulum; difficulty swallowing
topoisomerase I is associated with what form of scleroderma?
what does crest stand for?
Raynaud's phenomen
Esophageal dysmobility
Telangiectasias "spider vein"
claw hand deformity is Dx of what?
scleroderma: extensive subcutaenous fibrosis has virtually immobilized the fingers, creating a claw like flexion deformity
what are 3 symptoms of importance in Sjogren's syndrome?
Keratoconjunctivits: inadequate tear prodxn caused by lymphocyte and plama cell infiltrationg of lacrimal glands
Xerostomia: difficulty swallowing
Parotid gland enlargement: stuffed w/ plasma cells
clinical finding of woman with Sjogren's?
dry eyes
dry mouth
Rh factor
incrasing risk of lymphoma
what are the Ab markers for Sjogrens'?
Ab SS-A: Anti-Ro, specific for RNP's
Ab SS-B: Anti-La, specific for RNP's
what is the difference b/n primary and secondary Sjogren's
primary: only have Sjogrens
secondary: also have SLE, Scleroderma
in which Ct disease do we see lymphoma development?
b/c abnormal B cell production and activation
serology of Sjogrens?
anti ro- SS-a
anti la- SS-B
Rheumatoid factors
enlargement of salivary gland ?