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Neoplasia (CLINICAL CHARACHTERESTICS (SCREENING (common screening methods,…
Neoplasia
CLINICAL CHARACHTERESTICS
HISTOLOGIC
benign
organized growth
uniform nuclei
low nuclear to cytoplasm ratio
minimal mitotic activity
lack of invasion
malignant
unorganized growth
pleomorphic nucleus
high nucleus to cytoplasm ratio
high mitotic activity
invasiveness
Immunochemical methods are used to characterize tumors
SERUM TUMOR MARKERS
screening
monitor treatment and recurrence
GRADING
low grade
resembles normal tissue
well diffrentiated cancer
high grade
pooly differentiated
doesn't resemble normal tissue
STAGING
TNM system
tumor size and depth of invasion
spread to regional lymph node
metastasis
SCREENING
30 divisions occur before early clinical symptoms arise
each division result in increased mutations
screening seek to catch dysplasia or carcinoma before appearance of clinical symotoms
common screening methods
Pap smear
CIN
mammography
in situ breast cancer
hemoccult test
colonoscopy
PSA
prostate cancer
CARCINOGENESIS
ONCOGENES
result from mutations of proto-oncogenes
growth factors
Growth factor receptors
signal transducers
Ras (GDP bound)
activated by GFR (GTP state)
inactivated by GAP
sends growth signals to nucleus
mutation in GAP result in prolonged activation
cell cycle regulators
CD / CDK4 complex
TUMOR SUPPRESOR GENES
p53
DNA damage can be repaired
upregulation of repair enzymes
DNA damage cannot be repaired
Upregulation of BAX
which disrupts Bcl2
APOPTOSIS
both copies must be knocked out for tumor formation
mutations result in continuation of cell cycle from G1 to S phase w/ mutated genes
Rb
Holds E2f (transcription factor)
E2F is released when Rb is phosphorylated by CD / CDK4 complex
mutation result in continuously free E2f and continuous growth of cells
both copies must be knocked out for mutation to occur
REGULATORS OF APOPTOSIS
Bcl2
prevent apoptosis
follicular lymphoma
Bcl2 is over exptessed
B cells accumulate
CARCINOGENS
DNA damaging agents
chemical
radiation
ionizing
nuclear reactor accidents & radiotherapy
generate OH
nonionizing
UVB
pyrimidine dimers
oncogenic viruses
TUMOR DEVELOPMENT
ways to prevent mortality by malignant cells
Telomerase activity upregulated; prevents apoptosis
DAF upregulated degrades C3 & c5 convertases to prevent MAC formation
Angiogenesis
cellular changes
down regulation of MHCI for avoiding CD8 T cells
normal / atypical mitotic spindles; hyperchromasia
Both nucleus and nuclei are bigger with irregular borders
increased polysomes
fewer mito/ RER & loss of cadherins
metabolic changes
rely on anaerobic glycolysis for energ; + lactic acid
they store glycogen in cytosol
some cancers (prostate cancer) use B oxidation of FAs
basic principles
neoplasia (B&M)
MONOCLONAL
G6PD is an X linked gene that exist in multiple isoforms A & B
Androgen receptor isoforms
Clonality of B lymphocytes can be dected by Ig light chain phenotype (KAPA & Lambda)
Single progenitor
30 doublings to produce 1B cells (1g)
further 10 doublings to produce (1kg) mass
unregulated (autonomous)
irreversible
new tissue growth
composed of
parenchyma
neoplastic component
stroma
non neoplastic supportive component
benign
slow growing
mobile
No local invasion (capsulated)
do not metastasize
usually well differentiated (low grade cancer)
malignant
usually rapid growth rate
firm
metastisize to distant sites
invade locally
may be poor differentiated / anaplasia (high grade cancer)
Epidemology
2nd most leading cause of death in adults and children
most common cancers by mortality are
lung
prostate/breast (most common by incidence)
colorectal
TUMOR PROGRESSION
INVASIVENESS
Down regulation of E cadherin to disassociate
attachment to laminin and destroy basement membrane by collagenase IV
attachment to fibrenoctin in ECM and spread locally
METASTASIS
entrance into lymph nodes
characterestic of carcinoma
entrance blood vessels
characterestic of sarcomas and some carcinoma