oncology Flashcards
cell cycle
sequence of growth stages for mitosis and regeneration
G0, G1, S, G2, M
check points: DNA check, cancer cells often dont have these
G0
rest
cancer cells dont enter this at beginning cancer stage
G1
DNA rep prep, protooncogenes activated (control cell rep)
S
DNA rep + move to opposite ends with new nuclear membranes
G2
prep to divide
M
2 daughter cells
cancer cells
DNA make up change over time -> makes treatment particularly difficult - tries to impact cell cycle in some way
disregard normal cell cycle rules
large number of dividing cells, large variably shaped nuclei, large nucleus to cytoplasm ratio, variable size and shape, loss of normal cell features, disorganized arrangement, poorly defined tumor boundary
cancer cells: disregard normal cell cycle rules
constantly going through cycle -> not G0
no checkpoints -> DNA errors, apoptosis
disregard growth I released by neighboring cells
as they proliferate, they accumulate on top, around, beside each other, take over boundaries of organs, crowd normal cells, can break free and travel
immune surveillance
constantly survey for self v non self
non self antigen -> initiate attack to destroy invading substance
decrease with age therefore tumor development is easier
differentiation
well differentiated = function like cell or origin
extent that neoplastic cells resemble normal cells both structurally (shape and size) and functionally (normal cell cycle)
anaplasia = lack of differentiation -> cancer, total cellular disorganization, abn appearance, cell dysF
benign usually well differentiated
cancer cells break rules
contact inhibition - invade
cohesiveness - break away
communication - little to none
proliferation control - immortal/die unpredictable
proliferation rate - unpredictable, depends on differentiation (anaplastic = fast)
“self” HELA antigens - non self markers, attack may be muted, avoid
benign
well differentiated, resemble origin
progressive, slow growth
cohesive, well demarcated, often encapsulated (moveable)
no necrosis
malignant
poor dif, dont resemble origin, anaplastic
erratic growth (slow - rapid)
invasive and infiltrating, surround normal tissue
freq metastasis -> lymph or blood
can have necrotic core -> esp as age and size increase
- hard to get treatment there
tumor markers
biologic substances - shed by some tumors
measurable -> hormones, enzymes, antigens, genes
- blood, urine, CSF, tumor plasma membranes
- screen or dx (not always - some non malignant diseases also produce): follow course, treatment working?
ex: PSA, BRCA gene mutation
TNM: malignant
1 = well diff
2 = mod diff
3 = poorly diff or anaplastic
staging
classifies tumor according to size, invasiveness, spread
help to understand seriousness, survival, tm, trials
T = tumor size, location, involvement
N = lymph node involvement
M = metastasis to distant organs
staging: T
0 = no evidence of primary tumor
TIS = tumor in situ
T1-4 = progressive increase in size or involvement
1 = 1cm, 2 = 2cm, etc.
staging: N
N0 = no spread to regional lymph nodes
N1 = spread to closest or small # of regional lymph nodes
N2 = spread to most distant or numerous regional lymph nodes
staging: M
0 = none
1 = yes
4 stage classification
limited info
1 = confined to origin of organ
2 = locally invasive
3 = regional spread
4 = distant site
carcinogenesis
origin of cancer -> no simple answer, issue of gene expression
genes, carcinogens, promoters
carcinogenesis: phases - initiation
alteration, change, mutation of genes that arise spontaneously or are induced by exposure to carcinogen
carcinogenesis: phases - promotion
reversible -> alter/affect growth rate
actively proliferating cells accumulate
carcinogenesis: phases - progression
further mutation - more invasive with metastatic potential
carcinogenesis: phases - metastasis
spread of cancer
cancer genetics: mutations
hereditary or sporadic
sporadic = acquired during life
mutations dont = cancer, just increase risk
cancer genetic mechanisms
tumor suppressor genes = break pedal, p53 gene = controls apoptosis
if inactivated: proliferate out of control
oncogenes -> gas pedal stuck
mutated protooncogenes -> gas pedal
growth signal permanently on
carcinogens
can alter DNA, damage is cumulative, often require prolonged exposure
classify: known, probable, possible
known = tobacco, asbestos, estrogen therapy, OH, virus
probable = night shift F
possible = engine exhaust
promoters
promote dev
diet (increased fat)
OH, tobacco
hormones - estrogen (early menses, late menopause, no preg, HRT)
viral induced cancer
HIV = carcinoma
HPV = cervical cancer
insert into host which becomes manufacturer of virus
moa: always involve activation of growth promoting pathways or I of tumor suppressors in infected cells
metastasis
secrete vascular endothelial GF -> dev new BV = angiogenesis
primary and secondary tumor
spread = seeding, implantation, metastasis (lymph/vascular)
seeding
tumor erodes and sheds cells into body cavities
implantation
direct expansion to adjoining tissue
metastasis: lymph
1st stop, trapped in nodes
death, dormancy, flourish/proliferate
metastasis: vascular
penetrate local veins
liver 1st stop -> receives most of blood, clump, trapped, proliferate
secondary tumors
need nutrients and O2, access to blood (angiogenesis)
lung, bone, liver, brain
secondary tumors: lung
bone, brain
secondary tumors: colon
liver
secondary tumors: breast
bone, brain, liver, lung
secondary tumors: prostate
vertebrae
secondary tumors: melanoma
brain
lung cancer
leading cancer COD, dx early - most present with advanced or metastatic
>65, AA
lung cancer: etiology
smoking - promoter and known carcinogen, increase risk with # smoked -> pack per yr
overload of carcinogen and genetic predisposition
other common causes: 2nd hand, CPOD (chronic inflam), asbestos (construction), radon (test homes), arsenic, genetics, other (radiation therapy, pulm fibrosis)
get good hx
lung cancer: patho
carcinogen overload, genetic predisp -> paralyze cilia -> lesions -> cancer -> activate oncogenes and deactivate tumor suppressor genes -> rapid proliferation/destruction/invasion
lung cancer: types
non small cell lung cancer = slow growing
small cell = rapid, metastasize quickly
lung cancer: s/s
coincide with smoking
cough, hemoptysis, wheeze/stridor, chest pain, dyspnea, weight loss, excessive fatigue, weak, hoarsness (compression of larynx)
obstructive accumulation of secretions in bronchioles -> pna (appear as pna)
routine CRX, asymp, paraneoplastic S may be first sign -> secretion of hormone (too much) by tumor -> ACTH -> tan bc stim melanocytes
breast cancer
lining in ducts
overexposed estrogen receptors
overexposed human epidermal growth factor receptor
breast cancer: rf
> 50, prolonged reproductive life = early menses and late menopause, HRT, obese, late childbirth (30+), nulliparous, fam hx, jewish, BRCA1 +2 mutation (increased r/o breast, ovarian, colon, pancreatic, prostate (M))
can rest for presence of BRCA in high risk, genetic counseling, preventative mastectomy and oophorectomy (ovaries)
breast cancer: s/s
promote mamograms
single tumor, non tender, firm, irreg boarder, adherence to skin or chest wall, upper-outer quad of breast, nipple d/c, swelling in 1, nipple or skin retraction
peal d’orange = thickening of skin like orange peel
paget = redness, crsuting, pruritus, nipple tenderness
cervical
clinical course = long asymp phase, abn pap (q3 yr)
cervical: rf
smoke, hx STD, HPV! (genital wart type -> condylomata; or cancer type -> persistent infection), 2+ lifetime sexual partners, immunosuppression, genetics
colorectal
q10 yr after 50yr
start asymp (tumorous mass that projects into intestinal lumen) -> most are small and have low chance of malignancy
familial adenomatous polyposis = predispose
hereditary non polyposis coli HNPCC -> low chance of cancer
colorectal: rf
obsese (inflam), tobacco (polyps), physical inactivity (obese), insulin resistance, low fiber, high animal fat, high processed meats, decreased vits A, C, E (antioxidants); ulcerative colitis (inflam), high OH use
colorectal: s/s
fatigue, weak, weight loss, Fe def anemia (slow blood loss), change in bowel habits, melena, d, c
hematochezia (rectal bleed) and narrowing of stool caliber (ribbon life bc passing by tumor)
