Oncology Flashcards
stage G0
Cells at rest, not active
stage G1
cell enter cycle
Prepare for DNA replication
Proto oncogenes activated
stage S
Synthesis of structures
Structures move to opposite poles in preparation for division
To nuclear membranes develop around chromosome pairs
Stage G2
cells prepared to divide
Stage M
mitosis is completed
Two daughter cells created
T/F Cancer cells, utilize checkpoints to see DNA errors and complete apoptosis
False
what occurs with immune response in relation to age?
As age increases, immune response decreases
Tumor development increases
differentiation
Extend that neoplastic sells, resemble, normal cells, structure and function
what occurs with anaplasia?
Lack of differentiation
Total social disorganization, abnormal cell appearance, and dysfunction
T/F benign sells tend to be more differentiated
True
Factors of differentiation
contact inhibition
Cohesiveness
Proliferation control
Communication
Proliferation rate
Self HLA, antigens
which factors of differentiation are unpredictable with cancer cells?
Proliferation, control, and rate
do cancer cells avoid detection with antigens?
Yes, nonself markers
Benign tumors
well differentiated
resembles tissue origin
Slow, progressive
Well demarcated
Encapsulated
No meta-stasis or necrosis
malignant tumors
Poorly differentiated, anaplastic
slow to rapid
Invasive and infiltrating
Frequent meta-stasis
Necrotic core
tumor markers
Biological substances, measurable
Hormones, antigens, genes etc.
Found in blood, urine, cerebral, spinal fluid, tumor plasma, membranes
can tumor markers be used for screening to diagnose course of cancer?
Yes
TNM system
Grading of malignant tumors
T – tumor size, location, involvement
N– lymph node
M – meta-stasis to distant organs
Grade one TNM system
Cells are well differentiated
Grade 2 TNM system
Cells are moderately differentiated
Grade 3 TNM system
Cells are poorly differentiated/in a plastic
Classification of symptoms
stage one – confined to Organ of origin
stage two – local invasive
Stage three - regionally spread
Stage four spread too distant sites, meta-stasis
carcinogenesis
Origin of cancer
phases of carcinogenesis
Initiation
Promotion
Progression
Meta-stasis
tumor suppressor genes
Normally functions to restrain cell growth
inactivated with cancer
P 35. Gene – controls cellular apoptosis.
oncogenes
Mutated Protoncogenes
Growth signal permanently on
what occurs with the transition from proto-oncogenes to oncogenes
When mutated, constant, unrelenting cell growth and cycle
is a primary tumor started at the site of origin?
Yes, and stays there
what occurs with a secondary tumor?
Pieces of tumor, travel to other sites
carcinogens
Substances that cause development of cancer over many years
known carcinogens
Tobacco
HPV
HIV
Estrogen
promoters
Agents that promote development of cancer
Diet – high-fat
Alcohol
Tobacco
Hormones – estrogen
viral induced cancer
Virus inserts into genes host cell genome
host cell becomes manufacture of virus
Activation of growth promoting pathways or inhibition of tumor suppressor’s
- HIV, HPV, Hep B/C
Meta-stasis
cancer cells, secrete, vascular, endothelial, growth, factor
Capability to develop new blood vessels
seeding
Tumor sheds into body cavities
implantation
Direct expansion of tumor to other tissue
lymphatic meta-stasis
Cells, trapped in lymph nodes
vascular meta-stasis
Drainage, penetrate vessel/veins
where is usually the first stop of vascular meta-stasis
Liver, due to portal vein system
Secondary tumors
Need oxygen and nutrients and access the blood
what are most common secondary tumors?
Lungs
Bone
Liver
Brain
angiogenesis
Tumor creates own blood supply
metastasis from lungs?
To bone or brain
meta-stasis from colon
To liver
meta-stasis from breast
To bone, brain, liver, lung
meta-stasis from prostate
To vertebrae
Meta-stasis of melanoma
to brain
