oncology - patho E4 Flashcards
the parts of the cell cycle
stage G0
stage G1
Stage S
Stage G2
Stage M
cell cycle: G0
The cell is at rest and is not actively engaged in the cell cycle.
cell cycle: G1
Cells enter the cell cycle and prepare for deoxyribonucleic acid (DNA) replication. Proto-oncogenes, genes that control cell replication, are activated.
cell cycle: S
Synthesis of structures occurs and the structures move to opposite poles in preparation for division into two separate cells. The 46 chromosomes reorganize as two separate sets of 23 chromosome pairs arranged at opposite poles. Two nuclear membranes develop around the two separate sets of 23 pairs.
cell cycle: G2
Cells prepare to divide
cell cycle: M
Mitosis is completed and two daughter cells are created
compared to a normal cell cycle, what does a cancer cell cycle not have
-a rest phase (G0) -> rapidly reproduction
-check points to make sure everything is normal and correct -> allows for lots of cell changes (no DNA errors recognized, no apoptosis)
the goal of cancer treatment drugs is to do what
impact the cell cycle
what do cancer cell disregard
the growth inhibitors released by neighboring cells -> as they proliferate, they accumulate on top, around & besides each other, take over boundaries of organs, crowd out normal cells and may even breakfree and travel to distant body sites
immune surveillance
our immune system recognizes abnormal cells as “non self antigens” -> when discovered the immune system initiates an attack to destroy the substance
with age, this weakens -> increased risk of tumor development
differentiation
refers to the extent that neoplastic cells resemble normal cells both structurally and functionally
Lack of differentiation is called anaplasia, a term that indicates total cellular disorganization, abnormal cell appearance, and cell dysfunction
what does it mean when someone says “the cancer cell is well differentiated”
the cancer cell closely resembles & functions like the cell of origin
do benign tumors tend to be more differentiated or anaplastic
well differentiated -> remain localized, don’t break away, do not invade and destroy surround tissues
do malignant tumors tend to be more differentiated or anaplastic
anaplastic (or poorly differentiated)
review cancer cells break rules chart & differences between normal and cancer cells
tumor markers: what are they
biologic substances that some tumors put off that can be measured
tumor markers: what type of substances
hormones
enzymes
antigens
genes
tumor markers: where can they be found
blood
urine
cerebral spinal fluid
tumor plasma membrane
tumor markers: what are they used for
screening or diagnostic
can help us follow the clinical course of the cancer during treatment
tumor markers: are they diagnostic of cancer
not always but can help diagnose specific types of cancers
examples of tumor markers:
prostate specific antigen
BRCA gene mutation
can be elevated with benign tumor
maligant tumor grading
Grade I: cells are well-differentiated
Grade II: cells are moderately differentiated
Grade III: poorly differentiated or anaplastic cells
Staging classifies the tumor according to size, invasiveness, and spread using a TNM system:
T - tumor size, location, and involvement.
N - lymph node involvement.
M - metastasis to distant organs.
review TNM classification system
needs a biopsy
four stage classification system
doesn’t give much info, better for gen pop
Stage 1: Confined to organ of origin
Stage 2: Locally invasive
Stage 3: Regional spread
Stage 4: Spread to distant sites
four phases of carcinogenesis
initiation
promotion
progression
metastasis
what is involved in carcinogenesis
genes
carcinogens
promoters
carcinogenesis: intitation
the alteration, change or mutation of genes that arise spontaneously or induced by exposure to a carcinogenic agent
carcinogenesis: promotion
actively proliferation cells accumulate
reversible with chemotherapy
carcinogenesis: progression
when cells undergo further mutation & these cells tend to be more invasive with metastatic potential
carcinogenesis: metastasis
the spread of cancer
what are the two major classes of cancer genes
1) tumor suppressor genes (“car break doesn’t work” -> these cells are inactivated & nothing stops the proliferations of mutated genes and nothing tells the cell when to die)
2) oncogenes (“gas pedal controlling speed” -> mutated proto-oncogenes are permanently turned on and cells can keep dividing out of control)
how to classify carcinogens
-known (smoking, alc, HPV, HIV)
-probable (night shift), evidenced based
-possible (engine exhaust), insufficient evidence
what is a promoter
an agent that help the mutated gene proliferate
ex: high fat diet, alc, tobacco, hormones
viral induced cancer
certain malignancies are associated with cancer inducing viruses (like hiv)
MOA: always involve the activation of growth promoting pathways or inhibition of tumors suppressors in infected cells
how do tumors create their needed blood supply
they secrete vascular endothelial growth factor, a substance that gives them the capability to develop new blood vessels
with cancer spread we can have:
seeding
implantation
metastasis
cancer spread: seeding
the tumor erodes and sheds into the body cavities -> the “seed” can be planted in different body cavities
cancer spread: implantation
refers to the direct expansion of the tumor to an adjoining tissue -> prostate is right next to bladder so the prostate cancer grows right into the bladder
cancer spread: metastasis
2 primary routes are lymphatic & vascular
when the cancer moves to distant sites through the lymph or vas system
lymphatic spread
the first stop is the lymph system & get trapped in the lymph leading to:
1) cell death in the lymph
2) cells can go dormant in the lymph
3) flourish / proliferate
if they survive then they can start traveling around the entire lymph system
vascular spread
cancer cells can penetrate blood vessels that drain the tumor site and once they get into circulation, they can deposit anywhere
first stop is often the liver
common metastatic sites for tumors: lung
bone, brain
common metastatic sites for tumors: colon
liver
common metastatic sites for tumors: breast
bone, brain, liver, lung
common metastatic sites for tumors: prostate
vertebrae
common metastatic sites for tumors: melanoma
brain
