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32 Cards in this Set
- Front
- Back
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In general, why do cancer cells grow so much/fast? |
A loss of normal growth control There isn't a balance between new cell growth and cell death |
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Proto-oncogenes |
Normal growth factors Encode proteins for growth |
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Tumor suppressor genes |
Slow and stop growth of tumors |
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Oncogenes |
Mutant growth factor |
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Silenced tumor suppressor genes |
The tumor suppressing genes become silenced (inhibited) |
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What happens to cells as they mutate? |
Structural changes begin and result in uncontrolled growth of abnormal cells *Structural changes (exterior) occur at the third mutation |
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What are the 2 main differences between normal cells and cancerous cells? |
1) Cancer cells have no contact inhibition (they divide even when they form a complete layer and will keep dividing) 2) Cancer cells are anchorage-independent and don't need to attach to something to divide |
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Are benign tumors non-harmful? |
They can interfere with cell function, use up nutrients, and crowd out other cells |
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Characteristics of malignant tumors: growth rate, capsule, invasion, mitosis, metastasis? |
They grow fast Not encapsulated They can invade nearby structures High mitotic index Undergo metastasis |
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Mitotic Index |
The number of cells undergoing mitosis vs. the number of cells not undergoing mitosis |
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What is Carcinoma in situ? |
An abnormal growth of cells that is not considered cancer, but could become cancerous and remains in its original place where it was formed |
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Metastasis |
Spread of cancer cells from their original site |
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What are 3 possible outcomes of carcinoma in situ? |
1) Remains stable 2) Becomes invasive and metastasizes (becomes cancer) 3) Regresses and disappears (like quitting smoking) |
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Since tumors receive no blood supply, how can they make sure to get blood supply? |
They undergo angiogenesis and form their own blood vessels |
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What two ways do we classify cancer? |
The primary site where it first developed and the type of tissue where the cancer originated "-oma" |
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What is the leading cause of cancer death in PEI? |
Lung cancer (men and women) |
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In what age does cancer more commonly occur |
In the aging population Increased risk with age |
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Telomeres |
They are protective chromosomal caps that determine how many times a cell can divide |
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Telomerase |
An enzyme that maintains the telomeres * only found in germ and stem cells |
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Cancer is caused by ____________? |
Mutations |
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What are some risk factors for acquiring those mutations? |
Your genetics (BRCA1 - repairs genes, BRCA2 - suppresses tumors) Obesity (increased oxidative stress) Infection (HPV, EBV, H.pylori) Exposure to radiation |
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What advantage do mutated cells have? |
They have increased growth rate and decreased apoptosis |
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What are some clinical manifestations of cancer? |
Fatigue/lethargy Anemia Leukopenia/thrombocytopenia Cachexia Pain (later stages) |
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What are the advantages of screening? |
Improving the outcome and increasing survival |
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Can screening tests diagnose cancer? |
NOPE |
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How do we diagnose cancer? |
We look at the molecular (enzymes/proteins) and cytogenetic (chromosomes) studies Microscopic studies determine where cancer started and the type Any cellular properties "tumor markers" can be determined |
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What are tumor grades? |
It describes the type of tumor and its metastasis potential |
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GX - can't be assessed GI - well differentiated (low grade) G2 - moderately differentiated (intermediate grade) G3 - poorly differentiated (high grade) G4 - undifferentiated (high grade |
Tumor stage can be used with cancer stages to determine a plan, but they don't mean the same thing |
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What is cancer staging? |
Describes the severity of cancer based on its size/metastasis |
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Stage 1 - no metastasis Stage 2 - local invasion Stage 3 - spread to regional structures Stage 4 - distant metastasis |
:) |
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What is the TNM system? |
Developed by WHO T = tumor size and spread N = node involvement M = distant metastasis |
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Where do we NOT use the TNM system? |
For the brain and spinal cord, or blood and bone marrow cancers |
