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Storage for later > Cancer Patho from Thompson Spring 2016 > Flashcards

Cancer Patho from Thompson Spring 2016 Flashcards

1
Q

What are three mechanisms/modes of metatstatis?

A
  • Bloodstream
  • Lymphatics
  • Direct extension into neighboring tissues
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2
Q

What are two words used to describe metastasis through the blood stream?

A

(hematogenous or vascular)

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3
Q

What is “skip matastasis”?

A

Cancer cells bypass local lymph nodes and form distant modal mets

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4
Q

How does breast cancer spread? (Venous, lymphatic, both)

A

Both: Lymphatics and vertebral venous system

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5
Q

_What might happen if you resect a tumor without clear margins?

A

It can encourage mets, as new blood vessels form during healing process and the cancer can get into the bloodstream.

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6
Q

What are the most likely primary metastais sites for breast cancer? (6)

A
  • bones in
    • shoulder,
    • hip,
    • ribs,
    • vertebrae,
  • lungs,
  • liver
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7
Q

What is benign mechanical transport?

A
  • Mechanical disruption of the cancer cells cause them to break off and move (spread)
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8
Q

What are two ways you can get Benign Mechanical Transport?

A
  1. Lymphatic transport of epithelial cells displaced by biopsy of basic tumor
  2. Breast massage-assisted sentinel lymph node (SLN) localization
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9
Q

What are the early s/s of metasteses seen most often in a TP practice? (it seems more like she listed 5 systems where we would see it the most often)

A
  1. Integumentary
  2. Musculoskeletal
  3. Neurologic
  4. Pulmonary
  5. Hepatic
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10
Q

How many forms of cancer are there? Why do we care?

A
  • There are >250 forms of cancer
  • Just know there is a lot.
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11
Q

How can we find what the tumor of origin is?

A

The cell type will show the tumor of origin. Cancer cells have different characteristics depending on site of origin.

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12
Q

What are two things that characterize all cancers?

A
  1. Unregulated growth
  2. INVASION and spread of cells from the original site to other areas – METASTASIS
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13
Q

Does cancer always follow the normal pattern?

A

No, There are times where cancer cells don’t follow the general pattern.

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14
Q

When can cancer spread (metastasis)?

A

It can spread as many as 15-20 years after initial diagnosis and intervention.

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15
Q

What percentage of autopsies of pts who died from cancer show spinal metastases (in bone)?

A

70%

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16
Q

What is to important to remember when treating a pt with back pain?

A

HAVE THEY EVER HAD A DIAGNOSIS OF CANCER?? The mets may have spread to the spine (70% of autopsied pts who died of cancer had spinal mets)

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17
Q

Can cancer be detected easily? When might it be first detected?

A

Cancer may not detected until tumor starts to block organs, etc. or invades where pain receptors are

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18
Q

What is a cause of metaplasia? And example?

A

Usually in response to some stress.

Like metaplasia of bronchial epithelium in a smoker.

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19
Q

What is an example of benign hyperplasia?

A

Callous formation

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20
Q

Benign, malignant, and/or pre-cancerous?

  • Metaplasia
  • Dysplasia
  • Hyperplasia
  • Neoplasia
A
  • Metaplasia: benign (not malignant), but usually followed by dysplasia
  • Dysplasia : usually alerts us to pre-cancerous process
  • Hyperplasia: either pre-cancerous or benign
  • Neoplasia: benign or malignant
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21
Q

Are the terms for abnormal cells (metaplasia, dysplasia, hyperplasia, neoplasia) used consistently to mean certain things across credible sources? What does this mean to us and the pt?

A
  • Lots of variations of the use of terms. A lot of credible sources use some of these terms interchangeably.
  • Therefore, don’t hang your hat on what an MD calls the cells (as far as how serious it could be).
  • Any cell growing abnormally can be dangerous.
  • This is not a sequence, these are separate terms.
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22
Q

What are the three processes/mechanisms that regulate cell numbers?

A
  • Cell division
  • Cell differentiation
  • Apoptosis
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23
Q

How do the three process/mechanisms that regulate cell numbers relate to cancer interventions?

A

Each of the three processes presents an opportunity for intervention in unregulated cell growth.

(Processes are: Cell division, Cell differentiation, Apoptosis)

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24
Q

How the three processes/mechanisms that regulate cell numbers relate to development of cancer?

A
  • Cellular mutations can affect any of these processes, producing abnormalities in cell numbers

(Processes are: Cell division, Cell differentiation, Apoptosis)

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25
Q

When a cancer cell develops and goes crazy, what are the three processes where there is a chance to intervene with uncontrolled growth?

A

Any of the processes/mechanisms that regulate cell numbers

  • Cell division
  • Cell differentiation
  • Apoptosis
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26
Q

What are the 6 steps required of cancer cells to matastasize?

A
  1. Primary tumor
  2. Localized invasion: spread of tumor within the tissue of origin through local invasion of tissue (until it meets with blood vessels)
  3. Intravasation: spread into microvasculature
  4. Transportation by the circulatory system
  5. Arrest in microvasculature of organ
  6. Extravasation (and formation of secondary tumor)
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27
Q

What is intravasation?

A

Intravasation = invading the vascular system.

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28
Q

Why is the lung a very common site of mets?

A

Lung is a very common site of metastasis because it is the first filter encountered by blood.

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29
Q

What are 6 characteristics of all cancers (KNOW THIS!))

A
  1. Self sufficiency in growth signals
  2. Insensitivity to anti-growth signals
  3. Evasion of apoptosis
  4. Sustained angiogenesis
  5. Tissue invasion and metastasis
  6. Limitless reproductive potential
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30
Q

How do growth factors relate to normal cells?

A
  • In normal cells, growth and division requires external growth factors (GFs)
31
Q

Explain how growth factors are made, and get to and act on the cell? What is the end result?

A
  • Diffusible, produced by other cells & bind to cell receptors
  • Trigger intracellular kinases which in turn triggers cell division
32
Q

What are two abnormalities involving growth factors that contribute to uncontrolled growth in cancer?

A
  • Too many receptors & over-stimulation of growth
  • Self production & release of GFs which stimulate growth
33
Q

What are two things that could be a trigger for growth factor malfunction in cancer?

A

Trigger may be genetic, environmental (or both?)

34
Q

What are oncogenes? Where do they come from?

A
  • Small segments of DNA which can transform normal cells into malignant ones
  • Activated from “normal” proto-oncogenes by a mutation
35
Q

What causes oncogene mutation?

A
  • Mutation caused by abnormal environmentor genetics (maybe both)
36
Q

What happens with Anti-growth insensitivity? What is the normal process that goes wrong?

A

Cells stop listening to each other

  • In normal growth and division, cells are signaled to stop with anti-growth signals from other cells.
37
Q

What are the three types of anti-growth signals from other cells?

A
  1. Soluble growth factors
  2. Immobilized inhibitors embedded in the extracellular matrix
  3. Immobilized inhibitors on the surfaces of nearby cells
38
Q

What are the parts of the Cell Cycle? (do not need to memorize) – 6 things

A
  • G1 phase – cell growth in preparation for increased DNA synthesis
  • (G0 phase - resting phase where the cell has left the cycle and has stopped dividing)
  • (G1 check point)
  • S phase – DNA synthesis phase
  • G2 phase – cell growth preceding mitosis
  • M phase – mitosis, cell division
39
Q

What is the significance of the G1 phase?

A
  • G1 checkpoint is a regulatory step preventing move into DNA synthesis phase thus preventing cell division
  • Mature cells do not pass this checkpoint, they enter G0 here.
40
Q

Explain the significance of the cell cycle and chemo drugs:

A

cell cycle becomes the template for all chemotherapy. These are the opportunities where we can stop the cell.

If we look at the drugs, we will see these terms a lot. (G1 G2)

This is also why we have multiple regimens for chemotherapy. It is so we can take advantage of this so we can catch mature cells and developing cells.

41
Q

What are nectins?

What 2 roles do they play in normal cells?

What do they say?

A

Nectins (intercellular adhesive) & nectin-like substances

  • play a role in contact inhibition – prevention of mitosis once cells of a tissue come in contact with one another
  • also play a role in limiting the movement of cells – cell motility

Nectins say, “we’ve got enough; we don’t need any more cells.”

42
Q

What roles do nectins play in cancer cells? (2)

A
  • Nectins & nectin-like substances may be deficient so that there is a lack of normal contact inhibition and an overgrowth of cancer cells
  • Deficit of nectins & nectin-like substances may produce the excessive cell movement of cancer cells and spread of cells that begins metastasis
43
Q

What are anti-oncogenes/how do they relate to cancer? (2)

What is another name for them?

A

Anti-oncogenes, also called tumor suppressor genes

  • Can regulate growth and inhibit carcinogenesis (act like a break pedal)
  • Some meds are to try to get some of these cancer suppressor genes to work
44
Q

What are tumor suppressor genes?

A

Genes that when active decrease risk of a cell becoming metastatic (cancerous)

45
Q

How do Tumor suppressor genes work? (3-4 things)

A

Code for proteins which

  1. Have a repressive effect on progression thru the cell cycle
  2. Promote apoptosis
  3. Do both
46
Q

True/False: Activating Tumor Suppressor genes hold a lot of promise for treatment approaches.

A

True. For example, if p53 is turned off, maybe there is a way to turn it back on?

47
Q

What Tumor Suppressor gene is nicknamed “The Guardian of the Genome”? How does it work?

A

P53 Tumor Suppressor Gene

Forms P53 protein, which changes gene expression to halt cell proliferation & trigger apoptosis when DNA is damaged.

  • Halts cell division in G1 phase in response to DNA damage
  • Destroys potentially malignant cells via apoptosis
48
Q

What is found to be mutated or otherwise disrupted in the majority of all types of cancers?

A

P53

49
Q

Explain how Sustained Angiogenesis affects the cancer process? (4)

A
  1. Tissue survival requires nutrients & oxygen from blood
  2. Cells stop growing if they are any greater than a certain distance from a source of oxygen & nutrients
  3. Cancer cells have the unique ability to signal the growth of new blood vessels to themselves to sustain growth (using VEGF, vascular endothelial growth factor)
  4. P53 suppression allows mutation and proliferation
50
Q

Compare and contrast Normal versus abnormal vessel anatomy in cancer. How does this affect metastasis?

A
  • Normal architecture of vasculature is highly organized
  • Abnormal architecture with tumor vasculature is highly disorganized
  • Vessels are tortuous and dilated with uneven diameter, excessive branching and shunts
  • Numerous endothelial fenestrae, vesicles and transcellular holes, widened inter-endothelial junctions, and a discontinuous or absent basilar membrane
  • All of these changes result in high vessel permeability and promote metastasis
51
Q

What are three drugs that target Sustained angiogeneisis?

A
  1. Blocking VEGF receptor (Bevacizumab) - avastin
  2. Interfering with tyrosine kinase (Sunitinib & Sorafenib)
  3. Interfering with intracellular activator pathways (Sorafenib)
52
Q

4 points about tissue invasion and metastasis

A
  1. Every normal tissue has boundaries
  2. Even benign tumors don’t cross into other tissues, merely pressing against them
  3. Malignant tumors spread and invade into other tissues
  4. Cancer cells can break off too, spreading “seeds” around to other parts of the body(“soil”), which grow into new tumors
53
Q

What percentage of cancer deaths come from mets?

A

90%

54
Q

What does the environment have to do with metastasizing cells?

A
  • Metastasizing cells must adapt to new environments
55
Q

How does the metastasizing cells adapt to the new environment? (3 points)

A
  1. Adaption of cellular membrane proteins
  2. Intercellular signaling
  3. Changes from one configuration to another in different environments
56
Q

What is one one explanation for selective metastasis (why metastasis occurs in some tissues but not in others with certain cancers)

A
  • Certain cellular environments are conductive to particular tumor growth and others are not
57
Q

What is the “hayflick limit”?

A
  • Aside from being programmed to die, all cells have a limit to how many times they can divide before they cannot divide any more – referred to as the “Hayflick Limit”
  • (Cancer cells do not have this limit, so they are truly immortal cells)
58
Q

How does the hayflick limit work? (details on hayflick limit), include how many times normal human fetal cells in cell culture can divide.

A
  • Normal human fetal cells in a cell culture divide between 40 and 60 times
  • Cells then enter a senescence phase and stop
  • Cell reproduction with physical age as well
  • Each mitosis shortens the telomeres on the DNA of the cell
  • Telomere shortening in humans eventually makes cell division impossible, and correlates with aging
59
Q

What is a telomere? What is it for?

A
  • Telomere
    • Region of repetitive DNA sequences at the end of a chromosome
    • Protects the end of the chromosome from deterioration or from fusion with neighboring chromosomes
60
Q

What happens without telomeres?

A
  • Without telomeres, cells would lose the ends of their chromosomes at cell division, and the information they contain
  • Telomere goes bad is one of the genetic reasons for cancer.
61
Q

What happens to telomeres during cell division?

A
  • Telomeres are disposable buffers blocking the ends of the chromosomes & are consumed during cell division
62
Q

What enzyme is “the booger” in telomeres? Why?

A
  • Telomerase
    • Telomeres are replenished by the enzyme telomerase reverse transcriptase (TERT)
    • TERT is needed to extend lifespans of certain cells such as fetal stem cells
    • TERT activation has been observed in > 90% of all human tumors
    • Thus the immortality conferred by telomerase plays a key role in cancer development
63
Q

What are two main reasons for limitless reproductive potential of cancer?

A
  • Limitlessreproductive potential due to both loss of cell cycle checkpoints and
  • role of telomerase
64
Q

Explain the genetics of cancer

A
  • Cancer is the result of genetic changes to the cell
  • Cancer requires an accumulation of mutations, creating a progression from a healthy cell to a malignant cell
65
Q

What are some types of mutations in cancer? (4)

A
  1. Changes in single bases
  2. Insertion of individual bases or sequence
  3. Chromosome translocations
  4. Chromosome deletions
66
Q

What is the difference between inherited vs somatic mutations

Inherited (when acquired? Passed to next generation? Cancer risk? Associated with familial syndromes?)

A

Inherited

  • Present at birth, and in every cell
  • Passed from one generation to the next
  • Increase the risk of cancer exponentially
  • Are found in many familial syndromes

Somatic

  • Acquired throughout life in individual cells
  • Not passed on to next generation
  • Increased risk of cancer, but less than inherited
  • Not associated with familial syndromes
67
Q

What do BRCA1 and BRCA2 do? (2-3)

A
  • BRCA1 and BRCA2 are expressed in the cells of breast and other tissues, where they helps repair damaged DNA, or destroy cells if DNA cannot be repaired
  • Function as tumor suppressor proteins
68
Q

What happens if BRCA1 or BRCA2 genes are absent or mutated?

A
  • Absence or mutation of these proteins increase risk for breast and ovarian cancer, which can be inherited – called a “founder” effect
69
Q

What is the “founder” effect?

A

When an increase risk for breast and ovarian cancer can be inherited (from absence/mutation of BRCA1 , BRCA2)

70
Q

What is an example of “founder” mutation?

A
  • Example of “founder” mutation is found in Iceland, where a single BRCA2 mutation accounts for virtually all breast/ovarian cancer families
71
Q

What is another type of cancer besides breast cancer where BRCA2 mutation is also implicated?

A
  • Increased risk for leukemia also reported
72
Q

what percentage of hereditary breast cancer is caused by BRCA1 mutations? BRCA2 mutations

A
  • 28% of hereditary breast cancer is caused by BRCA1 mutations
  • 19%of hereditary breast cancer is caused by BRCA2 mutations
73
Q

What is the percent risk of developing breast cancer in women with an abnormal BRCA1 or BRCA2 gene?

A

Up to 60% risk

74
Q

What is the risk of developing ovarian cancer in women with BRCA1 mutation? BRCA2 mutation?

A
  • 55% for women with BRCA1 mutations
  • 25% for women with BRCA2 mutations

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