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Thompson- spring > Day 3- Cancer (Patho) > Flashcards

Day 3- Cancer (Patho) Flashcards

1
Q

What are 3 modes/ mechanisms that cancer can travel?

A

~Bloodstream (hematogenous or vascular)
~Lymphatics
~Direct extension into neighboring tissues

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2
Q

How can the cancer grow to the neighboring tissues?

A

*The cells will just keep growing/ dividing until it gets to the neighboring tissues

~Local invasion and tumor angiogenesis
~Venous drainage and further spread via metastatic cascade
~“skip metastasis” – bypass local lymph and form distant nodal mets

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3
Q

Are there normal patterns that metastatic of cancer will follow?

A

Yes

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4
Q

What determines the normal metastatic pattern of cancer?

A

Patterns of regional venous drainage, blood flow, and lymphatics determine common metastatic patterns

**there’s a huge table in the book on the primary cancer, mode of dissemination, and location of mets (just if you are interested- Table 13-4)

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5
Q

What is an example of metastatic patterns of cancer?

A

~breast cancer spreads via lymphatics and vertebral venous system to bones in shoulder, hip, ribs, vertebrae, lungs, liver

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6
Q

Why should the doctor be careful when resecting a tumor?

A

If the tumor does not have clear margins when resected, mets can occur. new blood vessels with form during the healing process from resection

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7
Q

What is benign mechanical transport?

A

~lymphatic transport of epithelial cells displaced by biopsy of basic tumor

*breast massage-assisted sentinel lymph node (SLN) localization can cause the tumor to dislodge- resulting in benign mechanical transport

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8
Q

What are all cancers characterized by?

A

~Unregulated growth

~Invasion and spread of cells from the original site to other sites - metastasis

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9
Q

Up to 70% of autopsies of patients who died of cancer showed….

A

spinal metastases

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10
Q

Metaplasia

A

~replacement of one differentiated cell type with another mature differentiated cell type.
~Not malignant
~the basal cells (epithelium stem cells) switch to making another cell type, usually in response to some stress (think metaplasia of bronchial epithelium in a smoker)
~dysplasia can easily follow

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11
Q

Dysplasia

A

~expansion of immature cells with decrease in the number and location of mature cells
~usually signals a pre-cancerous process

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12
Q

Hyperplasia

A

~increased number of cells, which may or may not signal a pre-cancerous or cancerous process
~may be very benign, such as a callous

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13
Q

Neoplasia

A

~“new growth”

~may be benign or malignant

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14
Q

What are the 3 basic processes in which our body regulates cells?

A

~Cell division
~Cell differentiation
~Apoptosis

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15
Q

Where in the normal processes can a problem occur?

A

ANYWHERE!

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

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16
Q

What are the steps for metastasis of cancer cells?

A 
~Primary tumor
~Localized invasion
~Intravasation
~Transportation thru the Circulatory System
~Arrest in microvasculature of organs
~Extravasation
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17
Q

What does Intravasation mean?

A

the entrance of foreign matter into a vessel of the body and especially a blood vessel

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18
Q

What does Extravasation mean?

A

the escape from a vessel into a tissue

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19
Q

More details on the steps for metastasis of cancer cells

A

~Spread of tumor within the tissue of origin through local invasion of tissue

~Spread into micro-vascular by intravasation

~Circulates through the vascular before being trapped in the microvasculature of other organs

~Tumor cells then extravasate into the other organs to form a secondary tumor

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20
Q

What are the 6 hallmarks of cancer?

A 
~Evading apoptosis
~Self-sufficiency in growth signals
~Insensitivity to anti-growth signals
~Tissue invasion & metastasis
~Limitless replicative potential
~Sustained angiogenesis
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21
Q

growth and division requires

*Nice to know- not on exam

A

external growth factors (GFs)

**I will put- “nice to know- not on exam” in the parts where she said it; I’m guessing she meant it for a good bit of this section, but I will put it in where she said it.

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22
Q

Growth Factors (GFs)

*Nice to know- not on exam

A

~Diffusible, produced by other cells & bind to cell receptors
~Trigger intracellular kinases which in turn triggers cell division

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23
Q

Abnormality of growth in cancer cells occurs when:

*Nice to know- not on exam

A

~Too many receptors & over-stimulation of growth
~Self production & release of GFs which stimulate growth
~Trigger may be genetic, environmental

*she wants us to know that a trigger makes the growth increase

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24
Q

What are oncogenes?

A

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

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25
Q

What happens when cells stop listening to each other?

*Nice to know- not on exam

A

Cancer cells don’t respond to signals and keep dividing over normal cells that have stopped growing

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26
Q

In normal growth and division, cells are signaled to stop with ….

*Nice to know- not on exam

A

anti-growth signals from other cells which include:

~Soluble growth factors
~Immobilized inhibitors embedded in the extracellular matrix
~Immobilized inhibitors on the surfaces of nearby cells

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27
Q

In normal cells, how is the growth checked?

*Nice to know- not on exam

A

the cell responds to antigrowth signals associated with the G1 checkpoint of the cell growth cycle

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28
Q

What are the phases in the cell cycle?

*Nice to know- not on exam

A 
~G0
~G1
~S
~G2
~M
29
Q

What is G0 phase

*Nice to know- not on exam

A

resting phase where the cell has left the cycle and has stopped dividing

30
Q

What is G1 phase

*Nice to know- not on exam

A

cell growth in preparation for increased DNA synthesis

**G1 checkpoint is a regulatory step preventing move into DNA synthesis phase thus preventing cell division

31
Q

What is S phase

*Nice to know- not on exam

A

DNA synthesis phase

32
Q

What is G2 phase

*Nice to know- not on exam

A

cell growth preceding mitosis

33
Q

What is M phase

*Nice to know- not on exam

A

mitosis, cell division

34
Q

What does nectins and nectin-like substances do in normal cells?

A

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

35
Q

What does nectins and nectin-like substances do in cancer cells?

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

36
Q

What is another name for anti-oncogenes?

A

tumor suppressor genes

37
Q

What do anti-oncogenes do?

A

~Can regulate growth and inhibit carcinogenesis
~Genes that when active decrease risk of a cell becoming metastatic (cancerous)
~Code for proteins

38
Q

In anti-oncogenes, the can code proteins. What does this do?

A

~Have a repressive effect on progression thru the cell cycle
~Promote apoptosis
~Do both

39
Q

P53 Tumor Suppressor Gene

is nicknamed…

A

“The Guardian of the Genome”

40
Q

P53 Tumor Suppressor Gene

A

~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
~Found to be mutated or otherwise disrupted in the majority of all types of cancers

41
Q

Cancer cells and apoptosis

A

~Normal cells are programmed to die at a certain point

~cancer cells keep going (don’t die)

42
Q

Apoptosis occurs in a precisely choreographed series of steps:

*Nice to know- not going to be on exam

A

Cellular membranes are disrupted, the cytoplasmic and nuclear skeletons are broken down
Cytosol is extruded
Chromosomes are degraded, and the nucleus is fragmented
Shriveled cell corpse is engulfed by macrophages & disappear in 24 hours

43
Q

What are the two components of apoptosis?

A

~sensors

~effectors

44
Q

What are sensors?

A

~Cell surface receptors that bind survival or death factors such as: IGF, Interleukins, TNF-alpha & FAS (in TNF family)
~Internal sensors of DNA damage or other abnormality stimulate the release of effector agents

45
Q

What are effectors?

A

Stimulated by abnormality sensors, the mitochondria release chemicals to trigger apoptosis

46
Q

Example of cancer evading apoptosis:

A

~Lymphoma-related oncogenes depressing the FAS death signaling circuit
~Mutation of p53 tumor suppressor gene

47
Q

Self-Building Vascular Supply

A

~Tissue survival requires nutrients & oxygen from blood
~Cells stop growing if they are any greater than a certain distance from a source of oxygen & nutrients
~P53 suppression allows mutation and proliferation

48
Q

Vascular Supply and Cancer cells

A

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)

49
Q

Vessel Anatomy

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

50
Q

Examples of chemotherapy agents that target angiogenesis:

A

~Blocking VEGF receptor (Bevacizumab)
~Interfering with tyrosine kinase (Sunitinib & Sorafenib)
~Interfering with intracellular activator pathways (Sorafenib)

51
Q

Compare normal cells, benign tumors, and malignant tumors- boundaries

A

~Every normal tissue has boundaries
~Benign tumors don’t cross into other tissues, merely pressing against them
~Malignant tumors spread and invade into other tissues
~Cancer cells can break off too, spreading “seeds” around to other parts of the body (“soil”), which grow into new tumors
~90% of cancer deaths come from metastases

52
Q

Metastasizing cells must do what 3 things

A

~Intravasate into the vasculature
~Stop in the microvasculature of the invaded tissue
~Extravasate into the invaded tissue from the vasculature

53
Q

Details about Metastasizing cells must adapt to new environments

A

~Adaption of cellular membrane proteins
~Intercellular signaling
~Changes from one configuration to another in different environments
~Certain cellular environments are conductive to particular tumor growth and others are not – one explanation for selective metastasis (why metastasis occurs in some tissues but not in others with certain cancers)

54
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
~Cancer cells have unlimited dividing potential
~They never stop dividing
~They are true immortal cells

~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

**Easier to understand: The concept states that a normal human cell can only replicate and divide forty to sixty times before it cannot divide anymore, and will break down by programmed cell death or apoptosis. (there’s a limit to how many times the cell can divide.)

55
Q

What is a telomere?

A

~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

56
Q

What would happen without telomeres?

A

~Without telomeres, cells would lose the ends of their chromosomes at cell division, and the information they contain
~Telomeres are disposable buffers blocking the ends of the chromosomes & are consumed during cell division

57
Q

What is a TERT?

A

telomeres replenished by the enzyme telomerase reverse transcriptase (TERT)

58
Q

What do TERTs do?

A

~TERT needed to extend lifespans of certain cells such as fetal stem cells
~TERT activation has been observed in > 90% of all human tumors
~the immortality conferred by telomerase plays a key role in cancer development

59
Q

Limitless reproductive potential due to what two things?

A

~loss of cell cycle checkpoints

~role of telomerase

60
Q

What s the 7th characteristic of cancer?

A

genetic instability

61
Q

Genetics and 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

62
Q

types of mutations that can result in cancer

A

~Changes in single bases
~Insertion of individual bases or sequence
~Chromosome translocations
~Chromosome deletions

63
Q

Inherited genetic instability

A

~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

64
Q

somatic genetic instability

A

~acquired throughout life in individual cells
~not passes on to the next generation
~increased risk of cancer but less so
~not associated with familial syndromes

65
Q

Some familial syndromes known to increase cancer risk:

A

~BRCA1 and BRCA2

66
Q

BRCA1 and BRCA2

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

67
Q

BRCA2 mutation:

A

~risk for leukemia also reported
~Example of “founder” mutation is found in Iceland, where a single BRCA2 mutation accounts for virtually all breast/ovarian cancer families
~A large study in the US
**BRCA2 mutation found in 0.6% of the population
**72% of patients who were found to be carriers had a moderate or strong family history of breast cancer

68
Q

Stats with BRCA1 or BRCA2 mutation:

A

~Women with an abnormal BRCA1 or BRCA2 gene have up to a 60% risk of developing breast cancer
~28% of hereditary breast cancer is caused by BRCA1 mutations
~19%of hereditary breast cancer is caused by BRCA2 mutations
~increase risk of developing ovarian cancer
**55% for BRCA1
**25% for BRCA2

Thompson- spring (13 decks)

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