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ARCHIVED: Pathophysiology > Exam 1: Cancer > Flashcards

Exam 1: Cancer Flashcards

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1
Q

Define neoplasia:

A

Abnormal growth of tissue resulting from loss of response to growth control signals

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2
Q

Define cancer:

A

Malignant neoplasia

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3
Q

Define carcinoma:

A

Cancer of epithelial origin

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4
Q

Define sarcoma:

A

Cancer of mesenchymal origin

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5
Q

Examples of carcinomas:

A 
Lung
Breast
Colon
Bladder
Prostate
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6
Q

Examples of sarcomas:

A

Fat
Bone
Muscle

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7
Q

Define hyperplasia:

A

Increased number of normal cells

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8
Q

Define dysplasia:

A

Cellular and nuclear changes leading to loss of uniformity, abnormal organization

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9
Q

Define anaplasia:

A

Undifferentiated atypical cells varying in size/shape, loss of organization

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10
Q

At what level of abnormal growth does disorganization begin?

A

Dysplasia

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11
Q

What is the key characteristic of anaplasia?

A

Undifferentiation of cells

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12
Q

Characteristics of benign tumors:

A

Well differentiated cells with preserved functions

Demarcated, often encapsulated, no invasion

No metastasis

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13
Q

Characteristics of malignant tumors:

A

Anaplastic/lack of differentiation

Locally invasive

Metastasis

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14
Q

Types of normal adult cells that proliferate:

A 
Bone marrow myeloblasts
Immune cells
Epidermal cells
Epithelial cells
Healing tissue
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15
Q

Normally cellular damage is controlled by:

A

Apoptosis

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16
Q

Seven features of a cancer cell:

A 
Self-sufficiency
Insensitivity to growth inhibitory signals
Evasion of apoptosis
Limitless replicative potential
Sustained angiogenesis
Ability to invade and metastasize
Evasion of host immune response
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17
Q

Define proto-oncogene:

A

Genes that encode proteins that normally stimulate cell proliferation

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18
Q

Define oncogenes:

A

Altered forms of proto-oncogenes

In cancer, they have alterations that sustain gain of function

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19
Q

Type of mutation that typically happens to proto-oncogenes:

A

Dominant mutations in somatic cells

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20
Q

Oncogenes’ impact on growth factors:

A

Overexpression of autocrine (self-affecting) growth factors

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21
Q

Oncogenes’ effect on growth factor receptors:

A

Upregulation in amount or activation

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22
Q

Growth factor receptor associated with breast ca:

A

HER2

Massive # of HER2 found in breast ca

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23
Q

Oncogenes’ effect on signal transducing proteins:

A

Keeps them turned on (GTP remains unhydrolyzed and activated) so there is constant signal input from GF receptors

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24
Q

Define mitogen:

A

Chemical substance (usually protein) that encourages mitosis.

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25
What is RAS?
Gene that encodes the p21 G protein
26
What does the p21 G protein do?
Promotes cell division/propagation Transmits a mitogenic signal from activated growth factor receptors
27
What is notable about the RAS gene?
Most common gene abnormality in human cancers, especially colon and pancreatic
28
What is MYC? What are CDKs? How are they related?
MYC: Nuclear transcription factor that stimulates CDKs CDKs: Cyclin-dependent kinases - growth related genes
29
How is MYC related to cancer?
Most common nuclear transcription factor involved in cancer; particularly breast, lung, and other ca's
30
What role do CDKs play in the cell cycle?
Check the DNA during each phase of the cell cycle, particularly between G1 and S
31
Why is the G1 to S cell cycle phase transition so important in cancer?
Most common disregulations affect proteins involved in G1-S transition
32
Role of tumor suppressor genes:
Inhibit proliferation and stimulate apoptosis when cell is damaged
33
How are proto-oncogenes and tumor suppressor genes related?
Normally are balanced in opposition
34
Most tumor suppressor genes are:
Recessive
35
Most oncogene mutations are:
Dominant
36
Hereditary cancers vs. sporadic malignancy:
Hereditary: earlier development, more locations Sporadic: later in life, more likely isolated
37
What is p53? How does it act under normal circumstances?
Tumor suppressor gene/protein that is normally bound to MDM2, which inhibits/degrades it
38
How does p53 act under stress?
Releases from MDM2 and stimulates transcription of p21 (not the same p21 as RAS encodes for) which leads to G1 growth arrest and activates DNA repair systems
39
Relationship between p53 and cancer:
Loss of quality control; leads to accumulation/propagation of damaged/mutated cells
40
Structure of p53:
Tetrameric
41
Three types of p53 mutations and their consequences:
Loss of function: not harmful alone, does not interfere with complex's function Gain of function: changes transcription process; activates different genes; stops cell cycle arrest/apoptosis; can even stimulate proliferation Dominant mutant allele: prevents complex from functioning altogether; cannot even bind to target gene promoters
42
Relationship between DNA repair genes and cancer:
Lack of DNA repair activity --> more mutations in oncogenes, tumor suppressor genes
43
DNA repair genes implicated in breast ca:
BRCA1, BRCA2
44
BRCA1 predisposes women to:
Breast and ovarian ca; mutation is almost entirely familial, not sporadic
45
BRCA2 predisposes women to:
Breast ca
46
How do cancer cells achieve limitless replicative potential?
Upregulation of telomerase
47
What four features of cancer cells are internal?
Self-sufficiency in growth hormones Insensitivity to growth inhibition signals Evasion of apoptosis Limitless replicative potential
48
What three features of cancer cells involve their interaction with the environment?
Sustained angiogenesis Ability to invade/metastasize Evasion of immune response
49
Which vessels typically carry metastatic cancer cells?
Veins (easier to degrade, get cells into)
50
What stimulates angiogenesis?
Hypoxia
51
What organs typically host metastatic tumors?
Liver and lungs due to rich blood supply
52
What do we call the turning point between a tumor being aneovascular and the start of angiogenesis?
Angiogenic switch
53
How do cells invade the extracellular matrix?
Alterations in cell-cell adhesion molecules Changes in attachment to basement membrane Increased activity of matrix degrading enzymes Autocrine motility factors/chemoattractants
54
How do tumors evade the immune system?
No MHC-1 or costimulant; T and B cells ignore the cancer cells Secretion of immunosuppressant (TGF-b)
55
Causes of cancer:
Chemicals (genotoxic and non-genotoxic) Viruses/bacteria Radiation
56
How does HPV cause cancer?
Synthesizes proteins that inactivate human genes involved in the cell cycle control
57
How does HBV (hep B) cause cancer?
Expresses proteins that stimulate proliferation | Injures tissues leading to regenerative processes
58
``` Name the associated cancers: Epstein-Barr Human papillomavirus Hepatitis B Human T-cell lymphotrophic virus Kaposi's sarcoma-associated herpes virus ```
``` Burkitt's lymphoma Cervical cancer Liver cancer Adult T-cell lymphoma Kaposi's sarcoma ```
59
General tumor progression pathway:
Mutation inactivates suppressor gene (p53) Cells proliferate Mutations inactivate DNA repair genes (BRCA) Proto-oncogenes mutate to oncogenes (MYC) More mutations, more genetic instability, metastatic disease
60
What physiologic factors can keep tumors dormant for long periods of time?
Lack of sufficient genetic mutation Lack of blood supply Immune response of host
61
Nonspecific s/s of cancer:
``` Weight loss Fever Fatigue Pain Skin changes ```
62
Imaging dx of cancer:
X-ray, US, CT, PET, MRI, thermal imaging
63
CD99 is specific to:
Ewing's sarcoma
64
Another way to view a tumor is as an:
Unorganized organ

ARCHIVED: Pathophysiology (18 decks)

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