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ARCHIVED: Pathophysiology > Exam 1: Cancer > Flashcards

Exam 1: Cancer Flashcards

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
Q

What is RAS?

A

Gene that encodes the p21 G protein

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26
Q

What does the p21 G protein do?

A

Promotes cell division/propagation

Transmits a mitogenic signal from activated growth factor receptors

27
Q

What is notable about the RAS gene?

A

Most common gene abnormality in human cancers, especially colon and pancreatic

28
Q

What is MYC? What are CDKs? How are they related?

A

MYC: Nuclear transcription factor that stimulates CDKs
CDKs: Cyclin-dependent kinases - growth related genes

29
Q

How is MYC related to cancer?

A

Most common nuclear transcription factor involved in cancer; particularly breast, lung, and other ca’s

30
Q

What role do CDKs play in the cell cycle?

A

Check the DNA during each phase of the cell cycle, particularly between G1 and S

31
Q

Why is the G1 to S cell cycle phase transition so important in cancer?

A

Most common disregulations affect proteins involved in G1-S transition

32
Q

Role of tumor suppressor genes:

A

Inhibit proliferation and stimulate apoptosis when cell is damaged

33
Q

How are proto-oncogenes and tumor suppressor genes related?

A

Normally are balanced in opposition

34
Q

Most tumor suppressor genes are:

A

Recessive

35
Q

Most oncogene mutations are:

A

Dominant

36
Q

Hereditary cancers vs. sporadic malignancy:

A

Hereditary: earlier development, more locations
Sporadic: later in life, more likely isolated

37
Q

What is p53? How does it act under normal circumstances?

A

Tumor suppressor gene/protein that is normally bound to MDM2, which inhibits/degrades it

38
Q

How does p53 act under stress?

A

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
Q

Relationship between p53 and cancer:

A

Loss of quality control; leads to accumulation/propagation of damaged/mutated cells

40
Q

Structure of p53:

A

Tetrameric

41
Q

Three types of p53 mutations and their consequences:

A

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
Q

Relationship between DNA repair genes and cancer:

A

Lack of DNA repair activity –> more mutations in oncogenes, tumor suppressor genes

43
Q

DNA repair genes implicated in breast ca:

A

BRCA1, BRCA2

44
Q

BRCA1 predisposes women to:

A

Breast and ovarian ca; mutation is almost entirely familial, not sporadic

45
Q

BRCA2 predisposes women to:

A

Breast ca

46
Q

How do cancer cells achieve limitless replicative potential?

A

Upregulation of telomerase

47
Q

What four features of cancer cells are internal?

A

Self-sufficiency in growth hormones
Insensitivity to growth inhibition signals
Evasion of apoptosis
Limitless replicative potential

48
Q

What three features of cancer cells involve their interaction with the environment?

A

Sustained angiogenesis
Ability to invade/metastasize
Evasion of immune response

49
Q

Which vessels typically carry metastatic cancer cells?

A

Veins (easier to degrade, get cells into)

50
Q

What stimulates angiogenesis?

A

Hypoxia

51
Q

What organs typically host metastatic tumors?

A

Liver and lungs due to rich blood supply

52
Q

What do we call the turning point between a tumor being aneovascular and the start of angiogenesis?

A

Angiogenic switch

53
Q

How do cells invade the extracellular matrix?

A

Alterations in cell-cell adhesion molecules
Changes in attachment to basement membrane
Increased activity of matrix degrading enzymes
Autocrine motility factors/chemoattractants

54
Q

How do tumors evade the immune system?

A

No MHC-1 or costimulant; T and B cells ignore the cancer cells

Secretion of immunosuppressant (TGF-b)

55
Q

Causes of cancer:

A

Chemicals (genotoxic and non-genotoxic)
Viruses/bacteria
Radiation

56
Q

How does HPV cause cancer?

A

Synthesizes proteins that inactivate human genes involved in the cell cycle control

57
Q

How does HBV (hep B) cause cancer?

A

Expresses proteins that stimulate proliferation

Injures tissues leading to regenerative processes

58
Q 
Name the associated cancers:
Epstein-Barr
Human papillomavirus
Hepatitis B
Human T-cell lymphotrophic virus
Kaposi's sarcoma-associated herpes virus
A 
Burkitt's lymphoma
Cervical cancer
Liver cancer
Adult T-cell lymphoma
Kaposi's sarcoma
59
Q

General tumor progression pathway:

A

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
Q

What physiologic factors can keep tumors dormant for long periods of time?

A

Lack of sufficient genetic mutation
Lack of blood supply
Immune response of host

61
Q

Nonspecific s/s of cancer:

A 
Weight loss
Fever
Fatigue
Pain
Skin changes
62
Q

Imaging dx of cancer:

A

X-ray, US, CT, PET, MRI, thermal imaging

63
Q

CD99 is specific to:

A

Ewing’s sarcoma

64
Q

Another way to view a tumor is as an:

A

Unorganized organ

ARCHIVED: Pathophysiology (18 decks)

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