Exam 1: Cancer Flashcards Preview

ARCHIVED: Pathophysiology > Exam 1: Cancer > Flashcards

Flashcards in Exam 1: Cancer Deck (64):
1

Define neoplasia:

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

2

Define cancer:

Malignant neoplasia

3

Define carcinoma:

Cancer of epithelial origin

4

Define sarcoma:

Cancer of mesenchymal origin

5

Examples of carcinomas:

Lung
Breast
Colon
Bladder
Prostate

6

Examples of sarcomas:

Fat
Bone
Muscle

7

Define hyperplasia:

Increased number of normal cells

8

Define dysplasia:

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

9

Define anaplasia:

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

10

At what level of abnormal growth does disorganization begin?

Dysplasia

11

What is the key characteristic of anaplasia?

Undifferentiation of cells

12

Characteristics of benign tumors:

Well differentiated cells with preserved functions

Demarcated, often encapsulated, no invasion

No metastasis

13

Characteristics of malignant tumors:

Anaplastic/lack of differentiation

Locally invasive

Metastasis

14

Types of normal adult cells that proliferate:

Bone marrow myeloblasts
Immune cells
Epidermal cells
Epithelial cells
Healing tissue

15

Normally cellular damage is controlled by:

Apoptosis

16

Seven features of a cancer cell:

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

17

Define proto-oncogene:

Genes that encode proteins that normally stimulate cell proliferation

18

Define oncogenes:

Altered forms of proto-oncogenes

In cancer, they have alterations that sustain gain of function

19

Type of mutation that typically happens to proto-oncogenes:

Dominant mutations in somatic cells

20

Oncogenes' impact on growth factors:

Overexpression of autocrine (self-affecting) growth factors

21

Oncogenes' effect on growth factor receptors:

Upregulation in amount or activation

22

Growth factor receptor associated with breast ca:

HER2

Massive # of HER2 found in breast ca

23

Oncogenes' effect on signal transducing proteins:

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

24

Define mitogen:

Chemical substance (usually protein) that encourages mitosis.

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