Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

5224 > Lecture 1 Cancer > Flashcards

Lecture 1 Cancer Flashcards

1
Q

What is cancer

A

a disease of cells involving dynamic changes (mutations) in the genome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are dynamic changes to cancer genome

A

not fixed - genome always changes. Will change before and after therapy -> makes therapy challenging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Three mechanisms of normal control

A

proliferation
differentiation
programmed cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

proliferation

A 
cell growth (number)
in cancer, out of control proliferation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Do cancer cells always grow faster than normal cells?

A

No. Some normal cells (skin and bone marrow) grow very quickly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

differentiation

A

the process by which a less specialized cell becomes a more specialized cell type.
In cancer - lose control of differentiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

de-differentiation

A

loss of differentiation (cancer cells). Happens to different degrees. Can use to grade cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

apoptosis

A

highly regulated in normal cells.

In cancer - resistant to apoptosis - refuse to die

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

poorly differentiated

A

immature cells, not in “order” (slide 5), invade other layers of the cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Tumorigenesis

A

malignant transformation or carcinogenesis. Multi-step process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

steps in tumorigenesis

A

Initiation:
Promotion:
Progression:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

initiation

A

first step: single cell targeted by carcinogen, grows

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

promotion

A

proliferates and shares same original mutations plus more mutations. Preclinical cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

preclincial cancer

A

before diagnosis
challenging to detect
patient feels fine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Progression

A

Clinical cancer

the cancer originally started in one site and spread

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Metastases

A

spreading of cancer from primary tumor - we don’t understand when and how this spreads - cells get into circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Intravasastion

A

tumor cells get into circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

extravasation

A

tumor cells leave circulation and form new mass in new tissue. Liver, lung, and brain are common sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

why do most cancers occur at an older age

A

mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

differences in normal vs cancerous cells

A 
structural 
energy use
blood vessels
growth factors
functional differences
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

structure of normal cell

A

normal cells: divide in orderly way to produce more cells only when body needs them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

structure of cancer cell

A
  • carry mutations for abnormal gene structure or numbers or chromosomes
  • no control or order; leads to a mass of tissue/tumor formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Energy use in normal cell

A

70% Krebs

20% glycolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Energy use in cancer cell

A

Defective Krebs
Most energy from glycolysis - up to 200x higher than normal tissues
either due to poor blood supply or over-expressed mitochondria
glycolysis EVEN in presence of oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

PET scan

A

utilizes high aerobic glycolysis by malignant tumors to diagnose, monitor, and treat by imaging uptake of 2-18F-2-deoxyglucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Blood vessels in normal cells

A

blood vessels that grow with tissue/built-in vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Blood vessels in cancer cells

A

not built in, cells grow first and then need blood supply (angiogenesis - build new vessels). Strategies to block this in cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Growth factor in normal cells

A

balanced amount of growth factors

normal level of activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Growth factor in cancer cells

A

overproduce growth factors = over active cells

30
Q

Function in normal cells

A

produce enzymes and hormones in a balanced manner

31
Q

Function in cancer cells

A

enzymes and hormones are either over or under active

32
Q

How is cancer classified

A

according to tissue it arose from

33
Q

carcinomas

A

from epithelial cells (line organs and skin)

34
Q

sarcomas

A

from connective or other deeper tissues (bone, cartilage, fat, muscle, vessels) and soft tissue

35
Q

Leukemia

A

Cancer of the blood (only circulatory cancer - all others are fixed)

36
Q

Lymphoma

A

cancer of the lymphatic system. Occur in a wide range of tissues/organs

37
Q

Which cancers are solid tumor

A

carcinoma
sarcoma
lymphoma

38
Q

Cancer staging describes

A

how far cancer (neoplasm) has spread anatomically (if metastasis has occurred)

39
Q

is staging applicable to leukemia

A

No b/c blood is not localized

40
Q

two staging systems for solid tumors

A
  1. the overall stage grouping system

2. tumor, nodes, and metastases (TNM) system

41
Q

what is the most powerful predictor of surival

A

stage at diagnosis - tx are often changed based on stage (dynamic)

42
Q

Stages 0 and I

A

small, localized cancers that are usually curable

43
Q

Stages II and III

A

Locally advanced and/or involvement of local lymph nodes

44
Q

Stage IV

A

Inoperable or metastatic cancer

45
Q

Locally advanced cancer

A

has spread from site of primary (original) tumor only to surrounding tissue or lymph nodes

46
Q

In situ

A

cancer that involves only the place in which it began and that has not spread

47
Q

TNM system

A

T: extent of primary tumor
T0 (in situ) or T4 (extensive invasion to other organs)
N: amount of regional lymph node involvement
N0 (none) or N4 (extensive)
M0: no metastasis
M1: metastasis

48
Q

Tumor Grading

A

measure of how abnormal cells appear under the microscope
degree of differentiation from parent tissue
Cancer cells often lack differentiation

49
Q

Gx

A

grade cannot be assessed (least aggressive)

50
Q

G1

A

well differentiated

51
Q

G2

A

moderately differentiated

52
Q

G3

A

poorly differentiated

53
Q

G4

A

undifferentiated (most aggressive)

54
Q

Etiology of cancer

A 
tobacco use
alcohol
radiation
dietary habits
chemicals
viruses
heredity (not environmental like others)
55
Q

Tobacco

A

30% of cancer deaths in USA
90% lung cancer due to smoking
lung, esophageal, bladder, and pancreatic cancer

56
Q

Alcohol

A

Can cause cancer in upper GI tract by increasing permeability of mucosa to carcinogens
indirect cause of cancer

57
Q

Radiation

A

Solar: squamous and basal cell carcinoma and melanoma
Ionizing: associated with development of leukemia and thyroid cancer

58
Q

Dietary habit that increase cancer risk

A

high fat, high calories
alcohol
salt cured, smoked, or charred foods
nitrate and nitrite

59
Q

Chemicals

A

Aflatoxin -> hepatoma (commonly found in mold)
Aromatic amines -> bladder cancer
Asbestos -> lung, mesothelioma (difficult to tx, doesn’t respond to drugs)
Benzene -> leukemia
Vinyl chloride -> liver angiosarcoma

60
Q

Viruses

A 
Epsein-Barr Virus -> non-hodgkin's lymphoma and nasopharyngeal cancer 
HIV -> Kaposi's sarcoma and lymphoma
HTLV1 -> cutaneous T-cell lymphoma
HPV -> cervical cancer
Hep B -> liver cancer
61
Q

EBV is associated with

A

Burkitt lymphoma (Africa) and nasopharyngeal carcinoma (mainly SE Asia)

62
Q

Genetic changes that lead to cancer

A
  1. activation of proto-oncogenes to oncogenes

2. inactivation of tumor suppressor genes

63
Q

What are proto-oncogenes

A

normal genes whose protein products stimulate growth and viability of cells
Also include genes that contribute to tumor growth by inhibiting cell death

64
Q

proto-oncogene examples

A

EGFR: duplications
HER2: amplifications
BCL2: overexpression

65
Q

What are oncogenes

A

mutated or damaged genes that contribute to tumor growth (defective proto-oncogenes

66
Q

proto-oncogenes activated to oncogenes by

A

mutation or amplification, chromosome abnormality (driver mutations), increased protein expression

67
Q

Epigenetics

A

WT sequence but expression level may be changed (increased)

68
Q

Tumor suppressor genes

A

genes whose protein products can directly or indirectly prevent cell division or lead to cell death

69
Q

Tumor suppressor genes inactivated by

A

mutation or deletion
decrease of protein expression
ex: P53

70
Q

How many pts can be cured? With chemo alone?

A

50%

Chemo alone only 10-15%

71
Q

Methods of cancer tx

A
  • surgery
  • radiotx
  • chemotherapy**
  • targeted tx**
  • Biologics (immunotx)**
  • photodynamic tx
  • endoscopic procedure
  • complementary and alt. tx
  • supportive tx
72
Q

Treatment depends on what

A

type of cancer, stage, and grade

5224 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions