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5224 > Lecture 1 Cancer > Flashcards

Lecture 1 Cancer Flashcards

(72 cards)

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1
Q

What is cancer

A

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

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2
Q

what are dynamic changes to cancer genome

A

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

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3
Q

Three mechanisms of normal control

A

proliferation
differentiation
programmed cell death

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4
Q

proliferation

A 
cell growth (number)
in cancer, out of control proliferation
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5
Q

Do cancer cells always grow faster than normal cells?

A

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

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6
Q

differentiation

A

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

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7
Q

de-differentiation

A

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

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8
Q

apoptosis

A

highly regulated in normal cells.

In cancer - resistant to apoptosis - refuse to die

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9
Q

poorly differentiated

A

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

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10
Q

Tumorigenesis

A

malignant transformation or carcinogenesis. Multi-step process

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11
Q

steps in tumorigenesis

A

Initiation:
Promotion:
Progression:

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12
Q

initiation

A

first step: single cell targeted by carcinogen, grows

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13
Q

promotion

A

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

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14
Q

preclincial cancer

A

before diagnosis
challenging to detect
patient feels fine

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15
Q

Progression

A

Clinical cancer

the cancer originally started in one site and spread

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16
Q

Metastases

A

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

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17
Q

Intravasastion

A

tumor cells get into circulation

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18
Q

extravasation

A

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

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19
Q

why do most cancers occur at an older age

A

mutations

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20
Q

differences in normal vs cancerous cells

A 
structural 
energy use
blood vessels
growth factors
functional differences
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21
Q

structure of normal cell

A

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

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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
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23
Q

Energy use in normal cell

A

70% Krebs

20% glycolysis

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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

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25
PET scan
utilizes high aerobic glycolysis by malignant tumors to diagnose, monitor, and treat by imaging uptake of 2-18F-2-deoxyglucose
26
Blood vessels in normal cells
blood vessels that grow with tissue/built-in vessels
27
Blood vessels in cancer cells
not built in, cells grow first and then need blood supply (angiogenesis - build new vessels). Strategies to block this in cancer
28
Growth factor in normal cells
balanced amount of growth factors | normal level of activity
29
Growth factor in cancer cells
overproduce growth factors = over active cells
30
Function in normal cells
produce enzymes and hormones in a balanced manner
31
Function in cancer cells
enzymes and hormones are either over or under active
32
How is cancer classified
according to tissue it arose from
33
carcinomas
from epithelial cells (line organs and skin)
34
sarcomas
from connective or other deeper tissues (bone, cartilage, fat, muscle, vessels) and soft tissue
35
Leukemia
Cancer of the blood (only circulatory cancer - all others are fixed)
36
Lymphoma
cancer of the lymphatic system. Occur in a wide range of tissues/organs
37
Which cancers are solid tumor
carcinoma sarcoma lymphoma
38
Cancer staging describes
how far cancer (neoplasm) has spread anatomically (if metastasis has occurred)
39
is staging applicable to leukemia
No b/c blood is not localized
40
two staging systems for solid tumors
1. the overall stage grouping system | 2. tumor, nodes, and metastases (TNM) system
41
what is the most powerful predictor of surival
stage at diagnosis - tx are often changed based on stage (dynamic)
42
Stages 0 and I
small, localized cancers that are usually curable
43
Stages II and III
Locally advanced and/or involvement of local lymph nodes
44
Stage IV
Inoperable or metastatic cancer
45
Locally advanced cancer
has spread from site of primary (original) tumor only to surrounding tissue or lymph nodes
46
In situ
cancer that involves only the place in which it began and that has not spread
47
TNM system
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
Tumor Grading
measure of how abnormal cells appear under the microscope degree of differentiation from parent tissue Cancer cells often lack differentiation
49
Gx
grade cannot be assessed (least aggressive)
50
G1
well differentiated
51
G2
moderately differentiated
52
G3
poorly differentiated
53
G4
undifferentiated (most aggressive)
54
Etiology of cancer
``` tobacco use alcohol radiation dietary habits chemicals viruses heredity (not environmental like others) ```
55
Tobacco
30% of cancer deaths in USA 90% lung cancer due to smoking lung, esophageal, bladder, and pancreatic cancer
56
Alcohol
Can cause cancer in upper GI tract by increasing permeability of mucosa to carcinogens indirect cause of cancer
57
Radiation
Solar: squamous and basal cell carcinoma and melanoma Ionizing: associated with development of leukemia and thyroid cancer
58
Dietary habit that increase cancer risk
high fat, high calories alcohol salt cured, smoked, or charred foods nitrate and nitrite
59
Chemicals
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
Viruses
``` 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
EBV is associated with
Burkitt lymphoma (Africa) and nasopharyngeal carcinoma (mainly SE Asia)
62
Genetic changes that lead to cancer
1. activation of proto-oncogenes to oncogenes | 2. inactivation of tumor suppressor genes
63
What are proto-oncogenes
normal genes whose protein products stimulate growth and viability of cells Also include genes that contribute to tumor growth by inhibiting cell death
64
proto-oncogene examples
EGFR: duplications HER2: amplifications BCL2: overexpression
65
What are oncogenes
mutated or damaged genes that contribute to tumor growth (defective proto-oncogenes
66
proto-oncogenes activated to oncogenes by
mutation or amplification, chromosome abnormality (driver mutations), increased protein expression
67
Epigenetics
WT sequence but expression level may be changed (increased)
68
Tumor suppressor genes
genes whose protein products can directly or indirectly prevent cell division or lead to cell death
69
Tumor suppressor genes inactivated by
mutation or deletion decrease of protein expression ex: P53
70
How many pts can be cured? With chemo alone?
50% | Chemo alone only 10-15%
71
Methods of cancer tx
- surgery - radiotx - chemotherapy** - targeted tx** - Biologics (immunotx)** - photodynamic tx - endoscopic procedure - complementary and alt. tx - supportive tx
72
Treatment depends on what
type of cancer, stage, and grade

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