Bld 204 Exam 3 Hallmarks Of Cancer2

Front 1

Interleaving

Back 1

Alternate the practice of two subjects

Front 2

Limitless Repicative Potential:
Max # of divisions is

Back 2

~60-70

Front 3

Limitless Repicative Potential is due to

Back 3

telomere shortening

Front 4

Limitless Repicative Potential:
Short telomeres are recognized as what happens?

Back 4

As dsDNA breaks leading to senescence
mediated by RB and p53

Front 5

Limitless Repicative Potential:
If RB and p53 are inactivated, what happens?

Back 5

the ends of two chromosomes get connected in a last ditch effort at repair → leads to
dicentric (2 centromeres) chromosomes

Front 6

Limitless Repicative Potential:
Telomerase is usually only present in
_____ _____, which maintains ______ ______

Back 6

-stem cells
-telomere length

Front 7

Limitless Repicative Potential:
Telomerase can be reactivated to maintain
____ ____ in ______ cells.

Back 7

-telomere length
-cancer

Front 8

Limitless Repicative Potential:
_____ _____ leads to telomere shortening

Back 8

Constant Proliferation

Front 9

Limitless Repicative Potential:
Telomere shortening leads to bridge-fusion-breakage cycle when

Back 9

p53 is absent

Front 10

Limitless Repicative Potential:
BFB cycle leads to

Back 10

mutations

Front 11

Limitless Repicative Potential:
When telomerase is reactivated, mutations are fixed and what results?

Back 11

cells continue to divide

Front 12

Development of Sustained Angiogenesis:
Tumors need _____ and _____ too

Back 12

food and oxygen

Front 13

Development of Sustained Angiogenesis:
Tumors bigger than 2mm can't...

Back 13

survive without vascularization

Front 14

Development of Sustained Angiogenesis:
Tumors bigger than 2mm can't survive without vascularization so they must...

Back 14

be able to induce angiogenesis, both benign and malignant tumors

Front 15

Development of Sustained Angiogenesis:
How are tumors vascularized?

Back 15

-neoangiogenesis
-vasculogenesis

Front 16

Neoangiogenesis -

Back 16

new sprouts from capillaries in the area

Front 17

Vasculogenesis -

Back 17

endothelial cells come from the bone marrow to make blood vessels

Front 18

Development of Sustained Angiogenesis:
-In Hypoxia, it stimulates the production of
_______ _______ like ______
-this happens through activation of ______

Back 18

-angiogenesis cytokines, VEGF
-HIF-1alpha

Front 19

Development of Sustained Angiogenesis:
If there's no hypoxia, VHL....

Back 19

binds to HIF-1alpha → signaling for destruction

Front 20

Development of Sustained Angiogenesis:
If there is hypoxia, VHL...

Back 20

no longer binds HIF-1alpha

Front 21

Development of Sustained Angiogenesis:
Angiogenic Factors is like
______ ______ growth factor (VEGF)

Back 21

Vascular Endothelial Growth Factor

Front 22

Development of Sustained Angiogenesis:
In Angiogenic Factors, FGF released from
_____ by ______

Back 22

-ECM
-proteases

Front 23

Development of Sustained Angiogenesis:
Inhibitory Factors (4)

Back 23

-Thrombospondin-1 (TSP-1)
-Protease-produced angiostatin, endostatin, and vasculostatin

Front 24

Development of Sustained Angiogenesis:
Thrombospondin-1 (TSP-1) is
-produced by _____ _______
-synthesis is induced by _____

Back 24

-produced by stromal fibroblasts
-p53

Front 25

Development of Sustained Angiogenesis:
In Cancer, when you lose p53, you lose _____

Back 25

losing p53 = losing TSP-1

Front 26

Development of Sustained Angiogenesis:
In cancer, VHL mutations are associated
with _____ ______

Back 26

renal cancers

Front 27

Development of Sustained Angiogenesis:
In cancer, they produce ____ and _____ that can swing the balance

Back 27

-VEGF and Proteases

Front 28

Ability to Invade and Metastasize:
Metastatic spread by ______ or ______ ______

Back 28

-lymphatics
-blood stream

Front 29

Development of Sustained Angiogenesis:
To invade tissues, you have to divide where?

Back 29

in place

Front 30

Ability to Invade & Metastasize:
Metastasis is the ____________________
with no _____________________________

Back 30

-2nd tumor site
-continuity with the first

Front 31

Ability to Invade & Metastasize:
In lymphatic spread, it's most common in ______
(example)

Back 31

-carcinomas
-carcinoma of the breast, malignant melanoma

Front 32

Ability to Invade & Metastasize:
In lymphatic spread, explain the invasion

Back 32

Invades the lymphatic vessels and spreads up along the lymphatic vessel to the node

Front 33

Ability to Invade & Metastasize:
In lymphatic spread, blood stream and _______ are connected

Back 33

lymphatics

Front 34

Ability to Invade & Metastasize:
In Spread via the bloodstream is most common
in _____

Back 34

sarcomas

Front 35

Ability to Invade & Metastasize:
In Spread via the bloodstream,
invasion can happen in

Back 35

-tumor's new blood vessels (angiogenesis)
-or in nearby normal vasculature

Front 36

Steps of Metastasis via the blood stream: (7)

Back 36

1. Liberation (setting/releasing free)
2. Invasion
3. Transfer as emboli
4. Adhesion at endothelium
5. Migration from vessel
6. Survival (angiogenesis)
7. Multiplication & growth

Front 37

Ability to Invade & Metastasize:
Degree of spread relates to _______

Back 37

survival

Front 38

Ability to Invade & Metastasize:
Common _______ of metastasis have been observe

Back 38

patterns

Front 39

Ability to Invade & Metastasize:
Common Patterns of Metastasis Secondary Sites:

Back 39

-Liver: most common
-Skeleton: second most common, source-breast,kidney,prostate,thyroid
-Brain: sources-lung, breast, adrenals
-Lung: sources-breast, stomach carcinomas, sarcomas
-Adrenals:most frequent endocrine gland site,
source-lung,breast