Cancer Flashcards

(41 cards)

1
Q

Most mutations are ______ and occur _______. They require _______

A

Somatic
post-fertilization
Multiple mutations

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2
Q

Oncogenes

A

Promote cell growth and division

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3
Q

Try more suppressor classes (2)

A

Caretaker

Gatekeeper

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4
Q

Caretaker genes

A

Prevent or repair damage to DNA

Lose these genes = promote genetic change

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5
Q

Gatekeeper

A

Restrain cell division or induce apoptosis

Lose these genes = uncontrolled proliferation

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6
Q

Loss of heterogeneity

A

Inheriting one bad copy can cause the good copy to go “bad”

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7
Q

Retinoblastoma caused by

A

Loss of function of Rb

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8
Q

Rb inhibits ____ which inhibits _____

A

E2F
G1/S transition
Rb prevents cell division

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9
Q

Sporadic Retinoblastoma

A

Late and rarely

1 tumor in 1 eye in 1 person in a family

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10
Q

Familial Retinoblastoma

A

Early and often
Bilateral tumors
Multiple members affected

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11
Q

P53 stimulates txn of: (2)

A

CDK inhibitors

Pro-apoptotic factors

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12
Q

P53 is destabilized by _____

A

Mdm2

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13
Q

P53 is stabilized by: (2)

A

DNA damage

P14ARF

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14
Q

P14ARF is a ______ made from _______ which encodes _______

A

Protein
Growth factors
CDK inhibitors

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15
Q

Proto-oncogene

A

Gene that can become an oncogene if mutated or expression increases

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16
Q

Oncogenes

A

Can cause cancer when activated or expressed

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17
Q

MTOR pathway

A

Promotes cell growth and protein synthesis

Commonly mutated in tumors

18
Q

Viral oncogenes

A

Normally promote cell division

Derived from genome of host cell

19
Q

Overproduction of c-myc by: (2)

A
Gene amplification (inc. number of gene copies)
Chromosomal translocations to inc. txn of c-myc
20
Q

Homogenously-staining region

A

Amplification of c-myc

Copies are duplicated in same region inside chromosome

21
Q

Double minute chromosome

A

Amplification of c-myc

Duplicated copies in same region outside of chromosome

22
Q

Detect overproduction of c-myc by:

A

Metaphase FISH

23
Q

Burkett Lymphoma

A

B lymphocyte cancer

C-myc controlled by antibody gene enhancer which increases lymphomas

24
Q

C-abl

A

Changes genetically to self-activate

Does NOT need regulatory stimuli

25
NF1 proteins is a
Ras-GAP | Mutation leads to Neurofibromatosis
26
Ras family (2)
Receptor signaling | Cell division
27
Ran family
Nucleus/ cytoplasm traffic
28
Rac family
Actin cytoskeleton
29
Rab family
Traffic of membrane vesicles
30
Oncogenic mutations in Ras
AA substitutions of gly12 and gln61 Reduce GTPase activity or ras Mostly in active state
31
C-ras mutation prevents
Inactivation
32
Clinical features of CML (3 main ones)
Splenomegaly Elevated WBC count Early satiety
33
CML is a ________ disorder so it _________ but does NOT ______
Myeloproliferative Increases proliferation Lose ability to differentiate
34
CML cause is a
Balanced translocation of chr22 (bcr) and chr9 (abl)
35
Philadelphia chromosome
Chimeric protein from the translocation
36
C-abl regulates ______ and is normally located in the _____
DNA damage repair response and promotes growth | Nucleus
37
Bcr-abl protein is
Trapped in the cytoplasm thereby altering the DNA damage repair response Constitutively active
38
Bc-abl promotes CML development by: (3)
Uncontrolled proliferation Escapes apoptosis Alter interaction with ECM
39
C-abl gains ______from bcr to facilitate _____
A domain | Dimerization
40
C-abl creates a ______ so it can _____ to ________
Gain of function Auto-phosphorylate Become active
41
C-abl is able to auto-phosphorylate because
It's a tyrosine kinase