Cancer Flashcards

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
Q

NF1 proteins is a

A

Ras-GAP

Mutation leads to Neurofibromatosis

26
Q

Ras family (2)

A

Receptor signaling

Cell division

27
Q

Ran family

A

Nucleus/ cytoplasm traffic

28
Q

Rac family

A

Actin cytoskeleton

29
Q

Rab family

A

Traffic of membrane vesicles

30
Q

Oncogenic mutations in Ras

A

AA substitutions of gly12 and gln61
Reduce GTPase activity or ras
Mostly in active state

31
Q

C-ras mutation prevents

A

Inactivation

32
Q

Clinical features of CML (3 main ones)

A

Splenomegaly
Elevated WBC count
Early satiety

33
Q

CML is a ________ disorder so it _________ but does NOT ______

A

Myeloproliferative
Increases proliferation
Lose ability to differentiate

34
Q

CML cause is a

A

Balanced translocation of chr22 (bcr) and chr9 (abl)

35
Q

Philadelphia chromosome

A

Chimeric protein from the translocation

36
Q

C-abl regulates ______ and is normally located in the _____

A

DNA damage repair response and promotes growth

Nucleus

37
Q

Bcr-abl protein is

A

Trapped in the cytoplasm thereby altering the DNA damage repair response
Constitutively active

38
Q

Bc-abl promotes CML development by: (3)

A

Uncontrolled proliferation
Escapes apoptosis
Alter interaction with ECM

39
Q

C-abl gains ______from bcr to facilitate _____

A

A domain

Dimerization

40
Q

C-abl creates a ______ so it can _____ to ________

A

Gain of function
Auto-phosphorylate
Become active

41
Q

C-abl is able to auto-phosphorylate because

A

It’s a tyrosine kinase