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MCM Exam II > Cell Cycle, Apoptosis, Cancer > Flashcards

Cell Cycle, Apoptosis, Cancer Flashcards

1
Q

in interphase, what happens at G1, S, and G2

A

G1: RNA and protein synthesis needed for DNA replication

S: DNA synthesis

G2: DNA stability is checked

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2
Q

G0 phase

A

In poor nutrient/environmental conditions, cells withdraw from the cell cycle

Also occurs following terminal differentiation in certain tissue types (brain, neurons, cardiac muscle, RBCs)

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3
Q

When is histone synthesis and centrosome formation

A

During S phase

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4
Q

Where is the one restriction point and three checkpoints in the cell cycle

A

Restriction point at the end of G1 two hours before S phase

  1. G1 checkpoint
  2. G2 checkpoint
  3. Metaphase checkpoint in M phase
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5
Q

How do growth factors affect the cell cycle

A

If growth factors are limiting then restriction occurs

Progression following the exit from restriction is growth factor independent

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6
Q

When does G1 checkpoint occur

A

At end of G1 phase in response to DNA damage

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7
Q

What is the purpose of the G2 checkpoint

A

To verify complete genomic duplication

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8
Q

What is the purpose of the metaphase checkpoint

A

Ensures that chromosomes are attached to the mitotic spindle

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9
Q

Mutations in Aurora B and BUB1 in spindle assembly cause

A

Colorectal, lung, and pancreatic tumors and T cell lymphomas

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10
Q

Mutations in BUB1B, BUB3 and MPS1 in spindle assembly cause

A

Colorectal cancer, lymphomas, MVA and PC55

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11
Q

Mutations in ATM during chromosome condensation cause

A

Lymphomas and breast cancer

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12
Q

ATR mutations in chromosome condensation cause

A

Stomach, endometrial, and breast cancer

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13
Q

CHK1 mutations in chromosome condensation cause

A

Stomach, endometrial, colorectal, and lung cancers

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14
Q

CDK1 and PLK1 mutations in centrosome duplications cause

A

Cancers of the liver, lung, stomach, and epidermis

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15
Q

Aurora A mutations in centrosome duplication cause

A

Several human tumors, for example, breast and colorectal cancers

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16
Q

CDK4 mutations in G0 phase cause

A

Melanoma, gliobastoma, osteosarcoma, and breast and Cervical cancers

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17
Q

CDK6 mutations in RB inactivation cause

A

Lymphomas, squamous cell cancer, and gloom a

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18
Q

CHK2 mutations before DNA replication in G1 cause

A

Bladder, colon, ovary, and other cancers

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19
Q

Myc

  • what is it
  • how does it regulate cellular division
A

Transcription factor

Increases CDK levels in G1
—>
which phosphorylates Rb
—>
which releases E2F allowing cell to enter S phase
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20
Q

How do cyclins affect cell division

A

Cyclin D-CDK4
Cyclin D-CDK6

Hyperphosphorylate Rb which releases E2F —> cell enters S phase

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21
Q

How does E2F allow the cell to enter and stay in the S phase

A

E2F has transcription genes for Cyclin E (so that the cell can transition to S phase) and Cyclin A (to keep Rb in hyperphosphorylated state)

Both Cyclin E and A activate CDK2 which maintains the hyperphosphorylation of Rb

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22
Q

Cyclins

A

Proteins that interact with and regulate CDK activity

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23
Q

How is cyclin-CDK activity inhibited

A

P27 and WEE1 inhibit the cyclin-CDK complex by inactivating the kinase activity of cyclin-CDK

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24
Q

CAK

A

CDK-activating kinase

Fully activates the cycle-CDK complex by phosphorylating the T loop that blocks the active site of the complex

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25
Q

G1 cyclin (D)

  • function
  • Cyclin-DKA complex(es)
A

Helps the passage of cells through the restriction point in late G1 phase

Cyclin D-CDK4
Cyclin D-CDK6

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26
Q

WEE1 kinase

A

Inhibits CDK activity by phosphorylating the “roof site”

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27
Q

Cdc25

A

Dephosphorylates “roof site” to increase CDK activity

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28
Q

P27

A

A type of CDK inhibitory protein (CKI)

Binds to both CDK and cyclin; primarily regulates early in cell cycle events (like G1 —> S)

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29
Q

APC/C

A

Anaphase promoting complex (also called cyclosome)

Key regulator in progression from metaphase to anaphase

Activated by binding to Cdc20
—> polyubiquinates its substrates (including S- and M- cyclin complexes)
—> cyclins targeted for destruction
—> absence of cyclins inactivates CDK

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30
Q

Cdc20

A

Activates APC/C

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31
Q

P53

A

Guardian of the genome

Normally kept inactive by E3 ubiquitin ligase (MDM2)

Stimulated by DNA damage and activated by phosphorylation
—> increase in p21 (a CKI)
—> cell cycle arrest

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32
Q

P21

A

A cyclin-dependent kinase inhibitor (CKI)

Active p53 causes transcription of the gene p21 which leads to inactivation of cyclin-CDK complexes for G1/S transition (CDK2); this keeps RB hypophosphorylated and active which sequesters E2F

Capable of inhibiting all cyclin/CDK complexes, but primarily associated with inhibition of CDK2

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33
Q

MDM2

A

Keeps p53 inactive in normal state

An E3 ubiquitin ligase

34
Q

Internal stimuli for apoptosis pathways

A

Abnormalities in DNA

35
Q

External stimuli for apoptosis pathways

A

Removal or survival factors

Proteins of tumor necrosis factor family (TNF-a)

36
Q

Intrinsic pathway of apoptosis

A

Mitochondrial dependent (cytochrome C is leaked from the mitochondria)

Activates apoptosome formation 
—> procaspase-9 (inactive)
—> caspace-9 (active) 
—> caspaces-3,6,7
—> apoptosis
—> phagocytosis
37
Q

Extrinsic pathway for apoptosis

A

Fas ligand binds to Fas receptor of membrane
—> procaspase-8
—> rest of cycle

TNF-a binds to TNF-a receptor on membrane
—> caspase-8
—> caspases-3,6,7
—> apoptosis

38
Q

BAX/BCL-2

A

Key regulator in intrinsic apoptosis pathway

39
Q

Initiator caspases

A

Caspase-8

Caspase-9

40
Q

Executioner caspase

A

Caspase-3

Executes apoptosis

41
Q

Apaf1 in the intrinsic pathway of apoptosis

A

Activated by the release of cytochrome C from the mitochondria

Activates BAX

Forms the apoptosome

Cytochrome c/Apaf1 complex activates caspase-9

42
Q

Proto-oncogene

A 
Growth factors
Receptors for growth factors and hormones
Transcription factors
Signal transducers
^normally promotes cell cycle

Gain of function mutations —> oncogene

43
Q

Oncogenes

A

Increase expression of protein products

Express altered proteins (oncoproteins) that do not respond to normal signals

44
Q

How do oncogenes cause breast cancer

A

HER2 receptor has a valine to glutamine mutation

Receptors dimerize and tyrosine kinase activity activated in absence of ligand (over-expression of HER2) causing breast cancer

45
Q

How do oncogenes cause glioblastoma

A

EGF receptor has a deletion mutation and the receptor’s tyrosine kinase activity is constitutively active causing gliobastoma

46
Q

How do oncogenes cause chronic myelogenous leukemia (CML)

A

Translocation between chromosome 9 and 22 producing BCR-ABL gene, which expresses the BCR-ABL fusion protein causing CML

47
Q

Retinoblastoma (Rb)

A

Tumor suppressor

Remains hypophosphorylated and sequesters E2F, blocking G1/S transition

When it is hyperphosphorylated by cyclin D-CDK4 and cyclin D-CDK6 it becomes inactive and released E2F which will then transition the cell to the S phase

48
Q

How is retinoblastoma (the phenotype) caused

A

Mutation/deletion of both copies of RB1 is needed to cause cancer (“two-hit hypothesis”)

Somatic mutation occurs and eliminates the second good copy of the gene which causes tumors form in highly proliferative tissues

49
Q

Sporadic form of retinoblastoma

A

Non hereditary

Abnormality in the RB1 gene develops on its own in only one cell in one eye

Found at a later age than hereditary retinoblastoma

50
Q

RB1 gene

  • what does it do
  • what do mutations cause
  • where is the mutation
A

Encodes pRb (Rb) protein

Mutations cause 100% of retinoblastoma

Chromosome 13 (regulates G1 phase of cell cycle)

51
Q

TP53

  • what does it do
  • what do mutations cause
A

Encodes p53

Mutations cause:

  • 65% colon cancers
  • 30%-50% breast cancers
  • 50% lung cancers
52
Q

PTEN (phosphate and tensin homolog)

  • what do mutations cause
A

70% of prostate cancers

53
Q

APC (adenomatous polyposis coli)

  • what do mutations cause
  • where is the mutation
A

Colon cancer (family adenomatous polyposis)

Mutation is in chromosome 5 which regulates cell proliferation

54
Q

What do metastasis suppressors do

A

They’re cell adhesion proteins

  • prevent tumor cells from dispersing
  • block loss of contact inhibition
  • inhibit tumor metastasis
55
Q

NF-1 gene

  • where is it located
  • what does it normally do
  • what does the mutated product do
A

Chromosome 17

Encodes p120GAP which normally turns off activated RAS protein

Causes neurofibromatosis

56
Q

BRCA1/BRCA2 gene

  • where is it located
  • what is its normal function
  • mutated product does what
A

Chromosome 17

Role in DNA repair and apoptosis

Breast cancer

57
Q

DCC gene

  • where is it
  • what does it normally do
  • mutated form does what
A

Chromosome 18

Role in cell proliferation, migration, and apoptosis

Colon cancer

58
Q

6 hallmarks of cancer

A
  1. Ability to grow along (oncogenes)
  2. Tumor suppressor failure
  3. Invading and metastasis
  4. Telomerase up-activation
  5. Angiogenesis
  6. Resisting cell death from apoptosis
59
Q

4 gene alterations than can lead to metastasis

A
  • loss of APC
  • activation of RAS
  • loss of a tumor suppressor gene
  • loss of p53 gene
60
Q

How can viruses cause cancer

A
  • normal virus infects host
  • viral genome incorporates into host genome next to proto-oncogene
  • virus replications containing proto-oncogene
  • proto-oncogene mutates into oncogene
  • virus containing oncogene infects normal cell transforming it into a tumor cell
61
Q

How does HPV cause cancer

A
  • E6+ binds to p53
  • degrades p53 and loses tumor suppression

Or

  • E7 binds to RB
  • Rb becomes inactive and releases E2F
62
Q

Epstein Barr Virus is associated with what tumors

A

Burkitt lymphoma

Nasopharyngeal carcinoma

63
Q

Hepatitis B virus is associated with what tumors

A

Liver cancer (hepatocellular carcinoma)

64
Q

HPV is associated with what tumors

A

Benign warts

Cervical and uterine cancers

65
Q

Human T Cell leukemia virus type 1 (HTLV-1) is associated with what cancer

A

Adult T cell leukemia/lymphoma

66
Q

Kaposi sarcoma-associates herpesvirus (KSHV) is associated with what cancer

A

Kaposi sarcoma

67
Q

How to alkylating agents act as chemotherapeutic agents

A

Block dna replication

68
Q

How do antimetabolites act as chemotherapeutic agents

A

Inhibit enzymes involved in dna synthesis

69
Q

How do topoisomerase I inhibitors act as chemotherapeutic agents

A

Inhibit topoisomerase I, an enzyme that removes supercoils in dna

70
Q

How to topoisomerase II inhibitors act as chemotherapeutic agents

A

Inhibit topoisomerase II, an enzyme that resolves tangles in DNA

71
Q

How to cytotoxic antibiotics act as chemotherapeutic agents

A

Intercalated between bases in dna to inhibit dna synthesis

72
Q

How do mitotic inhibitors act as chemotherapeutic agents

A

Arrest cells in mitosis during metaphase

73
Q 
Ifosfamide
Cyclophosphamide
Treosulfane
Carboplatin
Cisplatin
A

Alkylating agents

Chemotherapy

74
Q 
Cytarabine
5-fluorouracil
Gemcitaine
Mercaptopurine
Methotrexate
A

Antimetabolites

chemotherapy

75
Q

Etoposide

Teniposide

A

Topoisomerase I inhibitors

Chemotherapy

76
Q

Topotecan

A

Topoisomerase II inhibitor

Chemotherapy

77
Q

Daunorubicin
Doxorubicin
Epiruicin
Mitoxantrone

A

Cytotoxic antibiotics

Chemotherapy

78
Q 
Docetaxel
Paclitaxel
Vinblastine
Vincristine
Vindesine
Vinorelbine
A

Mitotic inhibitors

Chemotherapy

79
Q

Herceptin

Trastuzumab

A

Chemotherapy drug

  1. Blocks cleavage
  2. Blocks dimerization
  3. Activates antibody-dependent cell-mediated cytotoxicity that leads to tumor cell lysis
80
Q

Gleevec

Imatinib Mesylate

A

Chemotherapy drug

Blocks ATP from binding to Bcr/c-Abl enzyme and prevent chronic myelogenous leukemia

81
Q

Erbitux

Cetuximab

A

Chemotherapy drug

Blocks ligand binding to EGFR and prevents activation of signal transduction cascades (MAPK) leading to cancer

MCM Exam II (14 decks)

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