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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
G1 cyclin (D) - function - Cyclin-DKA complex(es)
Helps the passage of cells through the restriction point in late G1 phase Cyclin D-CDK4 Cyclin D-CDK6
26
WEE1 kinase
Inhibits CDK activity by phosphorylating the “roof site”
27
Cdc25
Dephosphorylates “roof site” to increase CDK activity
28
P27
A type of CDK inhibitory protein (CKI) Binds to both CDK and cyclin; primarily regulates early in cell cycle events (like G1 —> S)
29
APC/C
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
30
Cdc20
Activates APC/C
31
P53
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
32
P21
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
33
MDM2
Keeps p53 inactive in normal state An E3 ubiquitin ligase
34
Internal stimuli for apoptosis pathways
Abnormalities in DNA
35
External stimuli for apoptosis pathways
Removal or survival factors Proteins of tumor necrosis factor family (TNF-a)
36
Intrinsic pathway of apoptosis
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
Extrinsic pathway for apoptosis
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
BAX/BCL-2
Key regulator in intrinsic apoptosis pathway
39
Initiator caspases
Caspase-8 | Caspase-9
40
Executioner caspase
Caspase-3 Executes apoptosis
41
Apaf1 in the intrinsic pathway of apoptosis
Activated by the release of cytochrome C from the mitochondria Activates BAX Forms the apoptosome Cytochrome c/Apaf1 complex activates caspase-9
42
Proto-oncogene
``` Growth factors Receptors for growth factors and hormones Transcription factors Signal transducers ^normally promotes cell cycle ``` Gain of function mutations —> oncogene
43
Oncogenes
Increase expression of protein products Express altered proteins (oncoproteins) that do not respond to normal signals
44
How do oncogenes cause breast cancer
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
How do oncogenes cause glioblastoma
EGF receptor has a deletion mutation and the receptor’s tyrosine kinase activity is constitutively active causing gliobastoma
46
How do oncogenes cause chronic myelogenous leukemia (CML)
Translocation between chromosome 9 and 22 producing BCR-ABL gene, which expresses the BCR-ABL fusion protein causing CML
47
Retinoblastoma (Rb)
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
How is retinoblastoma (the phenotype) caused
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
Sporadic form of retinoblastoma
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
RB1 gene - what does it do - what do mutations cause - where is the mutation
Encodes pRb (Rb) protein Mutations cause 100% of retinoblastoma Chromosome 13 (regulates G1 phase of cell cycle)
51
TP53 - what does it do - what do mutations cause
Encodes p53 Mutations cause: - 65% colon cancers - 30%-50% breast cancers - 50% lung cancers
52
PTEN (phosphate and tensin homolog) - what do mutations cause
70% of prostate cancers
53
APC (adenomatous polyposis coli) - what do mutations cause - where is the mutation
Colon cancer (family adenomatous polyposis) | Mutation is in chromosome 5 which regulates cell proliferation
54
What do metastasis suppressors do
They’re cell adhesion proteins - prevent tumor cells from dispersing - block loss of contact inhibition - inhibit tumor metastasis
55
NF-1 gene - where is it located - what does it normally do - what does the mutated product do
Chromosome 17 Encodes p120GAP which normally turns off activated RAS protein Causes neurofibromatosis
56
BRCA1/BRCA2 gene - where is it located - what is its normal function - mutated product does what
Chromosome 17 Role in DNA repair and apoptosis Breast cancer
57
DCC gene - where is it - what does it normally do - mutated form does what
Chromosome 18 Role in cell proliferation, migration, and apoptosis Colon cancer
58
6 hallmarks of cancer
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
4 gene alterations than can lead to metastasis
- loss of APC - activation of RAS - loss of a tumor suppressor gene - loss of p53 gene
60
How can viruses cause cancer
- 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
How does HPV cause cancer
- E6+ binds to p53 - degrades p53 and loses tumor suppression Or - E7 binds to RB - Rb becomes inactive and releases E2F
62
Epstein Barr Virus is associated with what tumors
Burkitt lymphoma | Nasopharyngeal carcinoma
63
Hepatitis B virus is associated with what tumors
Liver cancer (hepatocellular carcinoma)
64
HPV is associated with what tumors
Benign warts | Cervical and uterine cancers
65
Human T Cell leukemia virus type 1 (HTLV-1) is associated with what cancer
Adult T cell leukemia/lymphoma
66
Kaposi sarcoma-associates herpesvirus (KSHV) is associated with what cancer
Kaposi sarcoma
67
How to alkylating agents act as chemotherapeutic agents
Block dna replication
68
How do antimetabolites act as chemotherapeutic agents
Inhibit enzymes involved in dna synthesis
69
How do topoisomerase I inhibitors act as chemotherapeutic agents
Inhibit topoisomerase I, an enzyme that removes supercoils in dna
70
How to topoisomerase II inhibitors act as chemotherapeutic agents
Inhibit topoisomerase II, an enzyme that resolves tangles in DNA
71
How to cytotoxic antibiotics act as chemotherapeutic agents
Intercalated between bases in dna to inhibit dna synthesis
72
How do mitotic inhibitors act as chemotherapeutic agents
Arrest cells in mitosis during metaphase
73
``` Ifosfamide Cyclophosphamide Treosulfane Carboplatin Cisplatin ```
Alkylating agents | Chemotherapy
74
``` Cytarabine 5-fluorouracil Gemcitaine Mercaptopurine Methotrexate ```
Antimetabolites | chemotherapy
75
Etoposide | Teniposide
Topoisomerase I inhibitors | Chemotherapy
76
Topotecan
Topoisomerase II inhibitor | Chemotherapy
77
Daunorubicin Doxorubicin Epiruicin Mitoxantrone
Cytotoxic antibiotics | Chemotherapy
78
``` Docetaxel Paclitaxel Vinblastine Vincristine Vindesine Vinorelbine ```
Mitotic inhibitors | Chemotherapy
79
Herceptin | Trastuzumab
Chemotherapy drug 1. Blocks cleavage 2. Blocks dimerization 3. Activates antibody-dependent cell-mediated cytotoxicity that leads to tumor cell lysis
80
Gleevec | Imatinib Mesylate
Chemotherapy drug Blocks ATP from binding to Bcr/c-Abl enzyme and prevent chronic myelogenous leukemia
81
Erbitux | Cetuximab
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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