MPM1 Test With Complete
Solution
Hallmarks of Cancer - Answer - Sustaining proliferative signaling
- Evading growth suppressors
- Avoiding immune destruction
- Enabling replicative immortality
- Tumour-promoting inflammation
- Activating invasion and metastasis
- Inducing or accessing vasculature
- Genome instability & mutation
- Resisting cell death
- Deregulating cellular metabolism
Genetic instability - Answer Increased rate at which mutations accumulate
Tumor suppressor - Answer Normally: inhibits cell proliferation
Deactivation: cancer
Oncogene - Answer Normally: growth
Overactivation: cancer
Driver gene mutations - Answer Genes involved in development or progression of
cancer
Mitogen - Answer Extracellular signal molecule/substance that stimulates cell
proliferation
G0 phase - Answer Quiescent state outside of cell cycle
G1 phase of interphase - Answer First gap, or growth phase
- Cell grows, synthesises proteins, prepares DNA for replication
- Monitors external & internal conditions to check if it should enter next phase
,- Cells responsive to mitogenic GFs & TGF-beta
S phase of interphase - Answer DNA replication (synthesis)
End result: each chromosome consists of 2 sister chromatids held by centromere
G2 phase of interphase - Answer Cell organelles are duplicated in preparation for cell
division (mitosis)
Checks for DNA damage & ensures DNA replication was successful
M phase (mitosis + cytokinesis) - Answer Mitosis + cytokinesis
1. Prophase: chromatin condenses, mitotic spindle forms
2. Prometaphase: nuclear envelope fully disintegrates, mitotic spindle attaches to
kinetochores on sister chromatids
3. Metaphase: chromosomes align at metaphase plate, mitotic spindle ensures each
sister chromatid attached to MT from opposite spindle poles
4. Anaphase: sister chromatids separate (pulled towards opposite spindle poles), cell
elongates
5. Telophase: 2 nuclei form around separated sister chromatids at opposite ends of cell,
chromosomes begin to decondensate
6. Cytokinesis: contractile ring constricts cytoplasm -> 2 daughter cells
G1 checkpoint (G1/S transition) - Answer Restriction point: sufficient size, nutrients
available, DNA undamaged, presence of GF
G2 checkpoint (G2/M transition) - Answer DNA integrity: DNA replication complete?
DNA damage repaired? If damage is extensive, cell may undergo apoptosis
Mitotic checkpoint (Meta-/Anaphase transition) - Answer Chromosome alignment &
attachment to mitotic spindle
Cyclin-dependent kinases (CDKs) - Answer Constantly expressed kinases, which control
cell cycle progression with cyclins
G1: CycD-CDK4/6
G1/S: CycE-CDK2
S: CycA-CDK2
S/G2: CycA-CDK1
M: CycB-CDK1
Cyclins - Answer Oscillatingly expressed proteins that regulate the timing of the cell
, cycle in eukaryotic cells
G1: CycD-CDK4/6
G1/S: CycE-CDK2
S: CycA-CDK2
S/G2: CycA-CDK1
M: CycB-CDK1
Cyclin-dependent kinase inhibitors (CKIs) - Answer can be activated by signals like P21
protein and halt CDK activity and cell cycle progression when surveillance indicates a
problem at a given stage (inhibit cell division)
G1: p16INK4A, p15INK4B, p18INK4C, p19INK4D
G1/S,S,S/G2,M: p57Kip2,
p27Kip1,
p21Cip1
Cdk-cyclin complexes - Answer G1: CycD-CDK4/6
G1/S: CycE-CDK2
S: CycA-CDK2
S/G2: CycA-CDK1
M: CycB-CDK1
Positive growth factors - Answer - Protooncogenes: Myc, RAS, HER/ERBB2, BRAF
- GFs: EGF, PDGF, IGF
- Cyclins & CDKs: cyclin D-CDK4/6, cyclin E-CDK2, mitogens (promote their expression)
- Checkpoint relievers: ATM/ATR kinases, CHK1/CHK2
Negative growth factors - Answer - Tumor suppressor proteins: p53, Rb1, PTEN,
BRCA1/BRCA2, TGFβ, (p16INK4a)
- CKIs: p21Cip1, p27Kip1, p16INK4a
c-Myc (protooncogene) - Answer - promotes cell growth
- rarely mutates, frequently amplified
- increases cyclin D -> G1-CDK activation (cyclin D-CDK4) -> Rb phosphorylation ->
increased E2F activity- > entry into S-phase
Solution
Hallmarks of Cancer - Answer - Sustaining proliferative signaling
- Evading growth suppressors
- Avoiding immune destruction
- Enabling replicative immortality
- Tumour-promoting inflammation
- Activating invasion and metastasis
- Inducing or accessing vasculature
- Genome instability & mutation
- Resisting cell death
- Deregulating cellular metabolism
Genetic instability - Answer Increased rate at which mutations accumulate
Tumor suppressor - Answer Normally: inhibits cell proliferation
Deactivation: cancer
Oncogene - Answer Normally: growth
Overactivation: cancer
Driver gene mutations - Answer Genes involved in development or progression of
cancer
Mitogen - Answer Extracellular signal molecule/substance that stimulates cell
proliferation
G0 phase - Answer Quiescent state outside of cell cycle
G1 phase of interphase - Answer First gap, or growth phase
- Cell grows, synthesises proteins, prepares DNA for replication
- Monitors external & internal conditions to check if it should enter next phase
,- Cells responsive to mitogenic GFs & TGF-beta
S phase of interphase - Answer DNA replication (synthesis)
End result: each chromosome consists of 2 sister chromatids held by centromere
G2 phase of interphase - Answer Cell organelles are duplicated in preparation for cell
division (mitosis)
Checks for DNA damage & ensures DNA replication was successful
M phase (mitosis + cytokinesis) - Answer Mitosis + cytokinesis
1. Prophase: chromatin condenses, mitotic spindle forms
2. Prometaphase: nuclear envelope fully disintegrates, mitotic spindle attaches to
kinetochores on sister chromatids
3. Metaphase: chromosomes align at metaphase plate, mitotic spindle ensures each
sister chromatid attached to MT from opposite spindle poles
4. Anaphase: sister chromatids separate (pulled towards opposite spindle poles), cell
elongates
5. Telophase: 2 nuclei form around separated sister chromatids at opposite ends of cell,
chromosomes begin to decondensate
6. Cytokinesis: contractile ring constricts cytoplasm -> 2 daughter cells
G1 checkpoint (G1/S transition) - Answer Restriction point: sufficient size, nutrients
available, DNA undamaged, presence of GF
G2 checkpoint (G2/M transition) - Answer DNA integrity: DNA replication complete?
DNA damage repaired? If damage is extensive, cell may undergo apoptosis
Mitotic checkpoint (Meta-/Anaphase transition) - Answer Chromosome alignment &
attachment to mitotic spindle
Cyclin-dependent kinases (CDKs) - Answer Constantly expressed kinases, which control
cell cycle progression with cyclins
G1: CycD-CDK4/6
G1/S: CycE-CDK2
S: CycA-CDK2
S/G2: CycA-CDK1
M: CycB-CDK1
Cyclins - Answer Oscillatingly expressed proteins that regulate the timing of the cell
, cycle in eukaryotic cells
G1: CycD-CDK4/6
G1/S: CycE-CDK2
S: CycA-CDK2
S/G2: CycA-CDK1
M: CycB-CDK1
Cyclin-dependent kinase inhibitors (CKIs) - Answer can be activated by signals like P21
protein and halt CDK activity and cell cycle progression when surveillance indicates a
problem at a given stage (inhibit cell division)
G1: p16INK4A, p15INK4B, p18INK4C, p19INK4D
G1/S,S,S/G2,M: p57Kip2,
p27Kip1,
p21Cip1
Cdk-cyclin complexes - Answer G1: CycD-CDK4/6
G1/S: CycE-CDK2
S: CycA-CDK2
S/G2: CycA-CDK1
M: CycB-CDK1
Positive growth factors - Answer - Protooncogenes: Myc, RAS, HER/ERBB2, BRAF
- GFs: EGF, PDGF, IGF
- Cyclins & CDKs: cyclin D-CDK4/6, cyclin E-CDK2, mitogens (promote their expression)
- Checkpoint relievers: ATM/ATR kinases, CHK1/CHK2
Negative growth factors - Answer - Tumor suppressor proteins: p53, Rb1, PTEN,
BRCA1/BRCA2, TGFβ, (p16INK4a)
- CKIs: p21Cip1, p27Kip1, p16INK4a
c-Myc (protooncogene) - Answer - promotes cell growth
- rarely mutates, frequently amplified
- increases cyclin D -> G1-CDK activation (cyclin D-CDK4) -> Rb phosphorylation ->
increased E2F activity- > entry into S-phase
