CANC 380 | UPDATED Questions with 100% Verified Answers
Q1: 2 most important research developments
A: 1. mapping of human genome
2. lifestyle contribution to cancer
Q2: Darwinian evolution: natural selection
A: All living things are descendants of a common ancestor where each new species are
more adapted to their native environment
Favourable trait in environment survive and reproduce and pass to offspring
Occurs by random genetic mutations
Q3: Requirements for natural selection
A: variation in population
heritable
influences survival and reproductive rates
Q4: clone vs subclone
A: clone group of cells from same parents
subclone product of mutant cells from a clone
Q5: selective pressures
A: environmental factors/conditions that reduce reproductive success of variant
populations
develop proliferative growth advantage
contributes to natural selection
Examples oxygen/nutrient availability, pH, tumour/stromal/immune cells growth factors,
hormones, angiogenic factors, extracellular matrix, interstitial pressure, therapies
Q6: Forms of evolution
A: divergent populations of single species have enough phenotypic differences to become
separate species (cancer cells > subclones with different mutations)
convergent 2 unrelated species develop similar structures due to similar environmental
selective pressures (mutations in subclones came from different clones)
parallel 2 unrelated species evolve on similar pass to produce similar phenotypic traits
(amplification of growth receptors is common in cancers even if gene amplified is
different)
,Q7: Tumour antigens
A: 1. mutated products: mutations in genes that favour uncontrolled growth result in
abnormal proteins and are expressed as antigens
2. protein levels: abnormal expression of growth proteins
3. glycolipids: overexpression of normal structure or presence of abnormal structure
4. oncogenic products: foreign product (viral proteins expressed)
Q8: Innate therapy
A: NK cells kills cells expressing tumour antigens
Macrophages become tumourcidal through cytokines (IFNy)
TNF stimulate coagulation (cuts of nutrient supply)
Q9: Adaptive therapy
A: Cytotoxic T cells through APCs
Helper T cells cytokines, stimulate cytotoxic T cells and innate response
Antibodies activate antibodydependent cytotoxicity and complement pathways
Q10: Immunoediting
A: immune system can destroy and influence development of malignant cells by acting as a
selective pressure
Q11: Immune surveillance
A: constantly surveilling dividing cells and ensuring normal function
Q12: Tumour destruction
A: lymphocytes in tumours recognize tumour antigens
Q13: Tumour promotion
A: immune system is involved in development of tumours
Q14: Staging system (TNM)
A: Tumour size, location
Node spread to lymph nodes, how many
Metastasis has it spread, where, how much
, Q15: TMN stages
A: Stage 0 in situ, highly curable
Stage 1 localised, begins to spread
Stage 2 &3 regional spread, grows into other tissues and nodes
Stage 4 metastatic
Q16: Bladder Cancer Staging
A: Non muscle invasive
TIS/Ta in situ, surface of bladder
Ti extands to lamina propria
Muscle invasive
T2a first layers of muscularis propria
T2b deeper layers
T3 perivesicle fat around bladder
T4 outside perivesical fat into tissues
Q17: Tumour grading
A: G1 (low) well differentiated, look and behave like normal cells, not aggressive, slow
growing
G2 (intermediate) moderately differentiated, most cancer cells
G3 (high) poorly differentiated, look and behave differently from normal cells,
aggressive, fast growing
G4 (high) undifferentiated, don't resemble normal cells, aggressive and rapid
Q18: Epithelial to mesenchymal transition (EMT)
A: Epithelial cells lose polarity and intracellular connections to acquire mesenchymal
phenotype (dedifferentiation, can assign stemcell characteristics)
Induces transcription factors (EMTIFs) to redefine epithelial status of cell
Promotes resistance to therapy
Q19: Gleason Score (prostate cancer)
A: Normal prostate tissue has defined glands with clear layers
Grade 3 variation in gland size
Grade 4 merging of cribiform glands
Grade 5 poor differentiation, do not form glands, visible sheets of cells
Q20: Cancer growth terms
A: Hypertrophy increased cell size, no increase in #
Hyperplasia increased # of cells
Metasplasia reversible replacement of one cell type with another
Dysplasia altered cell maturation, may progress to cancer or regress to normal cells
Anaplasia forms backwards, no differentiation
Neoplasia new growth, unregulated cell proliferation (genetic changes)
Q1: 2 most important research developments
A: 1. mapping of human genome
2. lifestyle contribution to cancer
Q2: Darwinian evolution: natural selection
A: All living things are descendants of a common ancestor where each new species are
more adapted to their native environment
Favourable trait in environment survive and reproduce and pass to offspring
Occurs by random genetic mutations
Q3: Requirements for natural selection
A: variation in population
heritable
influences survival and reproductive rates
Q4: clone vs subclone
A: clone group of cells from same parents
subclone product of mutant cells from a clone
Q5: selective pressures
A: environmental factors/conditions that reduce reproductive success of variant
populations
develop proliferative growth advantage
contributes to natural selection
Examples oxygen/nutrient availability, pH, tumour/stromal/immune cells growth factors,
hormones, angiogenic factors, extracellular matrix, interstitial pressure, therapies
Q6: Forms of evolution
A: divergent populations of single species have enough phenotypic differences to become
separate species (cancer cells > subclones with different mutations)
convergent 2 unrelated species develop similar structures due to similar environmental
selective pressures (mutations in subclones came from different clones)
parallel 2 unrelated species evolve on similar pass to produce similar phenotypic traits
(amplification of growth receptors is common in cancers even if gene amplified is
different)
,Q7: Tumour antigens
A: 1. mutated products: mutations in genes that favour uncontrolled growth result in
abnormal proteins and are expressed as antigens
2. protein levels: abnormal expression of growth proteins
3. glycolipids: overexpression of normal structure or presence of abnormal structure
4. oncogenic products: foreign product (viral proteins expressed)
Q8: Innate therapy
A: NK cells kills cells expressing tumour antigens
Macrophages become tumourcidal through cytokines (IFNy)
TNF stimulate coagulation (cuts of nutrient supply)
Q9: Adaptive therapy
A: Cytotoxic T cells through APCs
Helper T cells cytokines, stimulate cytotoxic T cells and innate response
Antibodies activate antibodydependent cytotoxicity and complement pathways
Q10: Immunoediting
A: immune system can destroy and influence development of malignant cells by acting as a
selective pressure
Q11: Immune surveillance
A: constantly surveilling dividing cells and ensuring normal function
Q12: Tumour destruction
A: lymphocytes in tumours recognize tumour antigens
Q13: Tumour promotion
A: immune system is involved in development of tumours
Q14: Staging system (TNM)
A: Tumour size, location
Node spread to lymph nodes, how many
Metastasis has it spread, where, how much
, Q15: TMN stages
A: Stage 0 in situ, highly curable
Stage 1 localised, begins to spread
Stage 2 &3 regional spread, grows into other tissues and nodes
Stage 4 metastatic
Q16: Bladder Cancer Staging
A: Non muscle invasive
TIS/Ta in situ, surface of bladder
Ti extands to lamina propria
Muscle invasive
T2a first layers of muscularis propria
T2b deeper layers
T3 perivesicle fat around bladder
T4 outside perivesical fat into tissues
Q17: Tumour grading
A: G1 (low) well differentiated, look and behave like normal cells, not aggressive, slow
growing
G2 (intermediate) moderately differentiated, most cancer cells
G3 (high) poorly differentiated, look and behave differently from normal cells,
aggressive, fast growing
G4 (high) undifferentiated, don't resemble normal cells, aggressive and rapid
Q18: Epithelial to mesenchymal transition (EMT)
A: Epithelial cells lose polarity and intracellular connections to acquire mesenchymal
phenotype (dedifferentiation, can assign stemcell characteristics)
Induces transcription factors (EMTIFs) to redefine epithelial status of cell
Promotes resistance to therapy
Q19: Gleason Score (prostate cancer)
A: Normal prostate tissue has defined glands with clear layers
Grade 3 variation in gland size
Grade 4 merging of cribiform glands
Grade 5 poor differentiation, do not form glands, visible sheets of cells
Q20: Cancer growth terms
A: Hypertrophy increased cell size, no increase in #
Hyperplasia increased # of cells
Metasplasia reversible replacement of one cell type with another
Dysplasia altered cell maturation, may progress to cancer or regress to normal cells
Anaplasia forms backwards, no differentiation
Neoplasia new growth, unregulated cell proliferation (genetic changes)
