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Kristine Krafts, M.D.
Neoplasia III (Epidemiology) and IV (Cancer Pathogenesis)
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Neoplasia Outline
• Tumor nomenclature
• Tumor characteristics
• Epidemiology
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Cancer Incidence
• Every year: 1.5 million new cases of cancer, >500,000 cancer deaths
• Cancer is 2nd leading cause of death (after heart disease)
• Most common cancers• Men: Prostate• Women: Breast
• Deadliest cancers• Men: Lung• Women: Lung
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Environmental Carcinogens
• Sunlight: skin cancer
• Smoking: lung cancer
• Alcohol: liver, breast cancers
• HPV: cervical carcinoma
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Three Types of Hereditary Cancer
• Familial cancers
• Inherited cancer syndromes
• Syndromes of defective DNA repair
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Familial Cancers
• Most cases of cancer are “sporadic” (random)
• A small number are “familial” (related to particular germline gene mutations)
• Example: certain BRCA1 gene mutations increase risk of breast, colon, ovary, and pancreatic cancers
• Familial cancers occur earlier and are more aggressive than their sporadic counterparts
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Inherited Cancer Syndromes
• Usually autosomal dominant
• Each has a specific gene mutation that increases risk of getting multiple cancers
• Example: Li-Fraumeni syndrome • mutation in p53 gene• 25x increased risk of getting sarcomas,
breast cancer, leukemia, and brain tumors, usually before age 50
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Syndromes of Defective DNA Repair
• Inherited mutations in genes encoding DNA repair systems
• Greatly enhance the occurrence of mutations in other genes (“genomic instability”)
• Example: xeroderma pigmentosum• mutations in genes in “nucleotide excision
repair” pathway (fixes UV-damaged DNA• Extreme sensitivity to sun; markedly
increased risk of skin cancer (in childhood!)
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Neoplasia Outline
• Tumor nomenclature
• Tumor characteristics
• Epidemiology
• Cancer pathogenesis
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What causes cancer?
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What causes cancer?
Non-lethal genetic damage.
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Autonomous cell proliferation
Resistance to growth-suppressing signals
Evasion ofapoptosis
Immortality
Ability to invadeand metastasize
Alteredmetabolism
Evasion ofimmune detection
Hallmarks of Cancer
Angiogenesis
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Autonomous cell proliferation
Hallmarks of Cancer
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Autonomous Cell Growth
• Proto-oncogene: a normal gene whose product promotes cell growth.
• Oncogene: a mutated proto-oncogene. Causes tumor cell to grow autonomously.
• Oncoprotein: the product of an oncogene.
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• RAS is a signal transduction protein
• Mutated RAS is always on…
• …therefore, always transducing signals…
• …therefore, cell is always dividing.
The RAS Gene
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Autonomous cell proliferation
Resistance to growth-suppressing signals
Hallmarks of Cancer
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Resistance to Growth-Suppressing Signals
• Tumor suppressor gene: a normal gene whose product suppresses the cell cycle (like brakes on a car).
• Mutate these guys, and you lose the brakes!
• Must mutate both copies of the gene to cause tumors.
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• RB gene product stops cell at G1 checkpoint
• Mutant RB is inactive; lets cells pass through G1!
• Patients with two mutated RB genes have way, way high risk of retinoblastoma (and an increased risk of getting other tumors).
The Retinoblastoma (RB) Gene
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The Cell Cycle
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Retinoblastoma
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Autonomous cell proliferation
Resistance to growth-suppressing signals
Evasion ofapoptosis
Hallmarks of Cancer
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Evasion of Apoptosis
• Many proteins are involved in apoptosis:• p53 • Fas (the “death receptor”)• Executioner caspases • BCL2 protein family
• If genes for these proteins are mutated, the cell will be able to avoid killing itself.
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• Nickname for p53: “guardian of the genome”
• If a cell’s DNA is damaged, p53 causes a pause in the cell cycle (via RB), so DNA can be repaired.
• If DNA damage is irreparable, p53 causes the cell to undergo apoptosis.
• Most human tumors have p53 mutations!
The p53 Gene
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p53 activated
cell cycle arrest
p53 not activated
no cell cycle arrest,no DNA repair
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Autonomous cell proliferation
Resistance to growth-suppressing signals
Evasion ofapoptosis
Immortality
Hallmarks of Cancer
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Immortality
• Normal cells can only undergo 60-70 doublings
• Main reason: telomere shortening!
• Stem cells and cancer cells use telomerase to maintain telomere length and keep replicating.
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Telomeres
As cells divide over time...
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Autonomous cell proliferation
Resistance to growth-suppressing signals
Evasion ofapoptosis
ImmortalityAngiogenesis
Hallmarks of Cancer
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Angiogenesis
• Tumor cells need blood too!
• Can’t grow >1-2 cm without new vessels
• Tumor cells eventually learn how to stimulate angiogenesis
• Lots of cytokines involved (i.e., VEGF)
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Tumor cells surrounding new vessel
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Autonomous cell proliferation
Resistance to growth-suppressing signals
Evasion ofapoptosis
Immortality
Ability to invadeand metastasize
Hallmarks of Cancer
Angiogenesis
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Ability to Invade and Metastasize
• To do this, tumor cells must:• Loosen contacts between cells• Degrade extracellular matrix• Migrate away from the original site
• Some tumors lodge in nearest capillary bed
• Some tumors show tropism
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clonal growth
intravasation
metastatic subclone
tumor cell embolus
extravasation
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Tumor cells surrounding and invading vessel
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Tumor cells now within vessel
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Autonomous cell proliferation
Resistance to growth-suppressing signals
Evasion ofapoptosis
Immortality
Ability to invadeand metastasize
Alteredmetabolism
Evasion ofimmune detection
Hallmarks of Cancer
Angiogenesis
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Autonomous cell proliferation
Resistance to growth-suppressing signals
Evasion ofapoptosis
Immortality
Ability to invadeand metastasize
Alteredmetabolism
Evasion ofimmune detection
Hallmarks of Cancer
Angiogenesis
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Grading and Staging
• Used for malignant tumors• Useful for determining treatment and prognosis• Grading
• Tells you how nasty the tumor looks (use microscope)
• Somewhat useful• Staging
• Tells you how far the tumor has spread (use imaging)
• Very useful
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Tubuleslots of tubules some tubules rare tubules
Mitoses0-9 mitoses/10 hpf 10-19 mitoses/10 hpf≥20 mitoses/10 hpf
Pleomorphismsmall, uniform cells larger, less uniform cellsmarkedly pleomorphic cells
Grading system for breast cancer
Low gradeIntermediate gradeHigh grade
123
123
123
3-56-78-9
add all points together
Grade Score 5y survival>95%80%60%
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Low grade breast cancer
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High grade breast cancer
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T=TumorTis – in situ tumor T1 – small tumorT2 – larger tumorT3 – larger or invasive tumorT4 – very large/very invasive
N=NodesN0 – no lymph node involvement N1 – a few regional nodesN2 – lots of regional nodesN3 – distant nodes
M=MetastasesM0 – no metastases M1 – metastases
TNM staging system for non-small cell lung cancer
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Overall stageStage 0
Stage I
Stage II
Stage III
Stage IV
TNM staging system for non-small cell lung cancer
TTis
T1 or T2
T1T2T3
T1 or T2T3
Any TT4
Any T
NN0
N0
N1N1N0
N2N1 or N2
N3Any N
Any N
MM0
M0
M0M0M0
M0M0M0M0
M1
TreatmentSurgery only
Surgery ± radiation
Surgery and radiation± chemotherapy
Chemotherapy ±radiation to debulk
Maybe surgery
Palliative careMaybe chemo or radiation
5y prognosis75%
50%
30%
10%
<2%
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Grading and Staging
Grading = microscopic
Staging = clinical
Staging is more useful.