Lecture 9 - Neoplasms Flashcards
tumour types, characteristics, epidemiology, aetiology, basis of cancer
what does neoplasm mean
abnormal mass of tissue which grows in UNCOORDINATED way and FASTER than normal tissue
remains even after initial stimulus has been removed
what does neoplasia mean
new growth
what is oncology
study of tumours
what is a tumour
swelling of part of the body generally without inflammation, caused by abnormal tissue growth
what two things can tumours be
benign and malignant
what 2 things are tumours made up of
neoplastic cells - constituite the tissue parenchyma
reactive stroma - made up of connective tissue blood vessels and immune cells
what 4 characterstics do malignant tumours exhibit
- malignant change is target cell -> transformation (anaplasia, metaplasia, dysplasia)
- growth of transformed cell
- local invasion
- distant metastasis
what is anaplasia
dedifferentiation
what is metaplasia
replacement of cell types
what is dysplasia
presence of abnormal cells in tissue (replaces normal cells)
what is the differentation
extent to which neoplastic parenchymal cells resemble to normal ones
what does a well differentiated neoplasm resemble
mature cells of origin
what is a poorly differentiated neoplasm composed of
primitive cells with little differentiation
how well are benign and malignant tumours differentated
benign - well differentiated
malignant - poor differentiation + poor prognosis
what is the rate of growth for benign anf malignant tumours
benign - progressive and slow
malignant - erratic, may be slow to rapid
what is the local invasion of benign and malignant
benign - non invasive
malignant - locally invasive
what is the metastasis for benign and malignant tumorus
benign - absent
malignant - frequent
what is pleomorphism
variation in size and shape
what is abnormal nuclear morphology
hyperchromasia, enlarged nucleus, chromatin clumping
what does loss of polarity mean
no orientation or organisation
what does dysplasia translate to
no growth
may not develop into malignancy
mildly abnormal
what is local invasion
progressive
invasion of basement from tumour causes it to spread
what is metastatis
spead of primary tumour to sites distant to where original tumour formed
benign do not exhibit this
what is the 3 step process on how tumour spread
- direct seeding of body cavities
- lymphatic spread
- haematogenous spread -> invasion of arteries and veins
what are cancer risk factors
age -> more likely wit old age apart from childhood cancers like leukamis
genetic predisposition -> 2 or more family members
non hereditory predisposition -> chronic inflammation, pre cancerous conditons
what are environmental risk factors of cancer
Infection e.g. human papilloma virus *
Smoking
Alcohol
Obesity
Reproductive history e.g. lifelong exposure to oestrogen *
Environmental carcinogens e.g. UV light, asbestos
what are the most popular cancers in females
breast
lung
bowel
what are the most common cancers in men
prostate
lung
bowel
name reasons why cancer is one of the most efficient cell types
does not need external signals to receive growth factors
altered cellular metabolism
evasion of apoptosis
can avoid immune response
what is the genetics and epigenetics of cancer
- non lethal genetic damage e.g. inherited mutations
- clonal expansion of single cell with geneic abnormalities
what are the principle target of cancer causing mutations (oncogenes)
- Growth promoting PROTO-ONCOGENES and ONCOGENES
- Growth inhibiting TUMOUR
SUPPRESSOR GENES - Genes involved in apoptosis
- Genes involved in DNA repair
what is oncogenesis
the process by which a normal cell becomes a cancerous cell
what are three mutation in growth promoting genes
proto-oncogenes
oncogenes
oncoprotein
what are proto oncogenes
normal cellular genes whose products promote proliferation
what are oncogenes
mutated or overexpressed versions of proto-oncogenes that have lost dependence on normal growth promoting signals
what is an oncoprotein
protein encoded by oncogene driving increased proliferation
what is the cell cycle process
mutation in cell growth genes
activation of oncogenes
leads to increased cyclin and CDK expression
drives cell through cell cycle continuosuly
what are three tumour suppressor genes
retinoblastoma gene (RB) - negative regulator of G1/S cell cycle
p53 (guardian of genome) - regulates cell cycle progression
apoptosis (can suppress tumours but is not a gene)
what is the mechanism of action of P53
G1 checkpoint
reads nad surveys DNA for damage
activates production of P21-> inhibit cyclin/cdk (cell cycle arrest), DNA repair proteins and apoptotic proteins
what does telomerase do in cancer
changes length of telomeres
makes cell have limitless replicative potential
