Oncology - Key Words

Question 1

oncogenes

Answer 1

mutated forms of proto-oncogenes that promote uncontrolled cell growth and proliferation, suppress differentiation and apoptosis

contribute to cancer development

Question 2

proto-oncogene

Answer 2

normal genes involved in promoting normal controlled cell growth and proliferation

Question 3

TS genes

Answer 3

tumour suppressor genes; important in inhibiting growth and proliferation and tumour formation

Question 4

cancer

Answer 4

the growth and proliferation of abnormal/transformed cells following mutagenic or epigenetic changes - results in the formation of tumour mass

Question 5

Li-Fraumeni syndrome

Answer 5

conditions where mutations in TP53 gene/ p53 protein lead to a higher predisposition/ susceptibility to various types of cancers from a young age

Question 6

RB1 gene

Answer 6

TS gene, encodes the Rb protein involved in the G1 to S phase checkpoint

two-hit mutations in the RB1 gene contribute to the formation of retinoblastoma

Question 7

TP53 gene, p53 protein

Answer 7

tumour suppressor gene and protein - maintains genomic stability by ensuring repair mechanisms work during enforced cell cycle arrest, binds to approx. 5000 gene promoters

Question 8

MYC oncogenes

Answer 8

master oncogene family - produces oncoproteins which act as transcription factors for many genes, have amplified effects across integral processes such as cell proliferation, growth, cycle, adhesion, metabolism, ribosomal biosynthesis and protein synthesis

Question 9

BRCA1 gene

Answer 9

TS gene involved in DNA damage repair - recruits other proteins to site of damage, ensures cell cycle arrest for repair mechanisms to occur

Question 10

Philadelphia chromosome

Answer 10

result of a chromosomal translocation/ inappropriate non-homologous end joining following a ds break between chromosomes 9 and 22 - produces fusion oncogene BCR-ABL on Philadelphia chromosome 22

Question 11

ERBB2 gene, HER2 receptor protein

Answer 11

ERBB2 gene encodes the HER2 protein which is expressed on cell surfaces, involved in cell growth and proliferation via growth signal transduction pathways

ERBB2 gene amplification can cause oversensitivity to growth signals = uncontrolled growth

Question 12

Ras

Answer 12

responds/activates by growth signals a component of many pathways - active when GTP bound

point mutations in Ras causing a G to T base change = constant activity = constant response to growth signals

Question 13

metastasis

Answer 13

spread of cancer cells from the place where they first formed to another part of the body

Question 14

angiogenesis

Answer 14

formation of new blood vessels from pre-existing vasculature

Question 15

Avastin

Answer 15

anti-angiogenic factor drug; antagonist to VEGF

monoclonal antibody that binds to VEGF-R2 and prevents angiogenic effects

Question 16

hypoxia

Answer 16

low oxygen tension, below 1%

Question 17

MMPs

Answer 17

matrix metalloproteases - degrade extracellular matrix and tissues

can also release latent growth factors and angiogenic factors

Question 18

VEGF

Answer 18

vascular endothelial growth factor; an angiogenic factor, binds to its receptor on endothelial cells and promotes the directional growth of sprouting blood vessels towards the tumour

Question 19

E-cadherin

Answer 19

homotypic adhesion molecule which ensures cell-cell contact, close proximity between cells and contact inhibition through Ca2+ dependent interactions with extracellular and intracellular domains

Question 20

B-catenin (beta)

Answer 20

central component of the Wnt signalling pathway - aberrant Wnt/β-catenin signalling facilitates cancer stem cell renewal, cell proliferation and differentiation

plays a key role in the regulation of cell proliferation, differentiation, and apoptosis

Question 21

intravasation and extravasation

Answer 21

intravasation = invasion into vessels

extravasation = exiting vessels (lymph/blood)