W11 Cancer Flashcards
what are 4 cancer cell features
large nuclei
many dividing cells
variation in shape/size
disorganised arrangement
what is the mechanism of cancer cell plasticity
-
what do cancer cells need to become invasive
- break off from primary tumour -> change cell adhesion molecules + release proteases
- undergo EMT
- enter local endothelia’s
- can form a 2ndary tumour back to epithelial cells (MET)
what is EMT
changes in cell shape and size from epithelial to mesenchymal
what are cells called when they are proliferating
epithelial cells
what is MET
changes in cell shape and size from mesenchymal to epithelial cells
what is intravasion
mesenchymal cells trying to enter neighbouring tissue
what are cancer cells able to bypass
normal proliferation controls
what is anchorage independent growth
doesn’t require a matrix -> can grow in suspension
what is density dependent inhibition
cell sense contact can stop growth
what type of growth are cancer cells
anchorage independant
what does cancer cell metabolism rely on
oxidative phosphorylation + aerobic glycolysis
which stages of mitosis do cancer cells bypass
G1 to S phase restriction points
what are cancer cells conditions that allow for dividing
abnormal stress responses
what process is limited in cancer cells to allow them to live for longer
no apotosis
what do cancer cells escape
replicative cell senescence
why are cancer cells DNA able to last this long
telomeres don’t shortern
which genes are expressed more during cancer cells
increased oncogenes
what are the 6 most common cancers
lung
breast
colon
prostate
stomach
liver
what is carcinomas
cancer from epithelial cells that cover body surfaces
what is sarcomas
development of cancer from connective tissues like bones
where does lymphomas/leukaemia’s begin
cells of lymphatic and blood origin
what is blastomas
cancer from blasts of embryonic tissue
what is osteosarcoma
cancer development in growing bones
how is osteosarcoma stained
H and E
what are symptoms of interest for lymphomas
enlarged lymph nodes + spleen
what are the requirements of cancer spreading
- brake off primary tumour
- invade local tissue
- spread to rest of body via blood vessels or lymph channels
what is angiogenesis
growth of blood vessels
what is metastasis
entering of cancer cells into bloodstream
what do tumour microenvironments do
influence cancer development
what does the microenvironment contain
endothelial cells
bone marrow cells
macrophages
monocytes
mesenchymal stem cells
how do tumour microenvironments promote cancer growth
- communication between tumour cells and stroma
- stroma provides framework for tumour
- during carcinoma cells secrete signal proteins for stromal cells
- stomal cells will turn on tumour cells
how is angiogenesis regulated
endogenous angiogenesis inhibitors
what are the 2 main activators of angiogenesis
basic fibroblast GF (VEGF)
vascular endothelial GF (FGF)
what are the 3 main inhibitors of angiogenesis
angiostatin
endostatin
thrombospondin
what does cell invasion rely on
cell adhesion changes
increased motility
protease production
what happens to cancer cells when they undergo metastasis
intravascular growth and adhesion to organ membrane
what are the 3 internal causes of cancer
oncogene activation
TSG loss
UV radiation
what is lung cancer linked to
asbestos
how does benzidine cause cancer
metabolise in liver
can cause bladder cancer
what do cancer cells do to DNA
crosslinks between 2 strands of double helix causing breaks in DNA strands
what cancer does the HPV cause
cervical cancer
which bacteria’s cause liver cancer
hepatitis B/C
what cancers can UV radiation cause
melanoma + carcinomas
what is changed in oncogenes to cause cancer
change in the Ras protein
how can oncogenes be activated
Point mutation
Gene amplification
Chromosomal translocation
Local DNA rearrangements
Insertional mutagenesis
what can chromosomal translocation lead to
increased oncogene expression
fusion proteins
what is Burkitt’s lymphoma caused by
chromosomal translocation affecting B lymphocytes
what are 3 mutations that disrupt proto-oncogenes
insertions
deletions
inversions
what is insertional mutagenesis
viral DNA integrated into host chromosome
stimulate expression of proto-oncogenes for too much proteins
what are proto-oncogenes
genes that control cell growth
how many human oncogenes are there
224-246
what are the 6 categories of oncogenes
growth factors
receptors
GTP-binding proteins
non-receptor kinases
transcription factors
apoptosis/cell cycle regulators
what do cell hybridization experiments do
supress malignancy by cell fusion
what does the Rb gene do
regulates progression of G1/S phase
where are Rb genes found
retinoblastomas
which is the most commonly mutated TSG and its job
p53 -> responds to DNA damage to trigger apoptosis
where are BRCA1/2 expressed
in breast
what are the jobs of BRCA1/2
repair DDSB
what are screening techs used for cancer
biopsy + pathology
what are 3 treatments of cancer
surgery
radio therapy
chemo
what do antimetabolites do as a chemo drug
inhibit DNA synthesis
what do alkylating agents/antibiotics do as a chemo drug
inhibit DNA function
what do plant derived drugs do as a chemo drug
block specific cell cycle progressions
what is hyperthermia treatment
using high temps to kill cancer cells
what is photodynamic therapy
treatment using photosensitizing agents
what does herceptin do
binds and deactivates HER-2 GF
how does inhibiting CTLA4 stop tumours
more activation of T cells to attack cancer cells
what is ipilimumab (anti-CTL4) used on
metastatic melanoma
where are PD-1 receptors expressed
cell surface of TILs
what is the oncolytic virus for
immunotherapy -> thrive in cancer cells to break open tumour cells
what does imatinib do
treats chronic myelogenous leukaemia (CML)
what does the inhibition of BRAF and MEK do
activates MAPK pathway
when is adjuvant therapy used
after primary treatments are used
