Bird (Molecular basis of disease: Cancer) Flashcards
What is cancer?
- group of diseases characterised by uncontrolled growth and spread of abnormal cells
- if spread not controlled can result in death
Why is uncontrolled growth of cells unusual?
- most cells don’t divide and only do when stimulated to
What is metastasis?
- 2º spread
- original cells break off and form new tumours
What is the incidence of cancer?
- 1 in 3 get it
- 1 in 5 die
- increases w/ age in humans (but cancers that are more common in children)
- skin most prevalent in younger people
What is the typical tissue structure?
- layer of epithelium separated from supporting mesenchyme by basement membrane
- support tissue (or stroma) made up of connective tissue and fibroblasts, may be supported on layer of muscle or bone depending on organ
- in some tissues (eg. skin, intestine) epithelium several cells thick
- may form tubes (eg. kidney, lungs)
- solid cords (eg. liver)
What is the 1st stage of cancer?
- carcinoma in situ
What happens if carcinoma in situ detected?
- recovery likely, before metastasis dev
- screening effective tool in preventing cancer by detecting early and removing it
What causes cancer?
- successive mutations
- usually in somatic cells, small no. germline, passed onto offspring increasing cancer risk
- usually 5-8 mutations
- each mutation creates cell increasingly well adapted for autonomous growth
What is the probability of a cell becoming cancerous, and why?
- probability of 1 cell simultaneously acquiring mutations v small
- can only get all mutations if initiated cell clonally expands
- 2nd mutation at critical locus gives growth advantage and 2nd clonal expansion occurs
- process repeats
Why is it surprising cancer isn’t more common?
- DNA v volatile inside cell
What is the traditional view on cancer developing?
- tumour cells heterogenous, but most cells can proliferate extensively and form new tumours
What is the more recent view on cancer developing?
not much evidence but gaining popularity
- tumour cells heterogenous and only cancer stem cell subset has ability to proliferate extensively and form new tumours
- self renew and prod differentiated daughter cells like normal stem cells
What are the characteristics of benign tumours?
- don’t metastasise
- grow locally
- may cause problems by pressure (brain) or obstruction (colon)
- histologically and cytologically resemble tissue of origin
- may prod wart like outgrowths containing all cell types, packed closely to form solid nodule
Where are benign tumours found?
- dev in any tissues
- cover or line tissues of skin, intestine, bladder etc.
What are the characteristics of in situ tumours?
- usually dev in epithelium
- usually small
- altered histological appearance (show morphological characteristics of tumour cells to greater or lesser degree
- don’t invade basement membrane and supporting mesenchyme
How do cells of in situ tumours differ from normal cells?
- loss of normal cell arrangement
- variation in cell size and shape
- increase in nucleus size
- presence of abnormal chromosomes
- increased mitotic activity
What are the characteristics of tumours of small intestine?
- rare
- despite high cell turnover rate in villus
- high proliferative rates not necessarily linked to high incidence of tumour formation
What are the characteristics of malignant tumours?
- specific capacity to invade and destroy underlying mesenchyme
- metastasise
- stimulate angiogenesis, dev of blood supply, but new blood vessels easily damaged and may increase metastasis and prod more 2º tumours
- difficult to treat once metastasised
How can 1º tumours be treated?
- surgery or localised chemo/radiotherapy
What are the 6 hallmarks of cancer?
- self insufficiency ingrowth signals
- insensitivity to antigrowth signals
- apoptosis evasion
- limitless replicative pot (must be over 60-70)
- sustained angiogenesis
- tissue invasion and metastasis
How is self insufficiency in growth signals achieved?
- by prod own growth factors or receptors in increasing no.s to increase stimulus
How does sustained angiogenesis occur?
- need O2 and nutrient supply to stop inhibition of growth
- late event
How does tissue invasion and metastasis occur?
- escape and colonise other areas
- only likely to dev once tumour mass of sufficient size
In what order are 6 hallmarks developed?
- no particular order or seq
- w/ each acquisition tumour state becomes more pronounced and more aggressive
What is normal cell proliferation in dev and adult life, and why?
- proliferation and cell death carefully regulated to ensure proper growth to adulthood and maintenance of adult state
What proliferation is there in adult tissues?
- cell birth and death rates determine adult body size
- some adult tissues show constant and continued cell proliferation as constant tissue renewal strategy
- cells of many adult tissues don’t normally divide except during healing processes
What happens when mutations occur in neurons and muscle cell and why?
- generally don’t induce tumour formation
- as highly differentiated and rarely divide
- so cancers rare in adults
Can cancers occur in tissues made up differentiated cells?
- they can and do
- eg. skin and gastro-intestinal tract
What is the series events that occur after DNA damage to form a tumour?
- transient mutation
- if not repaired becomes permanent mutation
- cell division leads to tumour
What causes DNA damage?
- exogenous agents, eg. ionising radiation, UV radiation, chemical carcinogens, viruses
- endogenous events, eg. errors in DNA rep, intrinsic instability, attack by free radicals
What does whether a permanent mutation leads to formation of tumour depend on?
- depends on which gene (or collection of genes) accum mutation
Which genes must accum mutation for tumour to develop and why?
- genes controlling cell proliferation or apoptosis
- to allow cells to evade normal controls reg tissue growth
What does 3% of human genome code for and why does this make tumour formation unlikely?
- protein and regulatory seq assoc w/ them
- so mutation v unlikely to be in coding seq
- even if it is must be in particular subset to bring about transformation to malignant state
What are 2 broad classes of genes involved in onset of cancer?
- proto-oncogenes –> excessively active in growth promotion
- tumour suppressor genes –> normally restrain cell growth, damage allows inapprop growth
What do many of the genes in both classes involved in cancer onset code for proteins involved in?
- entry into and passage through cell cycle
- apoptosis
- DNA repair
What types of mutation are commonly encountered in cancers?
- point
- frame shift
- mutation to stop codon
- amplification
- overexpression
- inapprop expression
- loss of gene
- fusion w/ another gene (chromosomal break and rearrangement)
- epigenetic mods (hypermethylation of cytosine in CpG islands)
Which mutations affect protein structure and how?
- frame shift and mutation to stop codon
- truncate protein or scramble seq
What effect do amplification, overexpression and inapprop expression mutations have?
- normal protein prod, but too much or at wrong time
Which mutations mean no protein prod?
- loss of gene
- epigenetic mod (gene silencing)
What effect does fusion w/ another gene have?
- chimeric protein w/ alt function
How is understanding of chemical events leading to cancer important?
- events causative in cancer dev, so prevention would be effective preventative measure
- several genetic diseases predisposing cancer involve mutations in gene which normally function to protect DNA from mutational events
- understanding events has direct clinical relevance
What are major causes of cancer?
- diet agents and lifestyle, approx 70% in Western world
- tobacco products, approx 30%
- dietary deficiencies in fruit and veg
- exposure to various chemical or physical agents in env
Can cancer occur w/o obvious exposure to env carcinogens?
- yes
- may occur in organs for which no env or genetic causes identified
- appears spontaneous DNA damage can occur and give rise to carcinogenic mutations
What are examples of spontaneous DNA damage that can occur?
- breakage of bonds between purines and deoxyribose, leading to random base insertions
- deamination of cytosine to uridine
- deamination of methylcytosine to thymidine
What is the most common spontaneous DNA damage and how frequently does it occur?
- deamination of cytosine to uridine
- 20x/cell/day
Why do few of spontaneous DNA damages usually accum?
- repaired by action of DNA repair enzymes
Why do DNA mutations occur?
- result of DNA rep
- inherent instability of DNA molecule
Is DNA stable, why?
- yes when isolated from cells
- no w/in cells, breakage of bond connecting purines to deoxyribose 10^4 events/cell/day
What other factor can cause DNA damage?
- chemical attack by products of oxidative metabolism
What are the characteristics of chemical carcinogens?
(DNA damage by endogenous agents)
- large chemical diversity
- may have great chemical stability
- stable chemical carcinogens known to undergo metabolic activation by enzymes normally involved in detox, and form highly reactive compounds which particularly react to guanine
How is guanine often affected by chemical carcinogens?
- converted to methylguanine
- mistaken for adenine when DNA rep
- paired w/ T in copied strand
- meaning eventually G-C replaced by A-T (point mutation)
What is the earliest discovered chemical carcinogen and what discoveries did this lead to?
- tumour induction in workers exposed to coal tar
- identification of polycystic aromatic hydrocarbons in coal tar
- discovery they acted as skin carcinogens in lab animals
What was identified as a carcinogen in rubber and chemical industry and what did it cause?
- 2-naphthylamine
- bladder cancer
What are the characteristics of physical carcinogens? (DNA damage by endogenous agents)
- ionising radiation
- UV radiation
How can ionising radiation result in direct and indirect damage? (Physical carcinogens)
- direct = ss and ds DNA breaks
- indirect (radiolysis of water) = damage from free radicals
How does UV radiation result in DNA damage? (Physical carcinogens)
- insufficient energy to prod ions
- absorbed by bases and induces chem reactions between 2 thymidines in helix
- forms covalent cross link
- disrupts normal bping
- obstacle to DNA pol
- mutations arise if not repaired
Where do 90% skin cancers occur?
- sun exposed areas
What is xeroderma pigmentosum and what can it lead to?
- acute sensitivity to UV
- if not recognised leads to high incidence of skin cancer
- defects in gene for repair of DNA damage
Which genes repair damaged DNA?
- p53 evolved to survey DNA for damage and to repair it
- other genes repair errors introd during rep
How are thymidine dimers repaired?
- removal of whole stretch of DNA
- resynthesis using opp strand as template
How are 0-6 methylguanine errors repaired?
- directly removed by breaking phosphate backbone
Can ss and ds breaks be repaired?
- ss directly repaired
- ds not easily repairable
How does p53 repair damage?
- delays DNA rep until repair completed
- apoptosis if damage too severe
Can p53 be mutated?
- mutated in over 50% of all human cancers
- mutations in 1 allele result in cancer susceptible state called Li-Fraumeni syndrome
What are growth signals generated by?
- diffusible growth factors
- extracellular matrix components
- cell to cell adhesion molecules
What are some examples of diffusible growth factors?
- EGF = epidermal growth factor
- FGF = fibroblast growth factor
- TGFα = transforming growth factor α
- PDGF = platelet derived growth factor
Do cells req growth signals to grow?
- normal cells don’t proliferate w/o signals
- many oncogenes of cancer cells subvert normal growth signalling in various ways
What is always the end result of cancer cells subverting normal growth signals?
- cont mitogenic stimulation
- centering on cyclin D in cell cycle
What to mechanisms of subverting growth signals differ between?
- between cancers and w/in specific tumour type by chance
What are 3 ways cancer cells can become growth signal autonomous?
- modulation of growth factor provision
- modulation of growth factor receptor activity
- modulation of intracellular signalling pathways
What occurs during modulation of growth factor provision?
- normally heterotypic signalling
- but many cancers acquire capacity for autocrine growth stimulation
- eg. glioblastomas, prod PDGF
- eg. sarcomas, prod TGFα
What is heterotypic signalling?
- growth factors made by 1 cell type and released to stimulate growth in different cell types
- in most normal tissues
What is autocrine growth stimulation?
- prod growth factor itself can respond to
- so doesn’t req growth factor prod by other cells w/in tissue
What occurs during modulation of growth factor receptor activity?
- growth factor binds to receptor in membrane
- receptor becomes active as Tyr kinase and autophosphorylates Tyr residues
- some proteins can then dock w/ active receptor and become activated
- some proteins act as substrates for receptor kinase and become Tyr phosphorylated
- these proteins usually protein kinases (Tyr or Ser kinases) and phosphorylate other proteins
- overexpression of receptor may allow cell to become hyper-responsive to normal low growth factor levels that wouldn’t normally induce growth response
- excessive overexpression of growth factor receptors may also result in ligand independent signalling
- receptors may also become structurally altered and become ligand independent as a result
What are some examples of growth factor receptors that can become unregulated in certain tumours?
- EGF-R (EGF receptor) and Erb (heregulin receptor) unreg in stomach, brain and breast tumours
- HERZ overexpressed in stomach and breast tumours
What occurs during modulation of intracellular signalling pathways?
- transmit signals gen at cell surface by growth factor-receptor interaction (subject to mod in many cancer cells)
- often involves 50S-Ras-Raf-MAPK cascade
- many tumours have mutated Ras protein, meaning mitogenic signals transmitted w/o any upstream activation of pathway
- suggested signalling pathways dereg in all tumours (hard to prove and not certain)
- direct interaction of Ras protein w/ survival promoting pI3 kinase enables growth signals to simultaneously gen survival signals (protecting cells from apoptosis)
What is the 50S-Ras-Raf-MAPK cascade known to interact w/?
- several other growth promoting pathways
What % of human tumours have a mutated Ras protein?
- approx 25% overall
- 90% pancreas
- 50% colon
- 30% lung
What is an oncogene?
- gene w/ pot to cause cancer
What family of proteins is Ras part of?
- GTP binding proteins that function as signal transducers
How does Ras function?
- GTP binds causing conformational change
- allows Ras to interact w/ other downstream signalling molecule
- Ras hydrolyses GTP –> GDP, released and Ras returns to inactive state
How does mutated Ras differ from normal Ras?
- decreased GTPase activity
- GTP not released
- constantly activated
What must happen to maintain normal tissue mass?
- response to growth signals when approp
- response to antiproliferative signals to stop growing
What do growth signals and antiproliferative signals both depend on?
- soluble growth inhibitors
- immobilised inhibitors bound to extracellular matrix and on surface of nearby cells
How are growth signals and antiproliferative signals generated?
- generated by inhibitors binding to cell surface receptors which then activate intracellular signalling circuits
What are 2 distinct mechanisms of blocking proliferation in normal tissues?
- cells become quiescent (inactive)
- cells differentiate (so can’t re-enter cell cycle)
How does cells becoming quiescent block proliferation in normal tissues?
- push actively dividing cells out of cell cycle into G0
- normally reversible
- may go back to G1 if approp growth stimuli
How does cells differentiation block proliferation in normal tissues?
- push cells into highly differentiated state, eg fully differentiated muscle fibres or nerve cells
- lose ability for future cell division
- often assoc w/ change in cell morphology, physically limiting cells pot to divide
What is TGFβ and how does it work?
- anti-growth factor
- upregulates expression of inhibitors of cell cycle (eg. p15, p21, p27)
- these are inhibitors of cyclin/CDK complexes which need to be activated for cell cycle to function
- in some cell types, suppresses expression of c-myc gene, which regulates G1 cell cycle machinery
What ways have tumours dev to block TGFβ acting?
- expression of TGFβ receptor down regulated
- receptor mutated to inactive or less active form
- intracellular signally disrupted by mutation of Smad4 protein
- mutation of Rb
How does mutation of Smad4 protein block TGFβ acting?
- disrupts intracellular signalling
- by elimination of p15
- or decrease in responsiveness of CDK4 cell cycle kinase to inhibition by p15
Why is Rb important?
- Rb important in control which acts at restriction point in G1 phase of cell cycle
- many antiproliferative signals operate through Rb
- important in non dividing cells as forms complex w/ E2F family of transcrip factors, preventing E2F acting, so preventing expression of genes involved in G1 to S transition
How does mutation of Rb block TGFβ acting?
- in DNA-virus induced tumours, Rb inactivated by being complexed w/ protein made by virus
What other aspect of insensitivity to antigrowth signals probably acts through Rb?
- can turn off expression of cell adhesion molecules that transmit antigrowth signals
How does c-myc function in normal cells?
- c-myc codes for transcrip factor Myc
- in actively dividing cells, active transcrip form of Myc complexed w/ Max
- Myc/Max complex = growth
- Mad/Max = differentiation
What is the mechanism for avoiding differentiation - involving c-myc oncogene?
- overexpression of c-myc (lots of Myc)
- favouring Myc/Max formation
- decreasing Mad/MAx formation
- maintains cells growth and blocks differentiation
What are the major steps in avoiding apoptosis?
- chromatin condenses and cyto shrinks
- nucleus fragmented, DNA “laddering”, blebbing and cell fragmentation
- phagocytosis of apoptotic bodies
What happens during apoptosis?
- cellular membranes disrupted
- cytoplasmic and nuclear skeletons degraded
- chromosomes broken down
- nucleus fragmented
- all w/in 30-120 mins
- dismembered cell engulfed by neighbouring cells
- usually completely eliminated wi/in 1 day
Can all cells apoptose?
- most have capacity to apoptose if directed to
Where are apoptosis initiating signals generated?
- from inside and outside cell
How are apoptosis initiating signals from outside cell transmitted?
- transmitted through receptors that bind death inducing factors (inc FAS ligand and TNFα)
- signals may be offset by signals gen by survival factors, eg. IGF1
How can apoptosis be triggered by cells gen intracellularly?
- unrepairable DNA damage
- signalling imbalance due to oncogene action
- lack of sufficient survival signal
- hypoxia
- loss of cell-cell contact or cell-ECM contact
The multitude of signalling opps means what for tissues?
- keeps normal cells in contact w/ neighbours
- regulates individual cell growth, survival or death in way approp for whole tissue
Why is cytochrome c important to apoptosis?
- potent apoptosis catalyst
- key process involves its release from mito
How are proteins of Bcl-2 family involved in apoptosis?
- in apoptotic cascade
- some pro-apoptotic and some anti-apoptotic
- regulate cytochrome c release
How is apoptosis a defence against tumour progression?
- if hormones removed, hormone dependent tumours undergo massive apoptosis
- suggests increase in cell growth and apoptosis occurred at same time
- apoptosis may be switched on by oncogene overexpression
- elimination of cells w/ activated oncogene expression 1º way that mutant cells continuously removed from tissues
What mutation is found in 50% lymphomas?
- mutation in c-myc and bcl-2
- further evidence for myc-bcl-2 interaction
In low conc serum, c-myc expressing cells show what level of apoptosis?
- high apoptosis
What could increased apoptosis be abolished by?
- addition of survival factors, eg. IGF1, to medium
- overexpression of Bcl-2 or Bcl-XL
- disruption of FAS pathway
What has been demonstrated about apoptosis evasion in transgenic mice?
- inactivation of Rb prod slow growing microscopic tumours w/ high rate apoptosis
- inactivation of p53 in same cells prod rapidly growing tumours
What can some lung and colon cancers do to evade apoptosis?
- prod decoy non-signalling receptor for FAS ligand
Do normal cells have limitless replicative pot?
- no, limited capacity for repeated divisions
- stop after certain no. doublings
How can tumour cells avoid cell growth stopping in cultured human fibroblasts?
- disabling p53 and Rb tumour suppressor proteins
- continue dividing until enter 2nd state termed crisis
- but small no. (appox 1 in 10^7) continue to divide w/o limit –> immortalisation
Why do tumour cells need to become immortalised?
- normal cells have capacity for 60-70 doublings
- should enable clones of tumour cells to expand to no.s vastly exceeding no. cells in body
- but during tumour dev, widespread apoptosis alongside cell division
- no. cell in tumour greatly under represents no. divisions req
- so generational limit of normal somatic cells may be barrier to cancer dev
What are human telomeres?
- simple seq of DNA repeats found at chromosome ends
- contain 2500 copies TTAGG
How does loss of telomeres lead to apoptosis?
- at each cell division 50-100bp of telomeric DNA lost from ends of every chromosome
- DNA pol unable to completely replicate 3’ ends during each S phase
- progressive shortening w/ each division
- eventually lose ability to protect ends of chromosomes
- end to end chromosomal fusion and apoptosis
What telomerase activity is there in malignant cells?
- telomere maintenance in most malignant cells
- most show upregulated expression of telomerase
- maintaining telomere length critical to state of immortality
What does telomerase do?
- adds hexanucleotide repeats onto ends of telomeric DNA
- keeping telomeres at length above critical threshold
- allowing unlimited multiplication of descendant cells
How is proximity of normal cells to blood vessels achieved?
- cells in tissue need to be w/in 100μm of capillary
- during organ dev
- once tissue formed, growth of new blood vessels, angiogenesis transitory and carefully reg
Why do cells need close proximity to blood vessels?
- oxygen and nutrient supply
- for cell function and supply
- for cancer cells, also gives route to rest of body
What is angiogenesis?
- growth of new blood vessels
Do cancer cells have angiogenic capacity?
- initially lack it, limiting initial expansion
- usually dev it in order to get to clinically detectable size
What signals do cancer cells of approx 2mm emit?
- to recruit surrounding connective tissue and vascular cells to tumour and induce them to grow into blood vessels
What are the most common positive angiogenic signals?
- vascular endothelial growth factor (VEGF)
- acidic and basic fibroblast growth factors (FGF1 and FGF2)
How do positive angiogenic signals act?
- through transmembrane Tyr kinase receptors on capillary endothelial cells
What are the most common negative angiogenic signals?
- thrombospondin-1, binds to transmembrane receptor (CD36) on endothelial cells
When is the ability to induce and sustain angiogenesis acquired and activated?
- acquired in discrete steps during tumour dev
- activated in mid-stage lesions, prior to appearance of full-blown tumours
How do tumours activate angiogenesis?
- changing balance of inducers and inhibitors
- many increase expression of VEGF and/or FGFs
- some downregulate expression of inhibitors, eg. thrombospondin-1
How do tumour cells increase expression of growth factors to activate angiogenesis?
- activation of ras oncogene may upregulate VEGF expression
How do tumour cells downregulate inhibitor expression to activate angiogenesis?
- positively reg by p51
- loss of p53 function (occurs in most human tumours) decreases levels
- releasing endothelial cells from inhibition
How are cells of normal tissues held in place?
- by cell adhesion molecules which bind them to neighbouring cells and to ECM by integrins
- cadherins linked to internal cytoskeleton of cell by catenins
What is the exception to the immobilised format of tissue and why?
- WBCs
- can migrate out of blood (and lymphatic system) to enter other tissues
What must tumours do in order to metastasise?
- acquire migratory properties usually restricted to WBCs
- break connections to neighbouring cells and ECM
- break through collagen and other proteins making up connective tissue that encapsulates organs and tissues
- inc breaking through basement membrane, separating epithelial cells from underlying mesenchyme
A poor prognosis is shown by spread of cancer to where?
- localised spread to lymph nodes
Where can tumours spread to?
- depends, certain tumours spread to particular organs
- not to do w/ distance
Are cells in 2º tumour the same as in 1º tumour?
- yes
- eg. if breast cancer spreads to lungs, still made up of abnormal breast cells
Are mutations in E-cadherin gene common?
- no, relatively rare
- as often result in poorly differentiated cancer cells w/ interior architecture that no longer resembles original structure
- decrease in amount more common
How do catenins (linking proteins) vary in tumour cells?
- often absent or nonfunctioning
How do integrins vary in metastasising cells?
- fewer prod
- different subset that help migration through connective tissue or blood vessel wall
What forms usually make up cadherin-catenin complexes?
- usually E-cadherin assoc w/ β-catenin
What is the role of β-catenin?
- in adhesion complex
- transcrip factor
What do integrins do?
- link cells to proteins such as collagen in surrounding connective tissue
- span the cell’s membrane, forming connections with connective-tissue proteins outside cell and proteins in the cell’s cytoskeleton
What do migratory cells extend into matrix of connective tissue and what is their role?
- cytoplasmic protrusions
- latch onto proteins in matrix w/ help of new integrins and pull themselves through
Is the ability to secrete proteases or induce
surrounding cells to, a property of cancer cells?
- yes, 1 of changes that turns normal cells to cancer cells and then to metastatic cancer cells
What must happen in order for cell to make protrusions?
- cytoskeleton reconfigured for mobility
Are cancer cells motile?
- most derived from cells that are not naturally motile
- so lack necessary skeleton giving motility
What shape are normal epithelial cells?
- cylindrical, cuboid, flattened
What shape are cancer cells?
- star shaped and elongated
- more closely resemble fibroblasts than epithelial cells
When is similar morphology to cancer cells observed in epithelial cells?
- during dev of embryo
What is req for tumour to pass through ECM?
- proteases to degrade basal membrane (proteolysis)
- breakdown of ECM proteins
What proteases can be used to degrade the basal membrane (allowing tumour to pass through ECM)?
- plasminogen activators (Ser activators), leads to conversion of plasminogen to plasmin
- Cathepsin B ( Cys proteases)
- Matrix Metalloproteinases (MMPs), often converted from inactive Pro form by plasmin
What are 2 mechanisms for survival of cancer cells in bloodstream?
- travel in clusters, increasing poss at least 1 will survive
- surround themselves w/ blood cells, eg. platelets, masking them from immune surveillance
What are the stages of metastasis?
- cancer cells invade surrounding tissues and vessels
- transported by circulatory system to distant sites
- reinvade and grow at new location
How do cancer cells interact w/ their 2º location?
- specific interactions between cancer cell surface and endothelial cells lining blood vessels in new host tissue
- carbs on cell surface bind to specific receptor on endothelial cells, called selectin
- more bonds mediated by integrins form between cells
How do cancer cells recognise diff tissues?
- diff selectins recognise diff carbs on cancer cell surface
- each cancer cell expresses diff set of carbs
What are carb-selectin interactions usually used by and why?
- WBCs
- to identify particular tissues to combat infection
