mollecular hallmarks of cancer and carcinogenesis Flashcards Preview

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Flashcards in mollecular hallmarks of cancer and carcinogenesis Deck (84)
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1

what are the main characteristics of the biological hallmarks of cancer?

there is no one single feature - they have acquired capabilities of cancer but not all cancers have the same acquired functional capabilities - various mechanistic strategies to acquire these

2

how are biological hallmarks used?

6 main and they are later used for prognosis, prediction and treatment

3

what are the six main biological hallmarks of cancer?

sustained angiogenesis, evading apoptosis, tissue invasion and metastasis, self sufficient in growth signals, insensitive to anti growth signals and limitless replicative potential

4

what are other biological hallmarks of cancer?

avoiding immune destruction, tumour promoting inflammation, deregulating cellular energetics, genome instability and mutations

5

what is meant by self sufficiency in positive growth factors?

a lot of signally pathways and targeted and changed in carcinogenesis. The most fundamental trait of cancer is the ability to sustain chronic proliferation. This occurs through signals by growth factors that bind to cell surface receptors and generally contain the intracellular tyrosine kinase domain. This then signals into the cell and the intracellular signalling pathways will regulate the progression through the cell cycle and growth

6

how are cancer cells monitored?

they are not monitored by the outside they progress independently.

7

how do tumours commonly evade growth supressors?

Rb protein is a key regulator of the cell cycle and controls the progression if G1 to S phase. There is negative GF control of the Rb protein - GF will inhibit the cell cycle by activating the Rb protein. A mutation in the Rb gene will render it resistant to the negative growth factor and make it inactive, therefore there is no gatekeeper between G1 and S phase.

8

how do tumours often evade immune destruction?

very often a tumour cell will have an infiltration of immune cells into the surrounding cells. There will be interaction between the tumour and immune cells.
The tumour cell will express receptor PD1 which will bind to T cell PDL1 - silences the T cell so cannot attack

9

how can the interaction between the T cell and tumour be stopped?

inhibitors can stop this through blocking binding. The antigen of the T cell and the T cell receptor of the tumour cell bind, anti PDL1 will bind to the PD1 receptor on the tumour cell and anti PD1 to the T cell and therefore it cannot bind with T cell a

10

how do cells normally stop replicating?

each cycle of replication the telomere of the daughter cell gets shorter so there is a finite replicative life

11

how can tumour cells enable replicative immortality?

the can maintain the length of the telomere and telomerase - infinite divisions

12

what is tumour inflammation?

there is dense inflammatory infiltrate of some tumours compared to others - the tumour associated inflammation can promote the progression of the tumour and cancer and therefore it benefits the tumour.

13

how can tumours be divided?

into categories depending on inflammation - different prognosis and amount of immune therapy

14

what are some cytokines that are released in TAI?

IFN-y, IL-6 and TNF-a

15

how can a tumour metastasise?

cancer becomes dysplastic and changes from a low to high grade dysplasia - breaks through the basal lamina and the ability to metastasis grows - can go to the endothelium of blood vessels and then metastasise into different tissue

16

what influences metastasis?

the tumour type

17

what is less worrying for a tumour?

when it has not metastasised - can locally destruct but not systemically
when there is a normal tumour that has a lining around it

18

how does metastasis result in a secondary tumour?

the cells will adhere to and penetrate a capillary wall and then through extravasation will form a secondary tumour once dividing

19

what process can be targeted in cancer therapy by antibodies?

inducing angiogenesis

20

how is angiogenesis induced?

small tumour will grow and will send different messangers to capillaries - these will start to grow and will supply the tumour will blood, oxygen and nutrients

21

how can angiogenesis aid the formation of secondary tumours?

the supply of nutrients and oxygen can help the spread

22

how does genomic instability help the tumour?

the instability allows it to progress quicker as it can react to changes more quickly

23

what are the three outcomes of DNA damage?

single stranded - apoptosis or DNA repair
double stranded - DNA repair or senescence/arrest

24

what is the deregulation of metabolism in cancer cells?

where normal tissue has oxidative or anaerobic pathways that will produce different ATPs depending on the pathway, tumour cells are adapted to lack of O2 and therefore do anaerobic metabolism

25

what are proto-oncogenes?

they are normal genes that promote cell proliferation, survival and angiogenesis

26

what are oncogenes?

they are mutated versions of proto that result in the increased expression/ overactivation of protos and therefore the increased and uncontrolled activity of expressed proteins - they are cancer causing agents

27

what does dominant gain-of-function mean?

oncogenes have this - it means that one mutant copy of the gene acts dominantly to the remaining normal parental gene
mutation in one of the two alleles is sufficient

28

where is the mutation to make oncogenes?

in somatic cells - it is not inherited
there is some tissue preference

29

what are TSGs?

they act to maintain checkpoints such as Rb and p53. They control genomic stability

30

how will a mutation be expressed in a TSG?

it is recessive so both copies of the gene/both alleles need to be affected - a mutation in one can easily happen when born