cancer, hallmarks of cancer, proto-oncogenes, tumor supressors, Metastasis, tumour microenviroment, and immunotherapy (25)

Question 1

angiogenesis

Answer 1

formation of new blod vessels

Question 2

benign

Answer 2

pose no to little risk because they are small and localised. eg. wart

Question 3

burkitts lymphoma

Question 4

cancer stem cells

Answer 4

tumor cells capable of seeding new tumors

Question 5

carcinogen

Answer 5

enviromental DNA-damaging agents. can be inherited or somatic mutation that prevent DNA repair to happen fast enough

Question 6

carcinoma

Answer 6

tumors derived from epithelial cells (endoderm cells form the gut, or ectoderm cells from the skin/neural epitelial)

Question 7

CAR T cells

Question 8

epithelial-to-mesenchymal transition (EMT)

Answer 8

a cells ability to go from a epithelial cell to a mesenchymal cell. this can a tumor cell use to get over the basement menbrane and the spread to other tissues (metastatis).

Question 9

immune checkpoint pathway

Question 10

immunoediting

Question 11

leukemia

Answer 11

type of cancer where the individual cells can circulate in the blood

Question 12

loss og heterozygosity (LOH)

Question 13

lymphomas

Question 14

malignat

Answer 14

tumor cells that can invade nearby tissue, spreading and making additonal tumors wihile growing itself

Question 15

metastasis

Answer 15

when a tumor can spread througout the body

Question 16

mulit-hit model

Question 17

mutagen

Answer 17

anything that can cause a mutation/error in the DNA/DNA replication

Question 18

incogene

Question 19

p53 protein

Answer 19

gardian og the genome. responesible for causing arrest in the cell cycle if something is not right before M-phase. if eznymes can fit it the damage, the cells move on in the cell cycle. if not, p53 activates apoptosis.
ift it does not work, the cells can keep dividing even though there are DNA-damage

Question 20

philadelfia chromosome

Question 21

proto-oncogene

Question 22

Ras-protein

Answer 22

GTPase switch. when Ras activates MAP kinase which can activate many TF that regulate cell proliferation. mutation in RAS can casue a constituve activation of MAP kinase pathway –> the cells thinks there are gwoth-hormone present –> they think they need go grow all the time

Question 23

Rb protein

Question 24

retrovirus

Question 25

sarcoma

Answer 25

tumors derived from mesodermal tissuse ( muscle, bines, connective tissue precursors, cartelage)

Question 26

telomerase

Answer 26

cancer cell can ipregulate telomerase expression –> they can keep dividing without dying

Question 27

transformation

Question 28

tumorigenesis

Question 29

tumor microenviroment

Answer 29

the immediate enviroment (nærmljø) of the tumor

Question 30

tumor supressor gene

Question 31

warburg effect

Answer 31

“tumors consume tremendous amounts of glucose relative to most non-transformed tissues, and that the majority of glucose consumed by tumors is fermented to lactate, rather than oxidized in pathways that require respiration”

the tumor cells prefer to fermentate lactate even though there are oxygen present

Question 32

SNV (single nucleotide variant or point mutation)
Indels (insertions or deletion)
SV (structural variant

Answer 32

SNV: where one nucleotide is switch with another
indels: insertion or deletion of one nucleotide in the DNA
SV: chromosomal rearangement, dupliations, abnomral number of chromosomes