tumour surpressors and oncogenes

Question 1

initial and later hallmarks of cancer

Answer 1

evade growth suppression and apoptosis rapid replication metastasis angiogenesis LATER- inflammation, avoiding immunity, mutations, and affecting cellular energetics

Question 2

later hallmarks of cancer

Answer 2

inflammation, avoiding immunity, mutations, and affecting cellular energetics

Question 3

what are protooncogenes and how do they become oncogenes

Answer 3

involved in cell growth/proliferation a SINGLE mutation produces an oncogene= cell division no longer in control

Question 4

how oncogenes are activated

Answer 4

point mutation/deletion in protooncogene produces abberant (unusual) protein, or overproduces protein can lead to chromosomal translocation OR INSERTIONAL MUTAGENESIS= enhances normal protein levels OR fusion protein eg Philadelphia chromosome

Question 5

DIAGRAM 2 types of receptors and downstream signalling with examples

Answer 5

tyrosine kinase= adapter proteins=kinase cascade G protein coupled- goes immediately to Ras Raf cascade met, neu affected at TK receptor, ras/raf affected in cascade myc, fos, jun affected at transcription

Question 6

what happens in mutant RAS

Answer 6

normally, when GTP converted to GDP , RAS switched off in mutant tase, GTP can’t be dephosphorylated

Question 7

example of tyrosine kinase mutation (oncogene)

Answer 7

SRC- C terminal deletion (thing that controls it)- occurs in breast/colon

Question 8

example of T.F mutations (oncogene)

Answer 8

MYC (Burkitt’s lymphoma) and Jun (lung)

Question 9

example of G protein mutations and location in cell

Answer 9

Ha Ras (bladder) and Ki Ras (colon)- both G proteins and TK are cytoplasmic, T.F’s are nuclear

Question 10

what are TMS and how many mutations needed

Answer 10

they CONTROL cell proliferation- needs to be 2 mutations

Question 11

knudsons 2 hit hypothesis

Answer 11

sporadic cancer= 2 acquired mutations needed hereditary cancer= 1 inherited+ 1 acquired mutation ie HAPLOINSUFFICIENCY

Question 12

features of inherited cancer susceptibility ie inherited TMS mutation

Answer 12

family history of cancers early age onset tumours in pair organs eg breast tumours in different organs at same time eg P53 mutations

Question 13

retinoblastoma and gene involved

Answer 13

malignancy of retinal cells- involves RB1 TMS gene (regulates cell cycle)

Question 14

classes of TMS and common feature of all

Answer 14

regulate cell cycle, or repair proteins, or cell death regulators they all supress NEOPLASTIC PHENOTYPE (stop cells from going wrong)

Question 15

cell cycle regulators and cancers

Answer 15

P53 (many) and BRCA1 (breast/prostate)

Question 16

mutation of p53

Answer 16

even though its TMS, only ONE mutation needed

Question 17

APC TMS- what is it, and effect of mutation

Answer 17

this gene involved in cell adhesion (regulates B catenin) + signalling, so deletion in gene causes many benign polyps in colon aka FAP, which is likely to become malignant

Question 18

development of colorectal cancer

Answer 18

epithelium normal, then APC mutation= hyperproliferative epithelium Kras mutation= adenoma (benign), and late p53 mutation= carcinoma

Question 19

TMS VS oncogene- types of mutations, heritability, specificity and type of tumour

Answer 19

TMS deletions vs translocations/joint mutation sometimes inherited vs rare tumour specific (ie often affects a certain region) vs broad tissue specificity solid tumours vs leukemia/lymphoma