BIOCH Y1 S1: Cancer

Question 1

what is cancer

Answer 1

• abnormal, uncontrolled growth of cells

Question 2

how does cancer occur

Answer 2

• one single cell has a mutation
• causes increased proliferation or decreased apoptosis > selective advantage
• form growing colony which can evolve and spread (metastasis)

Question 3

6 hallmarks of cancer

Answer 3

• continuous growth of cells
• evading growth suppressors
• invasion and metastasis
• replicative mortality: too many cells which can continue to divide > infinite survival
• angiogenesis: development of new blood supply to tumour
• resisting apoptosis
• active telomerase

Question 4

characterics of a cancer cell

Answer 4

• enlarged nucleus, little cytoplasm
• changes to cytoskeleton (to allow for more movement > metastasis)
• loss of specialised fts. > can’t carry out normal cellular functions
• many dividing cells > disorganised

Question 5

benign vs malignant tumour

Answer 5

• benign: don’t spread to other tissues (non-cancerous), resemble tissue of origin
• malignant: uncontrolled and can migrate to other organs/metastasise, don’t resemble tissue of origin (anaplasia)

Question 6

carcinoma
sarcoma

Answer 6

• epithelial cancer
• cancer of connective tissue

Question 7

leukaemia
lymphoma

Answer 7

• cancer of blood (WBC)
• cancer of lymphocytes

Question 8

how do cancer cells metastasise

Answer 8

• decreased adherence to neighbouring cells
• secretes proteolytic enzymes to degrade ECM
• intravasate into blood/lymph
• adhere to capillary walls + extravasates into tissue
• angiogenesis

Question 9

local cancer

Answer 9

• grown outside original body part but hasn’t spread to other tissues
• can block other tissues

Question 10

distant metastasis

Answer 10

• movement of cancer cells thru blood or lymph and spread to distal organs

Question 11

how and why does angiogenesis occur

Answer 11

• tumour can only grow to a certain size before it has a lack of oxygen and build-up of waste
• secretes growth factors e.g. vascular endothelial growth factor (VEGF) to stimulate formation of blood vessels through branching of nearby capillaries
• if angiogenesis doesn’t occur, cells can sit dormant for a while until it occurs

Question 12

mechanical factors which can impact where a tumour metastasises to

Answer 12

• site of OG tumour and where veins drain to
• size of cancer cell: can eventually be too big to progress through some blood vessels so stick and grow in new area
• e.g. colon cancer usually spreads to liver

Question 13

how can DNA damage occur to cause cancer?

Answer 13

• inherited (germline)> every cell in body will have one copy of DNA w/ defect
• acquired (somatic) mutations over time and not passed on b/c don’t affect gametes e.g. due to carcinogens like UV light, radiation, viruses etc - mostly acquired

Question 14

why does the risk of cancer increase with age?

Answer 14

• decreased DNA repair mechanisms
• longer exposure to carcinogens which can cause acquired mutations

Question 15

examples of predispositions to cancer

Answer 15

• processed meat preservatives
• carcinogen exposure
• obesity
• high fat and low fibre diet
• natural carcinogens in food
• chronic inflammation e.g. coeliac/IBD

Question 16

oncogenes

Answer 16

• altered forms of normal genes that promote inappropriate cell growth or cell growth in inappropriate circumstances
• gain of function mutation in only one oncogene can increase predisposition to cancer (one-hit)

Question 17

proto-oncogenes + examples

Answer 17

• normal genes which promote cell growth however if mutated can become an oncogene > cancer
• classes include growth factors, growth factor receptors, intracellular signalling proteins, transcription factors, cell cycle control proteins
• e.g. tyrosine kinase receptors

Question 18

how can a proto-oncogene become an oncogene

Answer 18

• 1. point mutation in coding sequence (hyperactive protein in normal amounts)
• 2. gene amplification (normal protein but overproduced)
• 3. chromosome rearrangement > hyperactive or overproduced proteins

Question 19

tumour suppressor genes

Answer 19

• prevent cancer by stopping cell cycle and/or causing apoptosis
• loss of function mutation (inherited or acquired) requires both copies of gene to be inactivated (2 hit hypothesis) and can cause cancer
• if only one copy is inactivated, still works but slightly unable to control cell cycle
• e.g. Rb/p53

Question 20

mismatch repair genes

Answer 20

• genes that repair mutated DNA during S phase
• 2-hit hypothesis + loss of function mutation

Question 21

local effects of cancer

Answer 21

• cancer displaces normal surrounding tissues > function deteriorates since cancer cells can’t carry out specialised function
• block vital passages e.g. colon, bronchi, blood vessels

Question 22

systemic effects of cancer

Answer 22

• signs and symptoms not directly related to location of tumour (can allow early detection of cancer)
• e.g. high metabolic weight which causes weight loss, fatigue, tiredness (cachexia), abnormal hormone secretion

Question 23

familial predisposition to cancer (ICPS)

Answer 23

• multiple family members with the same/ related cancers
• 2 family members with the same rare cancer
• early onset of cancer
• bilateral cancer in paired organs
• multiple cancers in different organs in one person

Question 24

penetrance

Answer 24

• % of ppl who have the cancer gene and then actually develop the cancer

Question 25

penetrance of APC > colorectal cancer

Answer 25

100%

Question 26

penetrance of BRCA1/BRCA2 > breast cancer

Answer 26

40-70%

Question 27

TNM staging

Answer 27

• tumour (size)
• node (swelling + texture of lymph nodes)
• metastasis