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MCB II Block 1 > Cancer II 5 > Flashcards

Cancer II 5 Flashcards

1
Q

tissue trophism

A

cancer cells may be attracted to particular tissue b/c of what they are expressin gon their surface

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2
Q

CXCR4 normally expressed by

A

WBC

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3
Q

in cancer they are expressing CXCR4 which binds to

A

CXCL12

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4
Q

CXCL12 is secreted by

A

lung, liver, bone

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5
Q

when cancer cells secreting CXCR4 where will they be attracted to

A

lung, ,liver, and bone b/c they express CXCL12 which will bind to CXCR4

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6
Q

CCR7 binds to

A

CCL21

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7
Q

CXCR4 is expressed in what type of cancer cells

A

breast

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8
Q

cancer cells being attracted to certain tissues, next step is

A

extravasation

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9
Q

migrated cell is called an

A

invadopodia

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10
Q

what has to happen cancer cell is ready to extravasate

A

has to secrete MMP to digest through endothelial cell and basal lamina to get out into new tissue

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11
Q

formation of second metastesis is major

A

limiting step

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12
Q

why is formation of second tumor major limiting step

A

hospitality of host envirorment
what cytokines, growth factors are present
what levels of TIMP (tissue inhibors of metalic proteases)

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13
Q

oncogene addiction

A

cancer cells are “addicted” to certain enviornment, maybe by the stromal cells from the ponit they originated from

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14
Q

in order to form macrometasesis what needs to happen

A

they need to proliferate rapidly adn then stimulate angiogenesis
then they can also metasetesize again

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15
Q

what drug do you use to block VEGF

A

Bevacizumab

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16
Q

chemolabelled antibodies

A

sot he drug will only go to the cancer cell to kill them, wont hurt our bodies other cells.
couple the chemotherapy stuff to antibodies targeting the cancer

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17
Q

immunoliposome

A

liposome coupled to antibodiy that will target some overexpressed receptor on cancer cell and within that liposome include cytotoxic drugs
liposome binds specifically to cancer body via monoclonal antibody

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18
Q

name some strategies to fight cancer

A

Cell Cycle Drugs
Inhibition of Signal Transduction Kinases
Inhibition of Angiogenesis
Hormone antagonists (ie. tamoxifen: arrests growth, not kill)
Enhancing immune response (to recognise tumour as foreign)

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19
Q

research into identifying cancer pathways is important for developing

A

diagnositc and prognositc tools

and biomarkers for cancer

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20
Q

why is it helpful to have better diagnositc and prognositc tools
and biomarkers for cancer

A

can identify the cancer earlier, needs to be easy and cheap to screen pop.

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21
Q

lead identificatoin

A

pharmecutical companies use research to identify drug that would be successful at targeting pathway

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22
Q

target identification and validation

A

what labs do, identify the biology and the pathways, etc.

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23
Q

list steps for new model for rational treatment of cancer

A

target identification and validation
lead identification
lead optimisation
clinical drug candidate

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24
Q

lead optimisation

A

look at structure of compound and see what and why it is having desired affect and try to optimize that u

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25
Q

what is phase 1 of clinical trial

A

very small group of ppl to evaluate safety and dosage, etc

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26
Q

what is phase 2 of clinical trial

A

larger group tested, still looking for effectiveness and safety

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27
Q

phase 3 of clinical trial?

A

compare the new drug with the existing therapy, if it’s not as effective then they won’t move forward

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28
Q

phase 4 of clinical trials

A

drug gets licensed and used in clinics - phase 4 is after drug is licensed. they follow up on use of drug long term, see if there is any long term side effects. physicians need to report back on side effects.

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29
Q

for a non-metastatic primary tumor what are some treatments

A

surgical excision
local radiotherapy (ionising radiation)
systemic chemotherapy (cytotoxic drugs & new signal transduction targeting drugs)
Immunotherapy (stimulate immune system)

30
Q

for metastatic cancer what are some treatments

A 
Non-metastatic primary tumour: 
surgical excision
local radiotherapy (ionising radiation)
systemic chemotherapy (cytotoxic drugs & new signal transduction targeting drugs)
Immunotherapy (stimulate immune system)
Metastatic cancer:
As above
palliative care (ease pain & discomfort)
31
Q

chemotherapy what does it do

A

systemic toxicity. damage DNA so much that cancer cells can’t cope b/c they have so many mutations and don’t have DNA repair enzymes. so when the drugs break up DNA they have a hard time with it

32
Q

what is the problem with chemotherapy

A

the cancer cells that survive these treatments then may aquire more mutations after and repopulate the cancer

33
Q

what is another problem with chemotherapy and cancer cells

A

they don’t have apoptosis signaling so might still not die with chemotherapy. (but most will)

34
Q

if cancer comes back, what will you do regarding chemotherapy

A

give them second drugs, hoping cancer cells wont be resistant to it

35
Q

PARP inhibitors are in trial to treat

A

hereditary breast cancer with LOF of BRCA gene

36
Q

in normal breast epithelial cells there are two ways ssDNA breaks can be repaired:

A

BRCA pathway

PARP pathway

37
Q

if pt with hereditary breast cancer is given PARP inhibitors and then chemotherapy what happens

A

normal cells can repair DNA breaks using the BRCA pathway, cancer cells get broken up and die b/c they can’t repair any of the damage happening to them. the normal cells can survive them

38
Q

cancer cells with loss of BRCA pathway will be very sensitive to what treatment

A

PARP inhibitors

39
Q

anti-cell drugs target

A

any rapidly dividing cell

40
Q

drugs that inhibit synthesis

A

inhibit S phase of cell cycle

41
Q

ex of drugs that damage DNA (chemotherapy)

A

cisplatin

carboplatin

42
Q

when pts are exposed to chemotherapy they are given

A

cocktail to approach cancer from differnet angles

43
Q

alkylating agents

A

abnormal base pairing, abnormal strand breakage etc as result

44
Q

drugs that block dna synthesis

A

Purine Analogues: Mercaptopurine
Pyrimidine Analogues: 5-Fluorouracil
Folic Acid Analogues: Methotrexate

45
Q

topoisomerase inhibitors ex of what type of therapy

A

chemotherapy

46
Q

topoisomerase enzyme involved in

A

inducing nicks in DNA and then ligating them after

47
Q

topoisomerase inhibitors

A

breakages in genome as a result

48
Q

ex of topoisomerase inhibitors

A

Doxorubicin, Daunorubicin

49
Q

mitotic spindle inhibitor drugs

A

Paclitaxel (Taxol)

Vinblastine, vincristine

50
Q

adenoviral p53 gene therapy

A

cells now express p53

51
Q

velcade good at treating

A

multiple myelomas

52
Q

what is used to treat multiple myeloma

A

Bortezomib (Velcade)

53
Q

activation of what pathway in multiple myeloma

A

IkB pathway

54
Q

draw out iKB pathway

A

pg 198

55
Q

velcade drug blocks

A

proteasome, so IKB can’t be degraded and still inhibits NFKB

56
Q

if you block proteasome in multiple myeloma

A

prevent IkB degradation

buildup of Bax & Bak → pores → apoptosis

57
Q

drug resistance in cancer treatment

A

amplification of diff. genes in cancer cells. amplification of Mdr1 is commonly found in cancer drugs exposed to chemotherapy, it’s ABC transporter which prevents the accumulation of cytotoxic drugs within the cancer cell, so they will be less susceptible to the chemotherapy.

58
Q

bcr-abl has overactive

A

tyrosine kinase domain

59
Q

drug tto block bcr-abl overactive tysoine kinase

A

imatinib

60
Q

bcr-abl fusion protein can activate

A

a lot of different pathways
ras-mapk
pi2k - pb
results in increased survival and proliferation

61
Q

gleevec/imatinib

A

first drug to turn off protein known to cause cancer. blocks bcr-abl

62
Q

what cancer does gleevec/imatinib treat

A

CML

63
Q

gleevvec resistance

A

bcr-abl structural alterations

too much bcr-abl expressed to be blocked

64
Q

endostatin stabilizes

A

endothelial cells

65
Q

Bevacizumab (Avastin) is given with what to be effective

A

cytotoxic drugs

66
Q

Bevacizumab (Avastin used to treat

A

metastatic cancer - like colorectal metastatic cancer

67
Q

women with metestatic breast cancer, stage IV, what would you do to treat?

A

estrogen and progesteron receptors were negative
induction chemotherapy: done before surgery - give some chemotherapy before, there’s a lot of inflammation in the primary site so it’s a way of getting rid of the inflammation before going in and surgically resecting it
right mastectom. sampling of bilateral axillary nodes (they will inject blue dye into cancer and see if it spreads to lymph nodes)

clinical case follow up pg 216-217

68
Q

how does Paclitaxel (Taxol) work

A

binds and stabilizes microtubules, so there’s no disassembly

69
Q

how does Vinblastine, vincristine work?

A

Binds tubulin subunits → prevents polymerization

70
Q

taxol and vinblastine and vincrisinte work when

A

during m phase of cell cycle, they are mitotic spindle inhibitors

MCB II Block 1 (12 decks)

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