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MCB II Block 1 > Cancer II 5 > Flashcards

Cancer II 5 Flashcards

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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
what is phase 1 of clinical trial
very small group of ppl to evaluate safety and dosage, etc
26
what is phase 2 of clinical trial
larger group tested, still looking for effectiveness and safety
27
phase 3 of clinical trial?
compare the new drug with the existing therapy, if it's not as effective then they won't move forward
28
phase 4 of clinical trials
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.
29
for a non-metastatic primary tumor what are some treatments
surgical excision local radiotherapy (ionising radiation) systemic chemotherapy (cytotoxic drugs & new signal transduction targeting drugs) Immunotherapy (stimulate immune system)
30
for metastatic cancer what are some treatments
``` 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
chemotherapy what does it do
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
what is the problem with chemotherapy
the cancer cells that survive these treatments then may aquire more mutations after and repopulate the cancer
33
what is another problem with chemotherapy and cancer cells
they don't have apoptosis signaling so might still not die with chemotherapy. (but most will)
34
if cancer comes back, what will you do regarding chemotherapy
give them second drugs, hoping cancer cells wont be resistant to it
35
PARP inhibitors are in trial to treat
hereditary breast cancer with LOF of BRCA gene
36
in normal breast epithelial cells there are two ways ssDNA breaks can be repaired:
BRCA pathway | PARP pathway
37
if pt with hereditary breast cancer is given PARP inhibitors and then chemotherapy what happens
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
cancer cells with loss of BRCA pathway will be very sensitive to what treatment
PARP inhibitors
39
anti-cell drugs target
any rapidly dividing cell
40
drugs that inhibit synthesis
inhibit S phase of cell cycle
41
ex of drugs that damage DNA (chemotherapy)
cisplatin | carboplatin
42
when pts are exposed to chemotherapy they are given
cocktail to approach cancer from differnet angles
43
alkylating agents
abnormal base pairing, abnormal strand breakage etc as result
44
drugs that block dna synthesis
Purine Analogues: Mercaptopurine Pyrimidine Analogues: 5-Fluorouracil Folic Acid Analogues: Methotrexate
45
topoisomerase inhibitors ex of what type of therapy
chemotherapy
46
topoisomerase enzyme involved in
inducing nicks in DNA and then ligating them after
47
topoisomerase inhibitors
breakages in genome as a result
48
ex of topoisomerase inhibitors
Doxorubicin, Daunorubicin
49
mitotic spindle inhibitor drugs
Paclitaxel (Taxol) | Vinblastine, vincristine
50
adenoviral p53 gene therapy
cells now express p53
51
velcade good at treating
multiple myelomas
52
what is used to treat multiple myeloma
Bortezomib (Velcade)
53
activation of what pathway in multiple myeloma
IkB pathway
54
draw out iKB pathway
pg 198
55
velcade drug blocks
proteasome, so IKB can't be degraded and still inhibits NFKB
56
if you block proteasome in multiple myeloma
prevent IkB degradation | buildup of Bax & Bak → pores → apoptosis
57
drug resistance in cancer treatment
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
bcr-abl has overactive
tyrosine kinase domain
59
drug tto block bcr-abl overactive tysoine kinase
imatinib
60
bcr-abl fusion protein can activate
a lot of different pathways ras-mapk pi2k - pb results in increased survival and proliferation
61
gleevec/imatinib
first drug to turn off protein known to cause cancer. blocks bcr-abl
62
what cancer does gleevec/imatinib treat
CML
63
gleevvec resistance
bcr-abl structural alterations | too much bcr-abl expressed to be blocked
64
endostatin stabilizes
endothelial cells
65
Bevacizumab (Avastin) is given with what to be effective
cytotoxic drugs
66
Bevacizumab (Avastin used to treat
metastatic cancer - like colorectal metastatic cancer
67
women with metestatic breast cancer, stage IV, what would you do to treat?
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
how does Paclitaxel (Taxol) work
binds and stabilizes microtubules, so there's no disassembly
69
how does Vinblastine, vincristine work?
Binds tubulin subunits → prevents polymerization
70
taxol and vinblastine and vincrisinte work when
during m phase of cell cycle, they are mitotic spindle inhibitors

MCB II Block 1 (12 decks)

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