Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacy Y2- Exam 3 > modern > Flashcards

modern Flashcards

1
Q

what kind of cells do chemotherapy target?

A

highly proliferating cells and then their process like cell cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the approaches for targeting only cancer cells?

A
  1. We can identify individual pathways that are aberrant in the cancer cell but not in the normal cell
  2. We can identify targets that are expressed/over-expressed in the cancer cell that are not expressed in the normal cell.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what mutation may women have that may result in them having a significantly higher risk of developing breast and/or ovarian cancer in their lifetime?

A

BRCA1 and BRCA2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what does BRCA1 do?

A

part of our double strand break repair machinery and binds to RAD51 to help identify mutations.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what happens when BRCA1 has a mutation?

A

it won’t repair the double strand break so we lose the repair, resulting in cell death of misread DNA and translocations and mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is personalised medicine?

A

Move away from the “one size fits all approach”
Moving closer to more precise, predictable and powerful medicine – customised for the individual patient
Growing understanding of genetics is allowing better diagnoses, safer drug prescribing and more effective treatments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what does personalised medicine classify tumours according to?

A

their genetic make-up instead of where they grow in the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the benefit of personalised medicine?

A

Drugs are often tested on broad populations and prescribed using statistical averages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are some aims for personalised medicines?

A
  • Shift the emphasis in medicine from reaction to prevention
  • Predict susceptibility to disease, improve disease detection, pre-empt disease progression
  • Customize disease-prevention strategies
  • Prescribe more effective drugs and avoid prescribing drugs with predictable side effects
  • Reduce the time, cost, and failure rate of pharmaceutical clinical trials
  • Eliminate trial-and-error inefficiencies that inflate health care costs and undermine patient care
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the name of the enzyme involved in DNA repair, it is an inhibitor?

A

Poly(ADP)ribose polymerase or PARP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what do PARP do?

A

-they repair DNA form duplex DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what does PARP inhibitors do?

A

result in the formation of a double strand DNA break as the sing strand break isnt repaired and is replicated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what does BRCA1 and 2 do?

A

prevent repair of double strand breaks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is BRAF mutation?

A

common in melanoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

WHAT IS THE PROTEIN-PROTEIN INTERACTIONS?

A

An interaction of two proteins at their domain interfaces that regulates
the function of the protein complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the domain intefaces?

A

is the part of a protein that can function and exist

independently from the rest of the protein

17
Q

why do we want to target PPIs?

A
  • molecular target driven
  • many cellular processes involve PPI
  • Understanding of how proteins engage and communicate
  • understand how Human diseases can be caused by irregular PPI’s
18
Q

what are some potential problem of PPI?

A

-often referred to as “undruggable”
-Affinity achieved from the accumulation of numerous weak interactions
-Hydrophobic nature results in drug leads that
are large and hydrophobic can be had for oral doseage

19
Q

how to target protein-protein interaction?

A

-fragment base drug discovery

20
Q

what are the BCL-2 family?

A
  • B-Cell Lymphoma-2 Family (BCL-2)

- Key regulators in cell apoptosis

21
Q

what does altering the balance of BCL-2 proteins do?

A

altering the balance of the pro survival and pro death provides one means by which cancer cells undermine
normal apoptosis

22
Q

what type of BCL-2 gene are over expressed in cancer?

A

the pro survival ones which increases the apoptosis threshold therefore preventing apoptosis

23
Q

how do pro death BCL-2 proteins work to result in apoptosis?

A

-pro death proteins BAK/BAX have activators that bind to the pro death protein to activate them resulting in MOMP forming holds in mitochondria

24
Q

how do pro survival BCL-2 proteins work to result in apoptosis?

A

-the pro survival proteins bind to activator proteins and pro death preventing them from binding together

25
Q

how do pro death BCL-2 proteins work to result in apoptosis?

A

when cell death signals come, sensitiser bind to pro survival protein that free up activator for pro death leading to apoptosis

26
Q

how does cancer cells benefit from pro survival?

A

cancer keeps up regulating pro survival even when there are death signals

27
Q

what does P53 do?

A

its the guardian of the genome

  • apoptosis
  • blocks angiogenesis
  • cell cycle arrest
  • DNA repair
28
Q

how is P53 avoided in human cancers?

A
  • it has a mutation so it can bind to DNA
  • up regulation of other proteins to prevent it from getting close to DNA like MDM2
  • is inactivated by several viral proteins
29
Q

what does MDM2 do?

A

MDM2 binds to P53 and stops it from finding DNA?

30
Q

how does MDM2 PRVENT P53 FROM WORKING?

A

-over express MDM2 and P53 is unable to get into the nucleus leading to proliferation?

31
Q

how does P53 bind to MDM2?

A 
 Binding site on MDM2: deep,
hydrophobic groove
 p53 binds in an -helical
conformation
 Forms 3 critical contacts through
the side chains of Phe19, Trp23, Leu26
(hot spots)
 300 Å2
 Backbone of p53: no interaction
except for 1 H-bond scaffold for the
side chains
32
Q

how do the nutlins work?

A
  • they displace P53 from MDM2

- Mimics the interactions of p53

33
Q

what are some possible plans to target PPIs?

A

Identify a peptide that will mimic a crucial peptide binding region for
one of the proteins

34
Q

why are peptides not good drugs?

A

BUT peptides are not good drugs – poor metabolic stability and low
bioavailability

35
Q

what is a method that can be done to alter peptides to make them better drugs?

A
  • peptide stapling

- photo

36
Q

how does peptide stapling work?

A

takes long chain and connects the staples along back bone to bring it closer in on its self into a helic

37
Q

how does photodynamic therapy work?

A 
light come towards our our photosensitiser and changed oxygen into single atoms with lead to cell death
-Non-invasive
-Minimal side effects
- Only activated in
irradiated cells
38
Q

what does gold nanoparticles take advantage of for delivery?

A

the fact that the blood vessels are leaky due to enhanced permeability and retention effect

Pharmacy Y2- Exam 3 (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions