Brainscape's Knowledge GenomeTM

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


See full index

IHO Week 4 (MJ) > Signal Transduction III > Flashcards

Signal Transduction III Flashcards

1
Q

How does overexpression occur?

A

At the mRNA or protein level:
DNA amplification
Increased transcription
decreased degradation

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

What usually causes constitutive activation

A

mutation (but NOT always)

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

The paradigm of protein over expression = sensitivity to inhibitor

A

NOT very general

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

Colon Cancer

A

4th most commonly diagnosed cancer
Second most lethal cancer
Universally accepted to screen

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

Chemotherapy for Colon Cancer

A

Metastatic : 5-fluorouracil with either irinotecan or oxaliplatin

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

EGFR

A

driver of proliferation and survival

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

Ras and Raf

A

downstream of EGFR - leads to cascade and transcription.

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

What does EGFR activation cause?

A 
Cell survival
Proliferation
Angiogenesis
Metastasis
Cell motility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

EGFR antibodies

A

Cetaximab (first used, not anymore, Martha Stewart)

Panitumumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is Panitumumab active in?

A

Colon cancer
Squamous cancers of head and neck
Squamous (HPV driven) cancers of the cervix and penis

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

EGFR in lung cancer

A

deletion on chromosome 19 or 20, mutation on receptor

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

EGFR in colon cancer

A

NOT a receptor mutation

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

When do blocking EGFR antibodies work?

A

When cells have wild type Ras/Raf

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

What is the most common leukemia?

A

Chronic lymphocytic leukemia (CLL)

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

CLL is a disease of ______, not ________.

A

accumulation, over-proliferation

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

SLL and CLL

A

same disease

17
Q

What does it mean when K67 is elevated?

A

cell cycling is active

in nucleus proportional to cell cycling activity

18
Q

What does % of K67 mean?

A

What percentage of cells are in active cell cycling

19
Q

Bcl-2

A

anti-apoptotic

20
Q

Bax

A

pro-apoptotic

21
Q

Low Bax/Bcl-2

A

low apoptosis (anti-apoptotic ratio)

22
Q

High Bax/Bcl-2

A

high apoptosis (pro-apoptotic ratio)

23
Q

What does CLL present with?

A

Commonly with autoimmune phenomena including:

  • Immune thrombocytopenic purpura (ITP)
  • Auto immune hemolytic anemia (AIHA)
  • Auto immune agranulocytosis
24
Q

What else do patients with CLL have?

A

typically hypogammaglobulinemia

virulent infections

25
Q

What often drives CLL?

A

constitutive expression of a non-mutated BTK

26
Q

Ibruntib

A

blocks PLC-gamma 2 (stops cascade)

27
Q

Fostamatinib

Entosplentinib

A

blocks SYK (which activates BTK)

28
Q

Dasatanib

A

blocks LYN (which activates BTK)

29
Q

what does BTK do?

A

phosphorylates PLC gamma 2 and activates a secondary messenger system

30
Q

How does BTK becomes constitutively expressed?

A

alterations in mRNA handling (not understood)

31
Q

Is BTK a receptor?

A

NOPE

32
Q

Why is fludarabine and cyclophosphamide with Rituximab dangerous to patients with CLL?

A

very immunosuppressive!

33
Q

Historical treatment for CLL

A

chlorambucil
CD20 antibody Rituximab
fludarabine and cyclophosphamide with Rituximab

34
Q

What revolutionized the treatment of CLL?

A

BTK inhibitors

35
Q

Ibrutinib MOA

A

Covalently modifies APT binding site (cysteine 481) on BTK

michael addition

36
Q

What types of CLL is Ibrutinib active against?

A

CLL with del 17p and del 11q

37
Q

Resistance against BTK inhibitors?

A

C481S (change from -SH to -OH on active site)
PLC-gamma
Clinically these are both difficult to treat

38
Q

Venetoclax

A

Bcl-2 modulator, resets apoptotic threshold

39
Q

Strategies for eliminating growth promoting signals?

A
  1. lower concentration of hormone in blood
  2. block the ability of the hormone to interact with its receptor (antagonists or antibodies)
  3. block down stream signal between receptor and effector apparatus

IHO Week 4 (MJ) (10 decks)

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