Exam 1- Lecture Content Flashcards

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1
Q

Keytruda: What is it?

A
  • A monoclonal antibody (mAb) drug
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2
Q
  • How is Keytruda effective?
A

o Its molecular target: PD-1 (programmed death receptor protein 1) expressed by immune cells.
o PD-L1/PD-L2: two ligands of PD-1 receptor
o Immune checkpoint

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3
Q

 Top cancers (males) %

A
  • Prostate – 26
  • Lung and bronchus – 12
  • Colon and rectum – 8
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4
Q

 Top cancers (females) %

A
  • Breast – 30
  • Lung and bronchus – 13
  • Colon and rectum – 8
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5
Q

Incidence rates - males

A

o Decreasing – lung, colon and rectum
o Stable – urinary bladder
o Increasing – melanoma

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6
Q

Incidence rates - females

A

o Decreasing – colon and rectum since 80’s, lung since mid 2000’s
o Stable – uterine
o Increasing – melanoma, thyroid

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7
Q

Lifetime probability of developing cancer - males

A
  • Males: lifetime risk – 40.5%
  • all sites – 1 in 2
  • prostate – 1 in 8
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8
Q

Lifetime probability of developing cancer - females

A
  • Females: lifetime risk – 38.9%
    o All sites – 1 in 3
    o Breast – 1 in 8
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9
Q

What is the top for sites for cancer death?

A

Males – 319,000 – 50%
o Lung and bronchus – 22
o Prostate – 11
o Colon and rectum – 9
o Pancreas – 8

Females – 289,000 – 53%
o Lung and bronchus – 22
o Breast – 15
o Colon and rectum – 8
o Pancreas – 8

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10
Q

Can cancer cells co-exist w/ normal cells in a microenvironment?

A

yes

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11
Q
  • How are cancer cells influenced by the microenvironment?
A

o When a tumor cell grows uncontrollably – uses the microenvironemtn to grow faster and spread, making more tumors.
o Components of the microenvironment interact w/ each other an w/ the tumor to enable cancer to grow.

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12
Q

How do cancer cells influence normal cells?

A

o Cancer cells shed tiny rna that can transform healthy cells into cancerous.
o They invade healthy cells and make them cancerous
o Normal cell cycle – grow, divide, die
o Cancer – grow, divide, reproduce

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13
Q

Nucleus

A

DNA and RNA synthesis

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14
Q

Plasma membrane

A

defining the extent of a cell - controls what exits and enters the cell

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15
Q

Golgi apparatus

A

secretion/ transportation of large molecules

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16
Q

Endoplasmic reticulum (ER)

A

Rough ER - protein synthesis
Smooth ER - lipid metabolism

17
Q

Mitochondria

A

energy production (ATP), etc.

18
Q

Cytoskeleton

A

Structure support/ cell shape and motion
ex. microfilament, microtubule, intermediate filament
-play a structural role to support

19
Q

Extracellular matrix (ECM)

A

cell interaction, etc. - anything top/side of cytoplasm - resp. for interaction w/ neighboring cell and how its related to its neighbor

20
Q

How is specific molecule (e.g. protein) detected in a cell?

A

immunostaining procedure

21
Q

Transcription

A

converting genetic info from DNA to RNA

22
Q

Post-transcription

A

from preRNA to mRNA; mRA stability

23
Q

Translation

A

Protein synthesis

24
Q

Post-translation:

A

protein modification; protein stability

25
Q

Promoter

A

determine transcription start site and the direction of transcription

26
Q

Enhancer

A

position - independent; orientation - independent

27
Q

Silencer

A

inhancer

28
Q

Tc Factors

A

(transcription co- factors) - DNA binding, transcription (usu. don’t directly bond w/ DNA)

29
Q

Processing of pre-mRNA

A

transcription rate
intron/Exon splicing
RNA stability

30
Q

Differential (or alternative) spicing

A

same pre-mRNA can be diff. splice in diff. tissue meaning that one gene could encode many mRNAs and proteins

31
Q

Potent mutagens are

A

powerful carcinogens

32
Q

weak mutagens are…

A

poor carcinogens