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PHRM 847 > Homework 1 > Flashcards

Homework 1 Flashcards

1
Q

ECOG

A

What? physical status of the patient

0: fully active
4: completely disabled

Aggressive treatment requires higher ECOG score to tolerate the treatment

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2
Q

NCCN

A

National Comprehensive Cancer Network

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3
Q

1st Line Therapy for Metastatic Pancreatic Adenocarcinoma

A

First:
- if jaundice present –> metal stent
- genetic testing for inherited mutations
- molecular profiling for tumor tissue

Second:
- Good PS: clinical trial (preferred) or systemic therapy
- Poor PS: palliative and supportive care and consider single agent chemotherapy or targeted therapy

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4
Q

2nd Line Therapy for Metastatic Pancreatic Adenocarcinoma

A

No disease progression (after 4-6 months of chemotherapy)
- Folfirinox
- modified Folfirinox
- Nalirifox
- Gemcitabine + paclitaxel

Disease Progression:
- Gemcitabine
- Capecitabine
- continious infusion of 5-FU

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5
Q

3rd Line Therapy for Metastatic Pancreatic Adenocarcinoma

A

re-biopsy
radiation therapy

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6
Q

Is it reasonable to have the same drug as both the 1st line and 2nd line drug regimen?

A

YOU WANT TO AVOID THE SAME DRUG IN BOTH 1st and 2nd LINE

  • when you give the drug the 1st time, the cancer cells have never seen the drug
  • the weaker cancer cells are killed (tumor shrinkage) but some of the cancer cells survive and form resistance
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7
Q

Biomarkers for PD1/PDL-1 Drugs

A
  • used to determine if certain patients are likely to benefit from immunotherapy

Examples:
- increased PDL1
- unstable MSI/dMMR
- increased TMD

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8
Q

CTLA-4 Inhibitor

A

Ipilimumab (Yervoy)

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9
Q

PD1/PDL-1 Interaction

A

Cancer cell expresses MHC and PDL-1 on the surface of the cell

PDL-1 on cancer cell interacts with PD1 on the T-cell
- PDL1 binds to PD1 on T-cell sending signal to the T-cell stating it is a good molecule

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10
Q

Should doctor order a test for PD1 or PDL-1 in tumor sample?

A

PDL-1

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11
Q

PD-1 Blockers

A

Pembrolizumab (Keytruda)

Nivolumab (Opdivo)

Cemiplimab (Libtayo)

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12
Q

PDL-1 Blockers

A

Atezolizumab (Tecentriq)

Avelumab (Bavencio)

Durvalumab (Imfinzi)

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13
Q

BRAC1

A

Olaparib

Niraparib

Talazoparib

Rucaparib

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14
Q

KRAS

A

Binimetinib

Trametinib

Cobimetinib

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15
Q

CDK4 and CDK6 Inhibitors

A

Palbociclib

Ribociclib

Abemaciclib

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16
Q

PARP Inhibitor to treat BRCA1 Mutation Cancers

A

When DNA is broken or damaged, the body can repair the DNA by both BRCA-mediated and PARP

In a patient with BRCA-mutated cells, the patient can no longer repair the DNA via the BRCA-mediated pathway; however, it can still repair the DNA via the PARP pathway (accuracy is low)

If we give PARP inhibitors, both the BRCA-mediated and PARP pathways for DNA repair are blocked and the cell (cancer) will die

Even if we give a PARP inhibitor that blocks PARP in good cell, the cell can still repair the DNA by the BRCA-mediated pathway as the BRCA cell is not mutated in a good cell

SYNTHETIC LETHALITY

17
Q

BRCA1 Mutations Gain or Loss of Function

A

most of the patients are loss of function

18
Q

HSB3

A

SOS –> KRAS

19
Q

Salirasib

A

membrane bound KRAS

20
Q

Lonafarnib & Tipifarnib

A

soluble KRAS

21
Q

Vemurafenib

A

RAF inhibitor

22
Q

Trametinib

A

MEK1/2 inhibitor

23
Q

Perifosine

A

AKT inhibitor

24
Q

Deltarasin

A

soluble KRAS to the membrane bound KRAS

25
Q

AMG 510

A
  • small molecule that specifically and irreversible inhibits KRAS G12C mutation by locking KRAS in inactive (GDP) state
  • normal KRAS is a ball that does not have clear binding pockets
  • when G12C mutation occurs, it forms a disulfide bond binding pocket that allows AMG 510 to bind into the pocket through C cysteine
26
Q

CDKN2A/B Loss

A

CDK2NA and CKD2NB encodes for tumor suppressors involved within the CDK4/6 and MDM2 pathways

This tumor suppression leads to disrupted cell progression and proliferation

27
Q

Melanoma Patients with NRAS Mutation

A

Ribociclib + Binimetinib (Mektovi)

PHRM 847 (11 decks)

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