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Pharmacogenomics > week 6 > Flashcards

week 6 Flashcards

1
Q

Genes for Malignant melanoma

A

BRAF

Codon 600

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2
Q

drugs for Malignant melanoma

A

Vemurafenib,
Dabrafenib,
Trametinib

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3
Q

drug action for Malignant melanoma

A

ATP-competitive inhibitor of kiase domain of BRAF

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4
Q

consequnce of identifying mutation for Malignant melanoma

A

Drug targets BRAF mutated at codon 600

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5
Q

Genes for Non small cell lung cancer

A

EGFR

Exons 18,19,20 and 21

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6
Q

drugs for Non small cell lung cancer

A

Gefitinib, Erlotinib, Afatinib, Dacomitinib

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7
Q

drug action for Non small cell lung cancer

A

EGFR Tyrosine kinase inhibitor

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8
Q

consequence of identifying mutation for Non small cell lung cancer

A

Drug targets EGFR over activity caused by mutation in the Tyrosine kinase domain of EGFR

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9
Q

drugs for Non small cell lung cancer

ALK

A

Crizotinib, Ceritinib, Alectinib

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10
Q

drug action for Non small cell lung cancer

ALK

A

Crizotinib, Ceritinib, Alectinib

Receptor tyrosine kinase inhibitor (including ALK and Met)

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11
Q

consequence for identifying mutations Non small cell lung cancer
ALK

A

Lung cancers can have the EML4-ALK translocation. This translocation causes ligand-independent dimerization and/or oligomerization of ALK, resulting in constitutive kinase activity

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12
Q

gene for Breast cancer

A

HER2

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13
Q

drug for Breast cancer

A

Herceptin

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14
Q

drug action for Breast cancer

A

Antibody to HER2 receptors blocking downstream signalling

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15
Q

consequence of identifying mtuation for Breast cancer

A

Breast cancers have to be positive for HER2 to work.

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16
Q

gene for Colorectal cancer

A

KRAS CODONS 12, 13, 59, 61 117 AND 146 NRAS CODONS 12,13, 59 and 61

17
Q

drug for Colorectal cancer

A

Cetuximab and panitumumab

18
Q

drug actionfor Colorectal cancer

A

Antibody to EGFR receptors blocking downstream signalling

19
Q

consequence of identifyign mutation Colorectal cancer

A

If patient has a downstream RAS mutation blocking the EGFR will be ineffective

20
Q

how is cancer a genomci disease

A

More and more mutations build up so not accurate replication and end up changing some hallmarks of cancer

21
Q

CML drug treats

A

Imatinib

22
Q

casue of CML

A

BCR-ABL1 fusion gene produced by trsanlocation
95% by (9;22) (q34;11) translocation
creates constitutively active tyrosine kinase leading to ucnrontrolled proliferation

23
Q

normal action of ABL1

A

ABL1 is tyrosine kinase- normall role in differentiation and reg of cell cycle

24
Q

imatinib action

A

blocks ATP binding centre of BCR-ABL so inhibits phosphorylation activity so less cancer protein produced

25
Q

effect of inbiting BRAF

A

no activation of MEK so no ERK so down cell prolif and survival

26
Q

Ras-RAf pathway

A

growth factor binds-
receptor tyrosine kinase activated- Ras activated-
BRAf activated,
Mek then Erk activated so normal cell prolif and survival

27
Q

EGFR pathway

A 
EGFR receptor activated
 KRAS,NRAS activated, 
activate RAF, MEK, ERK,
 trans factors,
 proliferation and survival
28
Q

Ras swithcing

A

Gdp is on GTP is off controlled by GEFs- guanine nucleotide exchange fact (sos1SOS2

29
Q

mechanism of GAOS

A

terminate On state by catalyzing hydrolysis of GTP to GDP

30
Q

waht is Gastrointestinal stromal tumours (GISTT

A

Sarcoma- tumour of soft tissue

31
Q

mutation in Gastrointestinal stromal tumours (GISTT

A

Caused by mutations in Kit and PDGFRA (receptor tyrosine kinase) so constitutive downstream pathways

32
Q

treatment of Gastrointestinal stromal tumours (GISTT

A

Imatinib bits of ATP bidnign sites of KIT and PDGFRA and bcr-abl inactivating signalling
Mek-Erk for proliferation and PI3K for survival
or Sunitinib is multi target TKI

Pharmacogenomics (11 decks)

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