Week 18 p2 Flashcards

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1
Q

Why do we need targeted therapy

A

• Standard treatment does not work
• Some cancer respond better to these treatments
• Side effects are bad
Given systemically i.e their action is limited

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2
Q

What is the aim of targeted therapy

A

Decrease the activity of onco-proteins

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3
Q

Give examples of cancer therapies

A
  • Antibody based therapies
    • Small molecules
    • Immune checkpoint blockades- AB that block pathways to prevent the immune from attacking cancer cells
    • Gene therapy based approached - use viral vectors to deliver corrected and functioning mutated gene
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4
Q

What is Kaplan Meier graph

A

Shows the probability of an event e.g. survival rate

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5
Q

What is antibody therapies

A
  • Antibody bind to spefic proteins that can reduce their activity
    • Bind to extracellular area
    • AB are serum protein produced by B lymphocytes in response to antigen
    • Hypervariable region detects antigens known as epitopes
    • AB are from clonal expansion of a single antibody producing cell called monoclonal antibodies (mb)

Hint drugs that end in mab

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6
Q

How does antibody therapies work

A
• AB can act as anti oncogenic agents by blocking spefic growth factor  receptors 
Eg Herceptin (Trastuzumab)
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7
Q

How does Herceptin (Trastuzumab) work

A
  • Has high affinity for the extracellular domain of HER2
    • Promotes an increased HER2 internalisation and degradation

Induces antibody dependent cytotoxic response

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8
Q

Evidence of Herceptin on survival

A

• Improves survival rate and disease free survival in women with HER+ BC

In this trial Herceptin was given to women after surgery and chemotherapy with or with RT

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9
Q

What is Cetuximab/Panitumumab

A
  • Anti EGFR
    • Used treat metastic colorectal cancer, lung cancer and head and neck cancer
    • AB binds to and inhibits extracellular domain of EGFR
    • Results in cell cycle arrest
    Given in combination with standard therapy
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10
Q

What are the side effects and resistance of antibody therapies

A
  • SE: Herceptin= serve cardiac problems +milder effects
    • R; Herceptin= HER2-,PI3K pathway mutation
    • SE: Cetuximab= serve aches+ rash +milder effects too

R: Cetuximab=KRAS and BRAF mutation

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11
Q

How does immunotherapy and AB therapies work

A
  • Trials for HE2 and EGFR antibodies
    • HER2 and PD1/L1 inhibiting ab
    • Causes secondary effects for resistances
    • Such as Herceptin may cause mutation in HE2,prevent Mab binding and causes over expression of EGFR

Cetuximab will cause EFGR or RAS mutation so HER2 can compensate

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12
Q

What is small molecule treatment

A
  • Chemical compounds that directly interfere with overactive signalling pathways in cancer cells
    • Small chemical molecular can penetrate inside the cell
    • Inhibit enzymatic activity
    Hint ends with ib
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13
Q

What is Imatinib (gleevec) small molecule based treatment

A

For BCR-ABL and has high kinase activity]causing an increase in growth signalling and reduction in apoptosis

This drug binds to ATP binding pocky and stabilises the inactive form of BCR-ABL

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14
Q

What is the resistances for Imatinib (Gleevec)

A
  • Resistance to treatment after an initial response and developed in 3 ways
    • 1.muatation of BCR-ABL to inhibit binding BCR-ABL
    • 2.overexpression by other mechanism
    • 3.reistances cells can gain an selective advantage and patients relapse
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15
Q

How would this be solved

A
  • Giving inhibitors such as bosutinib,nilotinin or ponatinib
    • Increase dosage
    • Last resort- bone marrow transplant
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16
Q

What is Dabrafenib, Vemurafenib

A
  • Melanoma VF 500
    • BRAF is a cytoplasmic serine threonine kinase B-RAF
    • Vemurafenib is much more effectivities’ and easily resistance
    • Resistances is caused in MEK
    Now Vemurafenib is given with trametinib (a MEK inhibitor)
17
Q

Show the drugs and cancer type for ABL, BRAF, EGFR and HER2

A

ABL-IMATININ-CML,ALL

BRAF-DEBRADENIB,VEMURFENIB-MELOMA WITH BRAF V600 MUT

EGFR, CETUXIMAB-METASTIC COLORECTAL LUNG CANCER HEAD AND NECK CANCER

HER2-HERCEPTIN/TRAMTUZIMAB-BC