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Interaction module: Environment and genes > Week 2 > Flashcards

Week 2 Flashcards

1
Q

3 types of cancer treatment

A

radiation
surgery
chemotherapy

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2
Q

examples of precision medicine

A

targeted therapy

immunotherapy

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3
Q

Neoadjuvant (preoperatively) are used for what

A

administered prior to surgery to facilitate resection and prevent metastasis.

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4
Q

Adjuvant (postoperatively) are used for

A

after surgical debulking to kill micrometastases and reduce risk of distant relapse; increase disease-free survival.

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5
Q

examples of alkylating agents

A

Cisplatin, Carboplatin, Oxaliplatin, Busulfan, Chlorambucil, Dacarbarzine,
Mechlorethamine (Nitrogen Mustard), Mephalan, Nitroureas, Procarbazine, Temozolamid

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6
Q

examples of antimetabolites

A

Methotrexate, Fluorouracil, Mercaptopurine, Thioguanine, Cytarabin, Hydroxyurea,
Fludarabine, Leucovorin, Capecitabine, Gemcitabine, Aracytidine, Pemetrexed, Trimexrexate

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7
Q

examples of mitotic spindle agents

A

Docetaxel, Paclitaxel [Taxol], Vincristine, Vinblastine, Cabazitaxel, Eribulin.

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8
Q

topoisomerase inhibitors examples

A

Topo I inhibitors – Irinotecan, Topotecan; Topo II inhibitors – Etoposide, Teniposide

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9
Q

what do Antimetabolites do

A

limit the synthesis of nucleic acid precursors e.g. methotrexate inhibits dihydrofolate reductase, reducing the synthesis of folate which is necessary for purine and pyrimidine production. Similar agents – 5-fluorouracil, cytarabine.

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10
Q

what do Topoisomerase enzymes do

A

participate in the winding and unwinding of DNA and are inhibited by anthracyclines (doxorubicin, daunorubicin, epirubicin), epipodophyllotoxins (etoposide, teniposide) and camptothecins (irinotecan, topotecan).

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11
Q

PARAMETERS TO BE EVALUATED IN SYSTEMIC TREATMENTS response

A 
Complete response (CR): disappearance of all target lesions.
Partial response (PR): at least a 30% decrease in the sum of the longest diameter (LD) of targeted lesions.
Stable disease (SD): neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD.
Progressive disease (PD): at least a 20% increase in the sum of the LD of targeted lesions.
Duration of response or time to progression (TTP): the time from response to progression.
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12
Q

PARAMETERS TO BE EVALUATED IN SYSTEMIC TREATMENTS SURVIVAL

A 
Disease-free survival (DFS): from the time of treatment to first recurrence.
Overall survival (OS): from the time of diagnosis to death.
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13
Q

what is mucositis and its symptoms and treatment

A

common complication of cancer chemotherapy
oral pain and burning
ulcerations
analgesia

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14
Q

how is P-glycoprotein (PGP) encoded by the MDR1 gene

A

multidrug resistance gene.
P-glycoprotein (PGP) mediates transport of certain drugs out of the cell thereby reducing their intracellular concentration and cytotoxicity.
PGP over-expression achieved increased expression of its mRNA with or without MDR1 gene amplification.

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15
Q

how can resistance be tackled

A

increasing the levels of platinum reaching tumours

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16
Q

tumour margin meaning

A

removing the rim of normal tissue surrounding the tumour

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17
Q

Drug resistance is effected by microenvironments give examples of what

A

fibroblasts
exosomes
vascualar abnormality

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18
Q

how is dna damaged included by ionizing radiation

A

doubled stranded base pair is damaged to stop replication leading to cell death
base and sugar damage, single-strand breaks,
double-strand breaks, and covalent intrastrand or interstrand crosslinking

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19
Q

what is the process of DNA

A

DNA damage is recognised by DNA damage sensor proteins,
(ii) transducer proteins then signal to effectors and (iii) this results in either cell cycle arrest, DNA repair or apoptosis

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20
Q

what factors affect the response of tumour to radiation

A

cell intrinsic
microenvironment
right ph and oxygen in the tumour

21
Q

types of radiotherapy

A 
Radical radiotherapy 
Adjuvant radiotherapy 
Palliative radiotherapy 
EXTERNAL BEAM RADIOTHERAPY
BRACHYTHERAPY
RADIOISOTOPE THERAPY
PROTON THERAPY
22
Q

Radical radiotherapy

A

intent to cure either as primary therapy (e.g. early stage Hodgkin’s lymphoma) or as an alternative to surgery
preserves normal anatomy

23
Q

Adjuvant radiotherapy and an example

A

administered as an adjunct to potentially curative surgery.
breast cancer

24
Q

Palliative radiotherapy what is it

A

control of distressing symptoms. Not curative. Improve quality of life. Relieve pain due to bone metastases and nerve compression. Reduce haemorrhage and obstructions. Brain metastases.

25
Q

EXTERNAL BEAM RADIOTHERAPY

A

X-rays, gamma rays and electron beams from linear accelerators. High intensity electron beam (4-20MeV) has greater penetration, less scatter, delivers high energy to deep-seated tumours while sparing normal tissues in its pathway.

26
Q

BRACHYTHERAPY

A

Use of radioactive sources implanted directly into a tumour or body cavity to deliver localised radiotherapy

27
Q

RADIOISOTOPE THERAPY

what are examples

A

Internal isotope treatment given either orally or systemically by injection.
Can only be used where a tumour is in a tissue that will preferentially accumulate a specific isotope.
Radioiodine (I-131) for the treatment of thyroid cancer.

28
Q

PROTON THERAPY

and its examples

A

Form of radiotherapy that uses protons instead of x-rays.
High energy proton beams target tumours more precisely.
Generated using a synchrotron or cyclotron.
Less radiation dose outside the tumour – less damage to healthy tissues.
Causes fewer short and long-term side effects.
Proven to be effective in adults and children – brain cancer.

29
Q

how does radiation induced immune response in cancer therapy work

A

Radiation induces the release of tumour antigens
captured and processed by antigen-presenting cells (APCs) to activate
cytotoxic T lymphocytes (CTL).
CTL are recruited to attack primary tumour or metastatic tumour cells (abscopal effect).
Radiation up-regulates PD-L1 and in combination with anti-PD-L1 therapy (immune checkpoint inhibitor therapy)
enhances MHC and Fas expression on tumour cells
increases CTL-mediated cytotoxicity
including the release of cytokines to further
enhance killing of primary and metastatic tumour cells.

30
Q

what are the types of immunotherapy

A

Therapeutic vaccines – modified tumour cells, tumour-associated antigens, dendritic cells, oncolytic viruses.
Immune system modulators – cytokines (e.g. IL-2), interferons.
Monoclonal antibodies – targets on tumour cells (e.g. CD20 on B cell lymphomas).
Adoptive T cell transfer – tumour-infiltrating T cells, peripheral T cells, CAR T cells.
Immune checkpoint inhibitors – taking the breaks off the immune system.

31
Q

how is tumour associated antigens classified

A

4 ways

32
Q

cancer germline what is it

A

Expressed only by tumour cells and adult reprodutive tissues

33
Q

Differentiation

A

Expressed by tumours and limited range of normal issues

34
Q

Over expressed

A

It is expressed by both normal and tumour cells but more in tumour cell s

35
Q

How does Dendritic cell vaccines work

A 
eluriated moncytes are cultured 
with IL-4 and GM-CSF
immature DCs are produced 
matured with CD40
pulsed with a peptide with an expression vector 
injected in a patient 
as a autologous vaccine 
induces T cell immune response
36
Q

Dendritic cells

A

cells are modified outside of the body after taking them from the patient then put back in as a form of therapy

37
Q

precautions and flaws

A

too much cytokines can interfere in the microenvironment and can cause the tumour to grow more

38
Q

what is pegalating to overcome half life

A

polyethalinegylcol with cytokine as single agents are better combined in other therapies

39
Q

Adoptive T cell therapy

A 
make t cells better killers
by in vitro stimulation 
tumour taken 
isolate them 
tils 
grown outside 
and then infused back into the patient
conditioning their body by imunosupress them the t cells then expand in the body
40
Q

IL2 does what

A

stimulates growth

41
Q

how doe CAR T cell therapy work

A 
blood in taken from the patient 
Then the CAR gene is inserted into the  T cells to produce CAR t cells
millions are made in the lab
in order to put them back into the body
so they can bind to cancer cells
to kill cancer cells alone
42
Q

Schemetic of a T cell

A 
Using T cell receptor as antibody
targets with a tumour 
the modifies antibody 
binds on the tail 
activate the t cell to be cytotoxic
then kills the cancer cells
43
Q

immune checkpoint inhibition

A

activation signal
inhibirity signal given to stop over stimulation
stimulation of T cell
CTLA 4 and PD1 important to put breaks on T cells to stop over stimualtion

44
Q

PD1 can do what

A

It can switch off T cells.

45
Q

Monoclonal antibodies can do what

A

block PD1 and stops the production of CTLA4

46
Q

problems with immune checkpoint inhibtion

A

over activatio. can over saturate the micro envrionment making it hard for t cells to kill cancer cells

47
Q

what does imatinib do and mec

A

competes with the atp for the able kinase
stops the bality of the kinsase to work
affects the progression of CML

48
Q

BCR2 controls what

A

apoptosis

Interaction module: Environment and genes (7 decks)

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