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
EXTERNAL BEAM RADIOTHERAPY
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
BRACHYTHERAPY
Use of radioactive sources implanted directly into a tumour or body cavity to deliver localised radiotherapy
27
RADIOISOTOPE THERAPY | what are examples
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
PROTON THERAPY | and its examples
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
how does radiation induced immune response in cancer therapy work
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
what are the types of immunotherapy
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
how is tumour associated antigens classified
4 ways
32
cancer germline what is it
Expressed only by tumour cells and adult reprodutive tissues
33
Differentiation
Expressed by tumours and limited range of normal issues
34
Over expressed
It is expressed by both normal and tumour cells but more in tumour cell s
35
How does Dendritic cell vaccines work
``` 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
Dendritic cells
cells are modified outside of the body after taking them from the patient then put back in as a form of therapy
37
precautions and flaws
too much cytokines can interfere in the microenvironment and can cause the tumour to grow more
38
what is pegalating to overcome half life
polyethalinegylcol with cytokine as single agents are better combined in other therapies
39
Adoptive T cell therapy
``` 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
IL2 does what
stimulates growth
41
how doe CAR T cell therapy work
``` 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
Schemetic of a T cell
``` 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
immune checkpoint inhibition
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
PD1 can do what
It can switch off T cells.
45
Monoclonal antibodies can do what
block PD1 and stops the production of CTLA4
46
problems with immune checkpoint inhibtion
over activatio. can over saturate the micro envrionment making it hard for t cells to kill cancer cells
47
what does imatinib do and mec
competes with the atp for the able kinase stops the bality of the kinsase to work affects the progression of CML
48
BCR2 controls what
apoptosis