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cancer > clinical oncology 1: cancer treatment > Flashcards

clinical oncology 1: cancer treatment Flashcards

1
Q

what are the main anti-cancer treatment modalities?

A

surgery
radiotherapy
chemotherapy
immunotherapy

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2
Q

what are the types of genetic mutations that can cause cancer?

A
  • chromosome translocation
  • gene amplification (copy number variation)
  • point mutations within promoter or enhancer regions of genes
  • deletions / insertions
  • epigenetic alterations to gene expression
  • inherited
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3
Q

what are the types of systemic cancer therapies?

A

cytotoxic chemotherapy

targeted therapies

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4
Q

what are some types of cytotoxic chemotherapies used?

A
  • alkylating agents
  • antimetabolites
  • anthracyclines
  • vinca alkaloids & taxanes
  • topoisomerase inhibitors
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5
Q

what are the types of targeted therapies?

A

small molecule inhibitors

monoclonal antibodies

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6
Q

how do cytotoxic chemotherapies work?

A

select’ rapidly dividing cells by targeting their structures (mostly DNA except taxanes affect microtubules)

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7
Q

how & when is cytotoxic chemotherapy given?

A

IV or orally

can be given:

  • adjuvant (post-op)
  • neoadjuvant (pre-op)
  • as monotherapy or in combination
  • with curative or palliative intent
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8
Q

what are the side effectes of cytotoxic chemotherapy and why do they arise?

A
  • hair loss
  • mucositis
  • immunnosuppression
  • nausea & vomiting
  • diarrhoea
  • nephrotixicity
  • neurotoxicity
  • tiredness
  • systemic effects mean all rapidly dividing cells in body are affected
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9
Q

how do alkylating agents work?

A
  • add alkyl groups to guanine residues in DNA
  • cross-link DNA strands and prevents DNA from uncoiling at replication
  • trigger apoptosis (via checkpoint pathway)
  • encourage mis-pairing (oncogenic)
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10
Q

what are some examples of alkylating agents?

A

chlorambucil
cyclophosphamide
decarbazine
temozolomide

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11
Q

how do pseudo-alkylating agents work?

A

add platinum to guanine residues in DNA

- same mechanism of cell death as alkylating agents

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12
Q

what are some examples of pseudo-alkylating agents?

A

carboplatin
cisplatin
oxaliplatin
(basically anything with platin in the name)

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13
Q

how do anti-metabolites work?

A

masquerade as purine / pyrimidine residues -> inhibition of DNA synthesis, DNA double strand breakage, apoptosis

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14
Q

what are some examples of anti-metabolites?

A
  • methotrexate (folate)
  • 6-mercaptopurine
  • decarbazine
  • fludarabine
  • 5-fluorouracil
  • capecitabine
  • gemcitabine
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15
Q

what are the side effects of anti-metabolites?

A
  • hair loss
  • bone marrow suppresion -> anaemia & thrombocytopenia
  • increased risk or neutropenic sepsis
  • nausea, vomiting
  • mucositis & diarrhoea
  • palmar-plantar erythrodysesthesia
  • fatigue
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16
Q

how do anthracyclines work?

A

inhibit transcription & replication by intercalating nucleotides within the DNA/RNA strand

  • also block DNA repair (mutagenic)
  • create DNA and damagine free oxygen radicals
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17
Q

what are some examples of anthracyclines?

A
  • doxorubicin

- epirubicin

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18
Q

what are the side effects of anthracyclines?

A
  • cardiax toxicity
  • alopecia
  • neutropenia
  • nausea & vomiting
  • fatigue
  • skin changes
  • red urine
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19
Q

how do vinca alkaloids & taxanes work?

A

inhibit assembly (VA) or disassembly (taxanes) or mitotic microtubules -> dividing cells undergo mitotic arrest

20
Q

what are some side effects of vinca alkaloids & taxanes?

A
  • nerve damage (peripheral neuropathy, autonomic neuropathy)
  • hair loss
  • nausea & vomiting
  • bone marrow suppression
  • arthralgia
  • allergy
21
Q

how do topoisomerase inhibitors work?

A

topoisomerases regulate torsional strain within DNA during replication & transcription by inducing temporary breaks in phosphodiester backbone of DNA -> specific topoisomerase inhibitors alter binding of complex to DNA -> DNA breaks permanently

22
Q

wha are some examples of topoisomerase inhibitors?

A
  • topotecan & irinotecan (topo I)

- etoposide (topo II)

23
Q

what are some side effects of topoisomerase inhibitors?

A
  • acute cholinergic type syndrome (diarrhoea, abdominal cramps, diaphoresis - managed with atropine)
  • hair loss
  • nausea & vomiting
  • fatigue
  • bone marrow suppression
24
Q

what are some mechanisms for cell resistance to cancer drugs?

A

DNA repair mechanisms upregulated & increased dna damage repair -> less likely for dna double strand to break

  • DNA adducts replaced by base excision pair
  • drug effluxed from the cell by ATP-binding cassette (ABC) transporters
25
Q

what are the pros and cons of dual kinase inhibitors?

A

reduce chance of alternate pathways continuing when one pathway is blocked
- however increased toxicity

26
Q

what are the 10 hallmarks of the cancer cell?

A
  1. self-sufficient
  2. insensitive to anti-growth signals
  3. anti-apoptotic
  4. pro-invasive and metastatic
  5. pro-angiogenic
  6. non-senescent
  7. disregulated metabolism
  8. evades immune system
  9. unstable dna
  10. inflammation
27
Q

how are normal cells stimulated to grow?

A

growth signals transmitted into cell via growth factors binding transmembrane receptors -> activates downstream signalling pathways

28
Q

how can signal amplification be increased in cancer cells?

A
  • overexpressoin of receptors (HER2, EGFR)
  • overexpression of ligand (eg VEGF in prostate, kidney + breast)
  • ligand independent receptor activation (eg EGFR (lung), FGFR (head+neck))
29
Q

how can receptors on cancer cells be targeted?

A

monoclonal antibodies

30
Q

what do the suffixes of monoclonal antibodies mean?

A

momab = derived from mouse

ximab = chimeric (murine component of variable region of fab is maintained integrally)

zumab = humanised (murine regions interspersed within light + heavy chains of fab portion)

mumab = fully human

31
Q

how do monoclonal antibodies work?

A

neutralise ligand -> receptor doesn’t dimerise -> no downstream signalling

  • target extracellular component of receptor
  • cause internalisation of receptor
  • complement-dependent cytotoxicity -> immune response
32
Q

what are some examples of monoclonal antibodies used in oncology?

A

bevacizumab (binds and neutralises VEGF) - improves survival in colorectal cancer)

cetuximab (targets EGFR)

33
Q

what do small molecule inhibitors do?

A

bind to kinase domain of tyrosine kinase within the cytoplasm -> blocks autophosphorylation & downstream signalling

34
Q

what is glivec?

A

small molecule inhibitor that targets ATP binding region within kinase domain

35
Q

what are some examples of SMIs inhibiting receptors?

A

erlotinib
gefitinib
lapatinib
sorafinib

36
Q

what are some examples of SMIs inhibiting intracellular kinases?

A

sorafinib, dasatinib

37
Q

what are some advantages of MABs?

A
  • high target specificity
  • cause ADCC, complement mediated cytotoxicity + induce apoptosis
  • can be radiolabelled
  • cause target receptor internalisation
  • long half-life
  • liked by regulatory authorities
38
Q

what are some disadvantages of MABs?

A
  • large with complex structure -> low tumour / BBB penetration
  • less useful against bulky tumours
  • only work against targets with extracellular domains
  • cause immunogenicity, allergy
  • parenteral administration
  • expensive
39
Q

what are some advantages of SMIs?

A
  • can target TKs without extracellular domain / which are ligand activated
  • oral administration
  • good tissue penetration
  • cheap
40
Q

what are some disadvantages of SMIs?

A
  • short half-life -> more frequent administration

- more unexpected toxicity

41
Q

what are some resistance mechanisms to targeted therapies?

A
  • mutations in ATP binding domain
  • intrinsic resistance
  • intragenic mutations
  • upregulation of downstream / parallel pathways
42
Q

what are anti-sense oligonucleotides?

A

single-stranded chemically modified DNA-like molecule

  • complementary nucleic acid hybridisation to target gene hinders translation of specific mRNA
  • good for ‘undruggable targets’
43
Q

what is RNA interference?

A

single stranded complementary RNA

44
Q

what is nivolumab?

A

anti PD-1 antibody - big success in treatment of melanoma

45
Q

what are some examples of new ways that cancer treatment can be delivered?

A
  • nanotherapies
  • virtual screening technologies
  • immunotherapies using antigen presenting cells to present ‘artificial antigens’
  • targeting cancer metabolism

cancer (22 decks)

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