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Biology of Cancer > Seminar 10 - Biological Basis of Cancer Chemotherapy > Flashcards

Seminar 10 - Biological Basis of Cancer Chemotherapy Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

What are the main ways in which tumours can spread?

A
  1. Local
  2. Blood
  3. Lymphatics
  4. Implantation
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2
Q

What is implantation?

A

Mechanical spread of detached clumps of tumour cells - peritoneum, ureters, CSF

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3
Q

Which types of tumour spread by lymphatics?

A
  1. Carcinomas

2. Melanomas

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4
Q

Which types of tumour spread via the bloodstream?

A
  1. Sarcomas

2. Carcinomas - later

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5
Q

If there is an abnormal connection between the bladder and bowel due to malignancy, what type of urine is formed?

A
  1. Fizzy urine - gas passed through

2. Possible feces in the urine

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6
Q

Where is the first site where secondaries from rectal cancer are observed? Why?

A

Lung - direct connection from the rectum to the lung via lymphatics

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7
Q

State the treatment options for cancer.

A
  1. Surgery
  2. Radiotherapy
  3. Chemotherapy
  4. Biological targeted therapy
  5. Hormones
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8
Q

State the options for chemotherapy.

A
  1. Primary treatment - radical
  2. Adjuvant
  3. Neoadjuvant
  4. Advanced disease - palliative
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9
Q

What is radical chemotherapy often used for?

A

Relatively rare but often used for haematological malignancies rather than solid tumours:

  1. Lymphomas
  2. Leukaemias
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10
Q

Define adjuvant therapy.

A

Post-operative treatment in a patient at high risk of microscopic metastases after removal of the primary tumour

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11
Q

What is neoadjuvant therapy?

A

Primary treatment of patients with a clinically localised tumour - it can be used to assess the biological responsiveness of the tumour

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12
Q

What is transcription?

A

DNA conversion to RNA

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13
Q

What is translation?

A

RNA conversion to amino acids which code for protein

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14
Q

Outline the sites of action of cytotoxic agents.

A
  1. Intercalating agents- DNA duplication and transcription
  2. Antimetabolites - DNA synthesis
  3. Alkylating agents - DNA
  4. Spindle poisons - mitosis
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15
Q

How do platinum compounds inhibit DNA synthesis?

A

Lead to formation of platinated inter- and intrastrand adducts leading to inhibition of DNA synthesis

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16
Q

State the percentage of platinated intrastrand adducts formed by Eloxatin (a platinum compound).

A
  1. G-G: 55%

2. G-A: 31%

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17
Q

How does topoisomerase-1 work?

A

Transient single strand cleavage: passage of the intact strand through the nick

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18
Q

What can be used to inhibit topoisomerase-1?

A

CPT-11

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19
Q

How does CPT-11 inhibit topoisomerase 1?

A
  1. CPT-11 binds to the Topo-I-DNA complex without affecting cleavage reaction
  2. Stabilisation of the cleavable complex = inhibition of the religation step
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20
Q

State 2 examples of anti-metabolite drugs.

A
  1. 5-Fluorouracil

2. Methotrexate

21
Q

Which enzyme does 5-fluoracil act on?

A

Thymidylate synthase (TS)

22
Q

Which enzyme does methotrexate act on?

A

Dihydrofolate reductase

23
Q

Which enzyme converts 5’-DUFR to 5-FU?

A

Thymidine phosphorylase - TP

24
Q

What are the 2 main ways microtubule binding agents affect microtubule dynamics?

A
  1. Inhibit polymerisation

2. Stimulate polymerisation and prevent depolymerisation

25
Q

What is the aim of combination therapy?

A
  1. Increased efficacy
  2. Activity - different mechanisms of action and mechanisms of resistance
  3. Safety - compatible side effects
26
Q

What is P-glycoprotein?

A

An ATP-powered efflux pump

Pumps cytotoxic agents out of the cell against the concentration gradient

27
Q

Outline the mechanisms of resistance to alkylating agents.

A
  1. Increased exit or decreased entry of agent
  2. Inactivation of agent in cell
  3. Enhanced repair of DNA lesions produced by alkylation
28
Q

Outline how double stranded breaks are repaired.

A

Recombinational repair:

  1. HR - ATM
  2. NHEJ - DNA-PK
29
Q

Outline how single strand breaks are repaired.

A

Base excision repair: PARP

30
Q

Outline how bulky adducts are repaired.

A

Nucleotide excision repair: XP, polymerases

31
Q

Outline how insertions and deletions are repaired.

A

Mismatch repair: MSH2, MLH1

32
Q

Outline how O6-alkylguanine is repaired.

A

Direct reversal by AGT enzyme

33
Q

What is the key enzyme involved in repair of SSBs?

A

PARP-1

34
Q

Outline the current endocrine therapies for prostate cancer.

A
  1. LHRH agonists: Goserelin
  2. Oestrogen: stilboestrol
  3. Castration
  4. Anti-androgens: cyproterone acetate, flutamide, bicalutamide
35
Q

State the mechanism of action of abiraterone in treatment of prostate cancer.

A

Inhibits CYP17A1 - enzyme crucial in conversion of pregnenolone and progesterone to testosterone

36
Q

What is the target for anti-cancer therapy in CML?

A

STI 571

37
Q

What is the mechanism of action of imatinib?

A

Magic bullet: bcr-abl tyrosine kinase inhibitor –> tumour selective, rationally designed targets and inhibitors

38
Q

What is trastuzumab?

A

A recombinant humanised IgG1 monoclonal antibody against the human epidermal growth factor receptor 2 (HER2)

39
Q

Outline the mechanism of action of herceptin (trastuzumab)

A
  1. Binds to HER2 positive tumour cells and flags them for destruction by the immune system
  2. Antibody-dependent cell-mediated cytotoxicity (ADCC)
40
Q

Which type of cancers is EGFR generally overexpressed in?

A
  1. Colorectal
  2. Breast
  3. NSCLC
  4. Prostate
  5. Ovarian
  6. Pancreatic
  7. Gastric
41
Q

What is high EGFR expression generally associated with?

A
  1. Invasion
  2. Metastasis
  3. Late stage disease
  4. Chemotherapy resistance
  5. Hormone-therapy resistance
  6. Poor outcome
42
Q

Why may EGFR-targeted therapies not work in patients with KRAS mutations?

A

When the KRAS gene is mutated, KRAS protein (p21 ras) is active regardless of EGFR activation
KRAS mutations associated with a poor prognosis - need to analyse NRAS

43
Q

Describe the biological role of VEGF.

A
  1. Involved in the migration and proliferation of endothelial cells
  2. Promotes angiogenesis in vivo by inducing endothelial cells to invade collagen gels and proliferate to form capillary-like structures
  3. New blood vessel formation
44
Q

Outline the process of angiogenesis.

A
  1. Endothelial cells migrate into the perivascular space towards angiogenic stimuli
  2. They proliferate, follow each other and adhere to create a lumen
  3. Blood vessel sprouts fuse to build new circulatory systems
45
Q

Outline the classes of drugs that can be used to target the VEGF pathway.

A
  1. Anti-VEGF antibodies
  2. Ribozymes - VEGFR1
  3. Anti-VEGFR antibodies
  4. Small molecule VEGFR inhibitors - tyrosine kinase inhibitors
  5. Soluble VEGFRs
46
Q

State an example of a CTLA-4 inhibitor.

A

Ipilimumab

47
Q

State an example of a PD-1 inhibitor.

A

Nivolumab

48
Q

Outline the routes of administration of cancer chemotherapy.

A
  1. IM: Rarely
  2. PO: convenient, dependent on oral bioavailability
  3. IV: most common, bolus, continuous pump infusion, infusional bag
  4. Subcutaneous: convenient in community setting
  5. Into a body cavity: bladder, pleural effusion
  6. Intrathecal - into the CSF: via lumbar puncture or omaya reservoir (directly into the ventricles)
  7. Intralesional: directly into the cancerous area- consider pH
  8. Topical: medication is applied onto the skin

Biology of Cancer (11 decks)

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