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Block 4 - Heamatology > Lecture 8 - Intro To Chemotherapy > Flashcards

Lecture 8 - Intro To Chemotherapy Flashcards

1
Q

Different treatments for cancer

A
  • treating the complications
  • cytotoxic therapy
  • local therapies
  • endocrine therapy
  • immunotherapy
  • enzyme inhibitors
  • molecular therapy
  • supportive care
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2
Q

Goals of systemic therapy

A
  • curative
  • debulking before surgery
  • adjuvant
  • radioenhancing
  • prolong survival
  • palliative
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3
Q

Chemotherapy

A
  • nitogen-mustard discovered during chemical warfare research
  • development of chemotherapy since mostly a result of empiricism
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4
Q

The ideal cytotoxic

A
  • would exploit unique property of tumour cells, thus providing tumour specific therapy
  • no such pure cytotoxic drug exists
  • collateral damage limits the effectiveness of systemic chemotherapy
  • autoloytic stem cell rescue allows you to give high dose chemotherapy before trasnplant - hematopoiesis resues
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5
Q

Spectrum of chemosensitivity

A
  • Drug resistant to curable: renal cancer, pancreas - colon - breast - ovarian lymphoma - germ cells
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6
Q

Cell cycle

A
  • cells with moderate amounts of DNA damage are arrested in G1
  • after DNA repair, the cell cycle resumes
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7
Q

P53: maintenance of fidelity

A
  • gives rise to P21 -> CDK4 -> cell cycle arrest, DNA repair
  • Apaf 1 -> caspases -> cleavage of vital molecules -> apoptosis

Killer molecules: Bax, Bak, Bad, Bim -> promote p53 pathway
Prosurvival molecules: Bcl2, Bcl3, BCl w molecule -> inhibit p53 pathway

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8
Q

How does a cell become malignant

A
  • increase activitiy of positive growht signals (activation of proto-oncogenes)
  • decrease activity of negatively acting growth signals: loss of tumour suppressor gene function (eg: P53)
  • decrease in the pathways leading to PCD
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9
Q

Conventional chemotherapy 5 main classes

A
  • alkylating agents: cross links DNA. Eg: cyclophosphamide
  • antitumour antibitotics: intercalate DNA base pairs (Daunorubicin), breaks DNA (Bleomycin)
  • platinum compounds: crosslink DNA (Cisplatin, Carboplatin)
  • anti-metabolites: Methotrexate (an anti-folate), 5FU, Ara-C… Competitive inhibitors of S phase enzymes
  • anti-microtubule drugs: taxanes and vincristine: bind microtubular proteins disrupting microtubule assembly during mitosis. Inhibition of the mitotic spindle leads to arrest in G2/M
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10
Q

Alkylating agents: classic cytotoxic

A
  • add alkyl groups to intracellular DNA/cross linking interferes with DNA synthesis
  • non-selective, toxicity to all rapidly dividing cells
  • eg: cyclophosphamide
  • side effects: anorexia, alopecia, amenorrhea, azoospermia, mutagenic, myelosuppressive (marrow suppression), immunosuppressive (AAAMMI). Nausea + vomiting
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11
Q

Combination chemotherapy 4 princiuples

A
  • drugs active as single agents should be selected
  • drugs with different MOA
  • drugs with different dose limiting toxicities
  • drugs with different susceptibilities to resistance
  • generally aim for max dose with minimum time interval between doses (2-3 weeks for recovery)
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12
Q

Multiagent chemotherapy: MOPP

A
  • Mustine
  • Oncovine
  • Procarbazine
  • Prednisolone
  • Hodgkin lymphoma
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13
Q

Multiagent chemotherapy: CMF

A
  • cyclophoaphamide, methotrexate, 5Fluorouracil

- for breast cancer

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14
Q

Mjultiagent chemotherapy: CHOP

A
  • Cyclophosphamide, H-adriamycin, Oncovin, Vincristine, Prednisone
  • for non-hodgkin lymphoma
  • R-CHOP: add rituximab
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15
Q

Assume all cytotoxics cause

A
  • anorexia, nausea, vomiting
  • alopecia
  • myelosuppression
  • gonadal damage
  • immune suppression
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16
Q

Which drugs dont cause hair loss

A
  • carboplatin, 5FU, vincristine, mitoxantrone
17
Q

Which cytotoxics dont damage the marrow

A
  • bleomycin
  • vincristine
  • cisplatin
  • 5FU
18
Q

Unite toxicities

A
  • Doxorubicin, idarubicin - cardiac toxicity
  • Bleomycin - lung toxicity
  • Vinca alkaloids - peripheral neuropathy
  • cyclophosphamide - haemorrhagic cystitis
  • Cysplatin - kidney toxicity
19
Q

Supportive care

A
  • pre treatment: counselling, education, teeth, fertility, nutrition
  • with treatment: anti-emetics (5HT3 receptor antagonist, aprepitant)
  • post treatment: anti-emetics, laxatives, g-CSF, autologous stem reinfusion, iv fluids, folinic acid after MTX
20
Q

Drug targets unique to cancer cell are rare but do exist

A
  • BCR–ABL in CML: blocked by imatinib and other tyrosine kinase inhibitors
  • PML/RAR in APML: differentiation therapy: ATRA: a vitamin A analogue lifts the block in myeloid differentiation
21
Q

Rituximab

A
  • anti-CD20 in B NHL

- 15% increase in response and survival rates

22
Q

Trastuzumab (herceptin

A
  • blocks the HEr2 receptor protein expressed in breast cande - increased survival when added to chemotherapy
23
Q

Monoclonal antibodies: Bevacizumab

A
  • inhibits VEGF: a protein that stimulates angiogenesis - new vessel formation
  • benefit in metastatic colon cancer
24
Q
  • monoclonal antibodies: brentuximab
A
  • anti-cd30 in T-NHL and HL
25
Q

Ipilimumab

A
  • blocks the cytotoxic T-lymphocyte-associated antigen 4 (CTLA4) on lymphocytes
  • blocking this immune checkpoint inhibitor allows CTL to destroy the melanoma cells
  • immune mediated side effects
  • PBS approved
26
Q

Vemurafenib - small molecule inhibitor

A
  • V600E mutated BRAF inhibitor present in 50% of melanomas
  • 600 patient trials
  • TGA approved, not PBS listed
  • photosensitive
27
Q

Other immuno-modulatory cancer therapies

A
  • replacing/complementing traditional chemotherapied in myeloma
  • thalidomide and lenalidomide
  • bortezomib inhibits the proteasome proteins the myeloma cells need for homeastis
  • multiple MOA: direct anti-tumour effect, induign apoptosis, anti-angiogenic, immune modulatory
28
Q

B cell enzyme inhibitors

A
  • BCR signalling blockade by ibrutinib: imhibitor of Bruton’s TK in relapse CLL, mantle cell lymphoma, waldenstrom

Block 4 - Heamatology (23 decks)

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