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Third year pharmacology > ls6003 solid cancer therapy (dr Modjthedi) > Flashcards

ls6003 solid cancer therapy (dr Modjthedi) Flashcards

1
Q

list 7 aetiological factors influcencing cancer

A

age
radiationchemicals
genetic dispostiion
ciruses and bacteria
dietary factors
immunosuppresion

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2
Q

what do carcinogens do/

A

cause genetic alterations and DNA damage leading to cancer

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3
Q

what are the 3 large groups of genes altered by carcinogens?

A

protooncogenes
tumour suppression genes
DNA repair genes

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4
Q

what are the function and what effect does carcinogenisis have on proto-oncogenes, tumour suppression genes, DNA repair genes

A

proto-oncogenes= promote cell division / function become enhanced
tumour suppression genes=code for cell division suppression / funciton loss
DNA repair genes = code for DNA repair before cell devisio/ accelerate accumulation of mutated tumour suppresor genes and proto-genes

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5
Q

Give examples for proto-oncogenes, tumour suppression genes, DNA repair genes

A

proto-oncogenes = Ras gene
tumour suppression gene = P53
DNA repair genes = ATM gene

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6
Q

name 6 common genetic alteration types

A

point mutation - Kras
gene amplification - HER2
epigenetic alterations - gene silencing, DNA methylation
genetic alteration due to insertion/deletion
exogenous sequences - viruses such as HPV, EBV
chromosomal transloction/changes - Ph chromosome

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7
Q

Oncogenes can be activate by 3 pathways, briefly describe these

A

A) mutation the DNA -> enhanced activity
B) Amplification results in increased amounts of normal protein
C) Translocation of part of DNA from one chromosomal location to another can produce a fusion protein

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8
Q

Define the tumour types
Neoplasm/tumour -
Cancerous:
carcinoma -
sarcoma -
Lymphoma (leukaemia) -

A

-abnomral mass of tissue
-from endo/ectodermal i.e forms in the skin or tissue cells
- from mesdermal connective tissues e.g. bone, cartilage, also poorly differentiated
- cancers of hamopoietic system
(over 80% of cancers are carcinomas)

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9
Q

cancers begin with accumulation of multiple mutatuions leading to genetic instability -> metastasis.
describe the general timeline for this

A

mutation inactivates tumour suppressor gene -> cells proliferate -> mutations inacrivate DNA reapir genes -> proto-oncogenes mutate to oncogenes -> more mutation, more genetic instability metatstatic disease (malignant tumour has broken through to blood vessels)

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10
Q

describe benign

A

rare, non-invasive, never metastasise, prognosis (likelyhood of survial) is very good

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11
Q

descrbe malignant

A

common on skin, invasive, often metastasize, prognosis is poor

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12
Q

list the 5 stages of tumour development

A

cells with genetic mutation
hyperplasia (increase in the number of cells in an organ or tissue that appear normal under a microscope)
dysplasia (change in organisation of cells)
carcinoma in situ
invasive cancer

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13
Q

list 7 hallmarks of cancer

A

uncontrolled proliferation
resistanc eot apoptosis
imoortaility
increased angiogenisis
invasion and metastasis
reprogramming of energy metabolisms
evastion of immune system
Tumor heterogeneity is one of the hallmarks of malignancy.

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14
Q

list some of the common metastatic sites for prmiary tumours

A

prostate
colorectal
breast
melanoma
neuroblastoma

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15
Q

what does stage 3 mean?

A

tumour has speead to lymph nodes

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16
Q

what factors are responsible for cancer morbidity/mortality

A

metastasis
ruptures in vessels
compression of vital organs
infection
organ failure
starvation

17
Q

3 approaches to fight cancer

A

A) prevention
B) early detection
C) treatment

18
Q

4 possible outcomes for treatment

A

complete response (CR)
partial (PR)
STABLE DISEASE (SD)
Progessive disease (PD)

19
Q

name 3 plainum based drugs

A

carboplatin
cisplatin
oxaliplatin

20
Q

give 5 characteristic of cytotoxic anti-cancer drugs

A

-disrupt bio processes essential for cell division
-not specific for cancer cells. (kills non-target cells)
-work best on cells in S+M phase of cell cycle, not G1 though
-typically used in combination with agents which act at different cell cycle phases
-often administered in cycles to allow for tissue recovery

21
Q

most cytotoxic drugs act at specific phases of cell cycle
what cllases act on M phase

A

Vinca alkaloids
taxanes

22
Q

most cytotoxic drugs act at specific phases of cell cycle
what classes work at S phase

A

Methrotrexate (antimetabolite)
Hydoxyurea
cytosine arabinoside (Ara-C) (purine antagonist)
Anthracyclines ( e.g. doxorubicin)

23
Q

most cytotoxic drugs act at specific phases of cell cycle
which are non-phase specific? i.e kill. both non-dividing and actively dividing cells

A

Alkylating agents (e.g bleomycin, carboplatin, cyclophosphamide)
Cisplatin
Nitrosoureas (Nitrosourea is both the name of a molecule, and a class of compounds that include a nitroso (R-NO) group and a urea) e.g. Streptozocin (Streptozotocin)
Antibiotics

24
Q

most cytotoxic drugs act at specific phases of cell cycle, what is the advantage of using a combination therpay, attacking at different stages

A

allows for lower dosage, resulting in lower toxicity and a higher efficacy for treatment

25
Q

what are the 3 clinical settings in which cytotoxic drugs are administered?

A

1) neoadjuvant (primary therapy prior to surgery, prevent metastasis)
2) adjuvant (after surgery/radiotherapy, reduce risk of relapse)
3) palliative care, improve patients QoL, palliaiting pain/symptoms

26
Q

what factors effect efficacy of cytotoxic drugs?

A

total dose of drug reaching tumour
duration of exposure
proliferation fraction of tumour
tumour size

27
Q

give 4 examles of antimetabolites used to treat cancer

A

methotrexate
doxorubicin
paclitaxel
irinotecan

28
Q

give 2 limitiations of anticancer drugs used in chemo

A

1)toxicity
2)development of resistance to drugs

29
Q

give 3 ways of reducing limitations surrounding anticancers drugs

A

-effective dosing and schedule
-combination therapy + differrent therapuetic apporaches (radiotherapy)
-supporting drugs

30
Q

list some of the symptoms from drug toxicity

A

-anaemia, neutropenia (low number of white blood cells), thromboctopenia (platelet count in your blood is too low)
-diarrehea, infertility, hair loss
-nausea and vomiting

31
Q

what are the 2 types of drug resistance?

A

primary (cancer does not respond to an immunotherapy strategy)
acquired (clinical scenario in which a cancer initially responded to immunotherapy but after a period of time it relapsed and progressed(

32
Q

what are 2 potentioal mechanims of drug resistance

A

1) inadequate drug exposure
2) alteration in cancer cell itself

33
Q

try to list 8 otehr factors associated with drug resistance

A

-slower cell cycle time
-geneitic instability -> high mutation rate
-expression of resistant phenotype prior to chemotherapy
-acquisition of additional genetic alterations folowing exposure to drug(secondary drug resistance)
-increased capacity for DNA repairs
-delivery of suboptimal dose due to poor tumour vasuclature i.e hypoxia
-EMT - mesenchymal cells are more resisant to chemo than epithelial
-presence of chemoresistance cancer stem cells

34
Q

define epithelial-to-mesenchymal transition (EMT)

A

involved in tumor progression with metastatic expansion, and the generation of tumor cells with stem cell properties that play a major role in resistance to cancer treatment

35
Q

name 4 strategies to overcome drug-resistance

A

-develop drugs that modulate/reverse resistance phenotypes
-moleular profiling, discovery and targeting of more cancer specific drug-resistant antigens
-combination therapy
-development of smarter drugs with novel MoA: mAbs, TKIs

36
Q

factors when designing combination therapy

A

-non-overlapping toxicity
-optimal dose anad ferquency
-non-overlapping mechanisms of drug resistance

37
Q

whats FOLFOX?

A

common combination therpay for advanced colorectal cancer
side effects: increased risk of infection, anaemia, bleeding, fatigue, nausea, pain

38
Q

name 3 factors effecting survival rate of cancer patients

A

-tumour grade
-cancer stage
-tumour type

Third year pharmacology (7 decks)

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