Cancer Chemotherapy Flashcards
(146 cards)
1
Q
Name the 9 Hallmarks of cancer:
A
*Sustaining Proliferative Signalling
*Evading growth suppressors
*Resisting cell death
*Enabling replicative immortality
*Inducing angiogenesis
*Activating invasion and metastasis
Deregulating cellular energetics
Avoiding immune destruction
Tumour promoting inflammation
2
Q
What should be the steps involved before initiating cancer treatment?
A
Self detection/ referral - 2 weeks max to see specialist
Diagnosis- staging, histology/genetics
Surgery/ radiotherapy/ chemo or supportive care
3
Q
Name and describe 4 classes of treatment for cancer:
A
Curative- aggressive treatment
Palliative- given to prolong life and reduce symptoms
Concomitant- studying the medicine (trials)
Subsequent line- one line of therapy up until a point e.g side effects
4
Q
What does palliative mean?
A
Means not going to cure, can survive for many years
5
Q
Name and describe the two classes of curative treatment for cancer:
A
Neoadjuvant- given before surgery to decrease tumour size
Adjuvant- given after surgery or with radiotherapy to ‘mop up’ dry cancer cells
6
Q
Name types of systemic therapy:
A
IV, IM, SC or oral
7
Q
Name types of regional therapy:
A
Intrathecal (spine), intra-arterial, intravesical
8
Q
What are important considerations to make when choosing a chemotherapy drug for a patient?
A
Performance status
Age
Previous treatment
Co-morbidities
Polypharmacy
9
Q
What is performance status?
A
From 0-5
0 is best
5 is death
4 is not well at all
2-3 is bed bound/ can do activities
10
Q
What is cytotoxic chemotherapy?
A
Anti-proliferative, inhibit cell division
Acts on all cells
11
Q
Name 3 cytotoxic drug targets:
A
Chemistry of nucleic acids
DNA or RNA production
Mechanics of cell division
12
Q
Why is combination therapy used in chemotherapy and the advantages:
A
Drugs with a different MoA, targets multiple pathways
Reduce toxicity of one class (as all low doses)
Each drug to be active alone on tumour type
Increase efficacy
Overcome drug resistance
13
Q
What occurs in drug resistance for chemotherapy?
A
Leads to discontinuation and progression
Decrease drug influx
Increase drug efflux
Inactivation of apoptotic pathways
Altered drug targets
Mutation of targets
Increase metabolism so deactivation (Cyp450)
14
Q
Describe hormone therapy as a type of therapy against cancer:
A
Remove the hormone that feeds the cancer to grow
Block the hormone
e.g Tamoxifen or enzalutamide (prostate cancer)
Not cytotoxic so not chemotherapy
15
Q
Describe how Bevacizumab fights against cancer:
A
Monoclonal antibody
Selectively binding to VEGF (vascular endothelial GF) so inhibits VEGF from binding to receptor
16
Q
Describe how Herceptin fights against cancer:
A
Monoclonal antibody
Selectively targets the extracellular domains of the HER2 protein
HER2 is a tyrosine kinase and an oncogene which provides the cell with potent proliferative and anti-apoptosis signals
17
Q
Why are antibody drug conjugates used and give an example:
A
Can use a monoclonal antibody to target HERT2 amplification
Attach to a very cytotoxic drug (so doesnt cause death)
Ado-trastuzumab Emtansine
18
Q
How are immune checkpoint inhibitors used as a chemotherapy?
A
Re-train the immune system
Blocks PDL1 or PD1 so allows T cell to kill cancer
19
Q
What are the benefits of oral chemotherapy?
A
◦ Home treatment
◦ Patient satisfaction
◦ Chair time
◦ Pharmacist role
◦ Less invasive
20
Q
What are the challenges of oral chemotherapy?
A
◦ Poor adherence
◦ Absorption - diet
◦ Polypharmacy – interactions
◦ Side effects
21
Q
Name a tyrosine kinase inhibitor:
A
Imatinib
22
Q
How do tyrosine kinase inhibitors work?
A
Targets the abnormal BCR-ABL1 (tyrosine kinase) protein that causes uncontrolled CML cell growth and blocks its function causing it to die
23
Q
What is CML?
A
Chronic Myeloid Leukaemia
24
Q
What are the side effects of chemotherapy?
A
*N&V
*Hair loss
*Diarrhoea
Mucositis (throat and mouth sores)
Constipation
Rash
Fatigue
Hypersensitivity
25
What are the two types of Chemo Induced N&V (CINV) and describe the onset of action:
Peripheral pathway (most common)- instant vomiting/ effects
Central pathway- delayed phase few days later
26
Describe how CINV occurs:
Chemo enters the enterochromaffin cell of the GI tract and it releases serotonin
Bind to 5HT3 receptor on vague affrent and causes side effects
27
How is CINV prevented/ stopped?
Using a 5HT3 antagonist such as ondansetron, anything ending in 'setron'
28
What are the risk factors for CINV?
Female
Non-smoker
Opioids
Age
Type of surgery
Migraine
Obesity
Lots of others
29
What are the complications in CINV?
Dehydration
Electrolyte disturbance
Nutritional deficiency
Oesophageal tears
Chemo dose delays
Aspiration pneumonia- going into lungs so risk of infection
Quality of life
30
Name and describe the types of CINV:
Acute- in 24 hours
Delayed- more than 24 hours
Breakthrough- CINV despite prophylaxis
Anticipatory- prior to admin of chemo
Refractory-CINV despite appropriate measures
31
Describe the treatment used for different types of CINV:
Acute- metoclopramide, domeridone, 5HT3 antagonists
Delayed- dexamethasone, NK1 antagonists
Breakthrough- 5HT3, NK1
Anticipatory- lorazepam
Refractory- levomepromazine, NK1, nabilone- not often used due to SEs
32
Name 3 types of chemotherapies that will very likely cause CINV:
Cisplatin
Dacarbazine
Carmustine
33
Name 3 types of chemotherapies that will not likely cause CINV:
Bevacizumab
Chlorambucil
Vincristine
34
What is mucositis?
Sore or ulcerated mouth or throat
Mucosal cells of mouth and GI tract are sensitive to chemo
From dryness to ulcers
Causes discomfort and pain
Takes 7-14 days to resolve
35
What are the preventative measures for mucositis?
Regular brushing- using a soft brush
Avoid floss and electric toothbrushes
Rinse mouth regularly-with salt water
Avoid alcohol containing products
Delay dental procedures if possible
Avoid spicy/ acidic foods
36
What is the pain treatment for mucositis?
Local anaesthetic mouthwashes or lozenges
Gentle mouthwash
Ice
Analgesics - paracetamol
37
What is the infection treatment for mucositis?
Treat by looking at clinical characteristics/ cultures
-fungal, systemic fluconazole or nystatin mouthwash
-viral, acyclovir
38
Name 3 high risk chemotherapy agents that cause diarrhoea and what do they treat?
5-fluorouracil
Capecitabine
Irinotecan
Colorectal and breast cancer
39
Name non-pharmacological interventions for chemotherapy induced diarrhoea:
Oral rehydration (8-10 glasses a day)
Dietary modifications
Small frequent meals
40
Name pharmacological interventions for chemotherapy induced diarrhoea:
Loperamide- 1st line
Oral antibiotics
Severe cases= hospitalisation, IV fluids and electrolytes
41
What is irinotecan chemotherapy used for and what side effects does this have?
Treatment of metastatic colorectal cancer
Early and late onset diarrhoea can occur
42
Describe the treatment for delayed diarrhoea in irinotecan chemotherapy:
Occurs after 24 hrs (3-10 days after)
Loperamide 4mg then 2mg every 2 hours until diarrhoea free for 12 hours
Ciprofloxacin 250mg BD for 7 days if lasts longer than 24 hrs
43
What is anticholinergic syndrome in irinotecan chemotherapy?
Inhibition of acetylcholinesterase
Increases sweating, saliva, stomach cramps and diarrhoea
SC atropine 300mcg or as prophylaxis
44
What are the causes of constipation with cancer?
Chemo- cisplatin, vinca alkaloids,
Supportive care- opioids, ondansetron
Other- inactivity, dietary changes
45
What advice should be given for the prevention of constipation?
Fluids (6-8 glasses)
High fibre foods
Excerise
46
What is the treatment for constipation?
Laxatives
Review medication (last resort as not changed as much as if it was diarrhoea)
47
Describe how chemotherapy can cause myelosuppression:
RBCs: anemia, fatigue
WBCs: risk of infection, neutropenia
Platelets: thrombocytopenia, easily bruised, may bleed longer than usual
48
Describe febrile neutropenia:
Fever, often with other sign of infection with a pt who has neutropenia
Requires urgent treatment with empirical antibiotics
49
What is febrile neutropenia caused by and how would you prevent it?
As a consequence of myelosuppressive chemo
Prevent with:
-prophylactic antibiotics
-G-CSF prophylaxis
-Dose reductions
50
What is the definition of febrile neutropenia?
Temp of more then 38ºC and absolute neutrophil count of less then 0.5 x 10^9/l
51
What is GCSF and how is it used?
Granulocyte colony stimulating factor
Stimulates production of neutrophils
Daily SC injections for 5-7 days following myelosuppressive chemo
52
Give two examples of GCSF medications:
Figrastim
Lenograstim
53
What are the indications of GCSF?
Chemotherapy with more than 20% risk of FN
Continuing chemo following episode of FN
54
What are the risk factors of febrile neutropenia?
Severe symptoms
Hypotensive
COPD symptoms
Leukaemia treatment
Dehydrated
More than 60 yrs old
Inpatient
55
If they are low risk, what is the treatment of neutropenic sepsis?
Oral antibiotics:
-ciprofloxacin
-co-amoxiclav
Iv stat then PO
Outpatient treatment or short admission
56
If they are high risk, what is the treatment for neutropenic sepsis?
Urgent empirical IV:
-Tazocin
-Ceftazidime
Admission
Review after 48 hours to see if can take orally
57
What is the advice given to help the side effect fatigue?
Move around and exercise when you can
Limit activities
Eat healthily
Drink plenty of fluid
58
What is the dermatological side effect of capecitabine?
Hand foot syndrome (57%)
Palms of hands/ soles of feet, tingling, redness, numbness, pain and swelling
59
What is the prevention of the dermatological side effect of capecitabine?
Avoid tight fitting shoes
Rubbing
Hot water
Moisterisers
60
What is the treatment for the side effect of capecitabine?
Lanolin containing creams
Dose reductions
61
Describe the severity of hand foot syndrome from capecitabine:
Grade 1- Numbness, dysesthesia and paresthesia, painless swelling, discomfort of hands and feet not effecting activities
Grade 2- painful erythema and swelling of hands and feet and discomfort, affecting activities
Grade 3- Moist desquaminiation, ulceration, blistering, severe pain, preventing work or performance of ADLs
62
What is Cetuximab used for?
EGFR inhibitor
Antibody to epithelial growth factor receptor
Treatment of colorectal and head and neck cancer
63
What is Erlotinib used for?
EGFR inhibitor
EGFR specific tyrosine kinase inhibitor
Treatment of lung cancer
64
What are the dermatological side effects of EGFR inhibitors?
Can cause severe papulopustular eruptions
65
Describe the treatment for EGFR inhibitor skin reactions:
Mild- topical antibiotic cream/lotion (clindamycin)
Moderate- Add topical steroid (hydrocortisone)/ oral antibiotics (doxycycline)
Severe- dermatology reference, dose reduction, consider stopping treatment if all else fails
66
What are long term side effects of chemotherapy?
Cardiac
Thromboembolic
Secondary cancers
Infertility
Respiratory
67
What is extravasation?
Accidental leakage of chemo from vein into surrounding tissue
Irritants
- inflammation
-pain
Vesicants
-necrosis
-pain
-blistering
68
Describe the different grades in a hypersensitivity reaction to chemotherapy?
Grade 1= transient flushing or rash, drug fever less than 38ºC
Grade 2= rash, flushing, urticaria, dyspnea, drug temp more than 38ºC
Grade 3= symptomatic bronchospasm with or without urticaria, oedema, angioedema, hypotension
Grade 4= anaphylaxis
Grade 5= death
69
Describe the pre-medication needed for patients when taking chemotherapy to stop hypersensitivity reactions:
Dexamethasone 20mg po every 6 hours for 4 doses
Ranitidine 150mg po every 8 hours for 3 doses
Chloramphenamine 4mg po every 6 hours for 4 doses
70
Where can molecules bind in DNA including DNA?
Proteins bind to major groove
Small molecules bind to minor groove via π, H- bond and electrostatic
DNA interacts by π-π stacking
71
Name four types of classical chemotherapies:
DNA Alkylators
Topoisomerase Inhibitors
Anti-mitotics
Anti-metabolites
72
Name a type of DNA Alkylator and how do they work against cancer?
Nitrogen mustards
They cross link DNA
Stops DNA polymerase being able to separate strands
The most predominant cross link is the N7 of guanine on two strands- inter strand crosslink
73
Name and describe the two types of cross linking and which one works as a chemotherapy?
Intrastrand (same strand)
Interstrand (different strand)
Interstrand crosslinking has been correlated with antitumour potency
74
What are SN1 reactions?
Nucleophilic substitution
Rate determining step is unimolecular (one molecule involved)- the loss of the leaving group
The rate ONLY depends on the conc of substrate
75
What are SN2 reactions?
Nucleophilic substitution
Rate determining step is bimolecular (two molecules involved)
The rate depends on the conc of the substrate AND the nucleophile
76
Describe the steps in the DNA Alkylation mechanism:
The nitrogen mustard forms an aziridinium ion (SN2 like- intramolecular substitution)
The aziridinium ion alkylates the N7 of guanine
The second Cl may then be displaced to form a second aziridinium ion (SN2) and the process repeats
77
Name 4 types of currently used nitrogen mustards:
Alkyl mustard
Aniline mustard
Melphalan (L-PAM)
Chlorambucil
78
Describe Cyclophosphamide as a nitrogen mustard:
It is a nitrogen mustard prodrug
Activated in the cellular environment, more by what a cancer cell has and a normal cell doesnt
79
How is acrolein produced?
A toxic product from the formation of a N mustard from cyclophosphamide
80
How does acrolein carry out its function?
Reacts with cysteine residues in proteins via Micheal addition
S-alkylation of cysteine thiols via acrolein leads to protein inactivation
81
Describe the mechanism of resistance in Nitrogen mustards and how is this over come?
Increased expression of glutathione-S-transferase and levels of glutathione
Increased expression of excision repair enzymes
Changes in drug uptake
May be countered by co-administration of glutathione-S-transferase inhibitors
82
Describe a DNA platinating agent and what does it help kill?
DNA Alkylator
Cisplatin is the most frequently used antitumour drug in the clinic
Used in the treatment of testicular, ovarian head and neck, lung and bladder cancers
83
Describe the mechanism of action of cisplatin:
The positively charged aquated platinum(II) reacts with biological nucleophiles
The biological target is thought to be N7 of guanine
95% of adducts are intrastrand crosslinks which are thought to inhibit DNA polymerase
84
How does resistance occur in DNA platinating agents?
Increased repair mechanism for intrastrand crosslinks
Increased expression of thiol containing proteins (glutathione, metallothionein)
85
What is DNA intercalation?
Causes the shape of the DNA helix to distort
This causes problems for DNA processing enzymes
This prevents cell replication and leads to cell death
86
Name an example of a Topoisomerase Inhibitors and how does it work?
Anthracyclines
DNA intercalators
Planar, aromatic structure sits between bases and interacts through π-π stacking
Amino sugar binds into the minor groove
Hydrogen bonds can be formed to the DNA bases
87
Name four types of anthracyclines:
* Doxorubicin
* Daunorubicin
* Idarubicin
* Epirubicin
88
What are the different side chains for the different anthracyclines?
1=bottom left 2=top right
Doxorubucin- OCH3, OH
Daunorubicin- OCH3, H
Idarubicin- H, H
Epirubicin- OCH3, OH
89
What are the functions of DNA topoisomerase I and II?
Release the strain in DNA during replication by cutting the strands, then reforming them
Topoisomerase I cuts one strand of DNA
Topoisomerase II cuts two strands of DNA
90
Describe the mode of action of topoisomerase II:
Topoisomerase II binds two double helices
Double strand break in one helix – covalent bonds are formed between TopoII and the broken DNA phosphate backbone
The full helix gets passed through the broken helix
DNA stands are released and the double strand break ligated back together, releasing its covalent bond to TopoII
91
Describe the mechanism of action of anthracyclines:
The intercalation distorts the shape of the double helix
Anthracyclines inhibit DNA Topoisomerase II by preventing it from fixing the double strand break
Most antitumour intercalators inhibit this enzyme
92
What is Mitoxantrone and what is it used for?
Topoisomerase II inhibitors
DNA intercalation through π-π stacking
Hydrogen bonding with DNA bases
Used in leukaemias, lymphomas and advanced breast and prostate cancer
93
How does resistance occur in topoisomerase II inhibitors?
* Increased expression of P-glycoprotein
* Increased efflux from the cell
94
What is an orthosteric inhibitor?
A molecule that binds into the active site of a protein, preventing its activity
95
What are the functions of microtubules?
They pull apart the chromosomes during mitosis and meiosis
Provide structural support
96
Name two ways in how anti-mitotics work:
Anti-mitotics target the microtubules in cells:
-Disruption of microtubule assembly
-Inhibition of microtubule disassembly
97
Describe how anti-mitotics cause disruption
of microtubule assembly?
They bind to free αβ-tubulin dimers
They disrupt the balance between polymerisation and depolymerisation
Results in the dissolution of microtubules and the destruction of mitotic spindle
In healthy cells this leads to cell cycle arrest
In cancer cells this leads to death by catastrophic mitosis
98
Name examples of anti-mitotics which causes disruption microtubule assembly and describe the difference:
Vinca alkaloids:
-Vinblastine (amine) at physiological pH can be protonated
-Vincristine (amide) not protonated and slighlty more potent
99
How do anti-mitotics cause inhibiton
of microtubule assembly?
Stabilisation of microtubules and prevention of their disassembly prevents cell replication
Leads to the formation of abnormal bundles of microtubuli
100
Name examples of anti-mitotics which causes inhibition microtubule assembly and describe the difference:
Paclitaxel (Taxol) ππ stacking (aromatic), only HBA, has amide
Docetaxel (Taxotere) no aromaticity, HBD+HBA, has carbamate and more soluble
101
How can resistance occur in anti-mitotics?
* Overexpression of p-glycoprotein
* Mutations in tubulin gene
102
What are the functions of antimetabolites in chemotherapy?
Toxic analogues of essential precursors for macromolecules (e.g DNA/RNA)
-Inhibit essential enzymes
-Disrupt the formation of macromolecules
103
What is folic acid important for in DNA?
Formation of pyrimidine bases
104
Describe how pyrimidine antimetabolites work:
5-FU is incorporated into RNA and DNA – less into DNA as it’s a uracil analogue
In RNA a disruption of function is observed
Intramolecular interactions may be affected by disruption of base pairings
105
Describe Capecitabine as an antimetabolite:
A prodrug of 5-FU
It is activated by three enzymes to release 5-FU
106
Describe how folate antimetabolites work and give an example:
Competitive inhibition of dihydrofolate reductase, e.g methotrexate
The affinity of Methotrexate for dihydrofolate reductase is
1000-fold that of folic acid
Methotrexate cannot be reduced by dihydrofolate reductase
Inhibits the synthesis of DNA, RNA, thymidylates and proteins
107
What is the difference between methotrexate structure and folic acid?
OH into NH2
NH to the left into NCH3
108
Name 2 types of modern chemotherapy and why are they modern?
NIBs- Tyrosine kinase inhibitors
RIBs- PARP inhibitors
Don't target all proliferating cells
109
What does PARP stand for?
Poly(ADP)Ribose Polymerase
110
How is PARP involved in cells?
Involved in DNA repair
Fixes single strand breaks e.g. those caused by Topoisomerase I
111
What is the function of BRCA1 and BRCA2 and what occurs if these are mutated?
Genes that produce proteins that help repair DNA damage
They are involved in repairing double strand breaks
Mutations in cancers result in proteins that cannot repair double strand DNA damage
Often seen in breast and ovarian cancers
112
How can PARP inhibitors be involved with mutated BRCA genes?
If PARP is inhibited, single strand breaks cannot be repaired
Results in DNA with lots of single strand breaks
During proliferation, this leads to double strand breaks
These are either repaired by homologous recombination (HR) in normal cells or lead to cell death in BRCA mutated cells
113
Name and describe a BRCA PARP inhibitor:
Olaparib
Used to treat advanced ovarian, fallopian tube and peritoneal cancers that carry faulty BRCA1 or 2 genes
Cyclopropylamide increased oral bioavailability
Conversion to piperazine increased both cell permeability and potency
114
Describe the BCR-ABL fusion protein and where is it found?
BCR and ABL are two genes, usually found on chromosome 9 and chromosome 22 respectively
Translocation of the ABL and BCR genes form the Philadelphia chromosome
Gene product is a protein that is always on
It acts as a tyrosine kinase and promotes proliferation
Found in chronic myelogenous leukaemia
115
Why could the BCR-ABL fusion protein be a target for a tyrosine kinase inhibitor?
Unique to cancer, as healthy cells don't have this or are over expressed in the tumour than healthy cells
116
Name and describe a BCR-ABL kinase inhibitor:
Imatinib
Introduction of the methyl group introduced selectivity for ABL kinase, but insoluble in water
Introduction of piperidine gave the molecule water solubility
117
Name three other ABL-Kinase inhibitors:
Dasatinib
Nilotinib
Bosutinib
118
What is BRAF?
Signalling pathway that promotes cell proliferation, gene expression, mitosis, cell survival, differentiation and apoptosis
119
How can a mutation in the BRAF protein cause cancer?
Many melanomas contain mutations in the B-Raf protein
Single amino acid mutation: V600E to a glutamic acid
This mutation allows for downstream signalling without upstream activation
Results in uncontrolled cell proliferation
120
Name and describe BRAF inhibitors including their selectivity:
Sorafenib- Approved for kidney and liver cancer, not selective for BRAF
Vemurafenib- Approved for melanoma, selective for BRAF
Dabrafenib- Approved for metastatic melanoma, selective for BRAF
121
Why would you replace an isopropyl in a drug to a terbutyl?
So it can't be oxidised which is better
As isopropyl find metabolites and very quickly changed which might be toxic
122
What does an IC50 and GI50 mean?
Lower IC50 (nm)= hitting target better
Lower GI50 (nm)= getting into cells better
123
How can resistance occur to tyrosine kinase inhibitors?
Small mutations in target protein can prevent the binding of the kinase inhibitor
In lung cancer, the EGFR receptor undergoes a T790M mutation which reactivates the pathway by preventing the binding of the TKI
Other pathways can be upregulated to promote cell proliferation and survival
124
Name two tyrosine kinase inhibitors:
BCR-ABL and BRAF inhibitors
125
Give the features of a carbocation:
Very electrophilic
Very reactive
Very little formed
126
How is cisplatin changed in vivo?
Chlorine ligands are displaced in vivo by water molecules
127
Describe folic acid metabolism:
Folic acid reduced by dyhydrofolate reductase into tetrahydrofolate
Methylene from sereine forms methylenetetrahydrofolate
Which can can be picked up by thymidylate synthase to reform dyhydrofolate
128
How does thymidylate synthase form dyhydrofolate?
Deoxyuracil monophosphate (dUMP) (methylenetetrahydrofolate) picks up a single carbon atom and converts it into deoxythymine monophosphate (dTMP) (dihydrofolate) using thymidylate synthase
129
What can be used to inhibit thymidylate synthase?
dUMP looks like a base
5-fluorouracuil 5-FU can be used to inhibit dUMP
This forms 5FdUMP
130
What type of nitrogens can be protonated?
Amine
Pyridine
Aniline
131
What does T, N and M mean in staging of cancer?
Tumour size
Lymph Nodes
Metastasis
132
Describe the TNM staging:
T1, less than 3cm
T2, more than 3cm
T3, any size but near airway
T4, any size but in air way
N0, no lymphs affected
N1-4 lymph nodes have been effected
M0, no metastasis
M1, metastasis
133
Name the 4 cancer P's:
Prediction
Prevention
Precision
Participation
134
What would be the prediction for breast cancer?
Faulty BRAC1/2
Diagnostic tests
HER2
135
What would be the prevention of breast cancer?
Weight management, alcohol consumption, contraceptive choice, physical activity, HRT
i.e. managing the risk factors for breast cancer development, breast feeding, smoking
136
What is the participation of breast cancer?
Mammogram screening
Mastectomy
Quitting smoking, regular exercise
137
What is a main risk factor for developing CML?
Radiation
138
What are risk factors in developing colorectal cancer?
Eating too much processed and red meat
Eating too little fibre
Overweight or obese
139
Name and describe the prediction of colerectal cancer:
Familial adenomatous polyposis (FAP)
If left untreated then likely to have cancer in 40's, recommend to remove colon in 20's
Lynch syndrome, or hereditary non polyposis colon cancer (HNPCC)
140
Name the 4 main types of leukaemia:
* Acute myeloid leukemia (AML)
* Chronic myeloid leukemia (CML)
* Acute lymphoblastic leukemia (ALL)
* Chronic lymphocytic leukemia (CLL)
141
Where does acute myeloid leukaemia start?
Starts from immature white blood cells called granulocytes or monocytes in the bone marrow
142
What is the age range in AML?
More than 40% are over 75 but any age
143
What are the main chemos for AML?
Cytarabine- anti metabolite
Daunorubicin- TOP II inhibitor
144
Where does acute lymphoblastic leukaemia start?
Starts from lymphocytes in the bone marrow
145
What is the age range in ALL?
Children 0-4
More common in females than males
146
What is the age range in CLL?
Rare to have it in people aged less than 40
More common in men than woman
