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Flashcards in The Big 4 Cancers Deck (65)
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how common? (2)
risk factors? (6)
mutations? (1)
pathogenesis? (1)
is colon or rectal more common? (1)

- 1 in 20
- 4th most common (10-15% all malignancies)

- men
- old age
- diet: animal fat/ low fibre
- Western countries
- IBD; UC (Crohns more controversial)
- familial association ~10%; FAP, HNPCC, APC

- APC mutations are associated with the development of benign adenomas whereas the progression to invasive carcinoma requires further mutations e.g. p53, DCC and RAS

- from well-demarcated polyp --> tumours

- colon 1.5* more common than rectal

mortality is decreasing due to better screening; reduced mortality between 15-18%


where are they located? (3)

- 1/3 in rectum
- 1/3 on left side
- 1/3 in remainer of colon

Future of treatments:
Agents acting through angiogenic mechanisms such as bevacizumab, and agents acting on epithelial growth factor receptors such as cetuximab can be effective when added to chemotherapy in advanced disease and their place in standard treatment regimens is being determined by research and the National Institute Health and Clinical Excellence (NICE).


colorectal caner:
red flags? (6)

- rectal bleeding
- change in bowel habit
- mucous PR
- anorexia
- weight loss
- abdo pain


rectal bleeding:
prevalence in UK? (1)
causes? (6)

~50% have it at some point, ~3% of all consultations
quite a COMMON symptom! lots of causes..

- cancer
- anal fissure
- trauma
- anticoagulants
- gastroenteritis/ IBD
- haemorrhoids


colorectal cancer:
examination signs? (4)

- abdo mass
- signs of anaemia
- mass on rectal exam
- weight loss


colorectal cancer: routes to presentation? (4)

- straight to test if 'fit'= colonoscopy/ flex sig OR colorectal surgeon review in 14 days
if cancer diagnosed should start treatment within 62 days

- 1:5 have red flat symptoms
- present with obstruction, perforation, bleeding, abdo pain


4) SCREENING ~10% of cancers
- every 2 years 60-74 years old
- FIT Faecal immunochemical testing
- one sample
- FOB Faecal Occult Blood: used to require 3 samples
Positive: treat as urgent suspected cancer

Bowel screening scope (sigmoidoscopy) at 55: one off to detect left sided polyps


colorectal cancer:
reoccurance risk more common in rectal or colon? (1)
how to prevent reoccurance in:
colon? (2)
rectal? (4)
what is Hartmans? (1)

- more common in RECTAL cancer

Surgery + consider neoadjuvant chemo
(hemicolectomy/ anterior resection)
(giving chemo before and after surgery is better than just after)

- consider neoadjuvant treatment:
low risk= surgery
medium risk= radiotherapy, anterior resection
high risk= radiotherapy+chemotherapy, APER (anteriorperitoneal resection), Hartmanns

Hartmans= Surgery involves removing the affected section of the bowel and creating an alternative path for faeces to be passed. i.e. colostomy
Essentially: the rectal is very susceptible to RADIOTHERAPY


what is DPD testing?
don't need to know this

- patients receiving 5FU chemotherapy tests for DPD enzyme deficiency (heterozygous)

patients who have the deficiency have a v severe reaction to the chemotherapy as unable to metabolism it


colorectal cancer:
follow-up investigations? (3)

- specialist-nurse led
- telephone-based

- CEA 6-monthly
- CT 18 months, 3 years, 5 years
- colonoscopy within 12 months, 3 years post last one


lung cancer:
prevalence? (1)
prognosis? (2)

- 13% of all cancers, 21% of all deaths
- 3rd most common in UK

- usually presents at advanced stages (stage IV)
- outcomes poor (5% 10 yr survival) but improving (3-5%)

mortality higher in men than women


lung cancer:
risk factors (7)

- deprivation
- smoking
- male
- genetic predisoposition
- history of COPD
- industrial exposure to asbestos, chromium, arsenic and iron oxide
- exposure to radiation


lung cancer:
subtypes? (4)
histology (1)
why is it important to identify which subtype? (1)

50% adenocarcinoma
30% squamous cell carcinoma
15% small-cell carcinoma
5% large cell carcinoma
It is not clear whether these distinct tumours arise from different cell types or from a single common progenitor which then differentiates to produce different tumour types.

- arise from epithelium of bronchi usually, only rarely from lung parenchyma itself

- important to differentiate type as different clinical features and management

adenocarcinoma is the most common for NON-smokers, but smoking is still a risk factor for ALL TYPES


lung cancer:
presentation in early (2) and late disease (8)

Early disease:
- cough
- breathless
(very non-specific symptoms!)

Advanced disease:
- haemoptysis
- chest pain
- weight loss
- bone pain
- RUQ pain
- headaches/ nausea/ neurological
- stridor (emergancy)
- recurrent chest infections
- Horners syndrome if affect sympathetic chain (Pancoast's)
- recurrent laryngel nerve palsy

haemoptysis is very central cancers... either means its spread lots already or centrally placed --> surgery not appropriate

lung cancer non-specific symptoms--> often an incidental finding!

Specific histologies may be associated with a particular pattern of presentation. For instance, clubbing is more frequent with squamous cell carcinoma. Sputum production may be excessive in bronchio-alveolar carcinoma.


lung cancer:
localized treatment? (2)
systemic treatment (3)

- surgery
- radiotherapy: curative/ palliative

- chemotherapy
- immunotherapy
- targeted therapy (biologics)


Pancoast tumour:
symptoms? (4)
what type of cancer often are they? (1)
where? (1)

- ptosis
- meiosis (pupil)
- anhidrosis
- pain in R arm
- weakness small muscles of R hand


- lung apex


Why is it important to know
performance status? (1)
co-morbidities? (1)
smoking - why quit after lung cancer diagnosis? (3)

- performance status lets you work our how aggressive you can be with the treatment/ how well someone is despite the cancer

- some drugs are contraindicated in co-morbidities

+ chemo side effects worse,
+ increases risk of recurrence:

- smoking makes the level of oxygen in your blood drop --> radiotherapy less effective
- tobacco smoke has chemicals in it that can reduce the levels of some chemotherapy drugs, making them less effective


histology of small cell lung cancer (5)

- small and oval cells
- scanty cytoplasm
- fine granular neoplasm
- absent nucleoli
- frequent mitosis
- dense neurosecretory granules


What is a paraneoplastic syndrome? (1)

What paraneoplastic syndromes does each lung cancer causes:
- SCLC? (5)
- squamous cell? (3)
- adenocarcinoma? (2)
- large cell/ NSCLC? (2)

- group of disorders where cancer causes an abnormal immune response
(can affect endocrine, dermatologic, haematologic and rheumatologic systems)

- small cell lung carcinoma SCLC
(has lots because it is a NEUROENDOCRINE subtype of cancer compared to the others)
1- ectopic ACTH--> crushing
2- SIADH -->hyponataemia
3- Eaton-Lambert Syndrome (similar to myasthania), NSCLC causes ~50% of cases
4- SVC syndrome (2nd most common cause after NSCLC)
5- carcinoid--> flushing and diarrhoea

1- PTHrp--> hyperCa2+
2- Horners--> ptosis, miosis, anhydrosis
3- Pancoasts--> 1st/2ns thoracic nerve--> shoulder pain--> ulner nerve pain

1- pulmonary osteoarthropathy--> pain in hands/legs
2- marantic endocarditis

1- SVC syndrome (most common cause)
2- gynaecomastia


treatment small lung cell carcinoma (SCLC)? (2)

SCLC is the RUBBISH one :( presents late..

1- CHEMOTHERAPY mainstay, responds well normally
2- radiotherapy to chest and brain

- often too late for surgery

only give radiotherapy to the brain in this circumstance and in childhood cancers (leukemia that might have gone to brain) (not normal!) --> can lead to short term memory loss and brain cancer (!!)


What are oncogene addicted tumours?

lung cancers
- targeted therapies have significantly improved outcomes


lung cancer:
which type is...
highly aggressive/ rapid? (1)
associated with paraneoplasic syndromes? (1)
often found centrally close to bronchi? (1)
often peripheral+non-smokers? (1)
previous asbestos exposure? (1)
less differentiated than other NSCLCs and tend to metastasis early? (1)
associated with mutations in EGFR and ALK?

- SCLC; often metastasised already and inoperable prior to diagnosis. responsive to chemo but relapse quickly. Poor prognosis.


- squamous cell carcinoma: central, close to bronchi, closely linked to cigarette smoking. Squamous cell cancers can also secrete PTH relate peptide (PTHrp) which can lead to malignancy-related hypercalcaemia

- adenocarcinomas; often in women

- adenocarcinoma

- large cell carcinoma

- adenocarcinoma (mutations)

other types of lung cancers include carcinoid, mesothelioma, sarcoma, and lymphoma.


lung cancer:
investigations (7)

- CT chest and upper abdomen
- PET scan
- bronchoscopy
- other biopsy techniques
- tumour markers
- pulmonary function tests
- cadiopulmonary exercise testing


lung cancer:
when to do CT? (1)
use of PET? (1)
bronchoscopy? (1)
other biopsy techniques? (1)
tumour markers? (2)

What are the uses of:
pulmonary fuction tests? (1)
cardiopulmonary exercise testing? (1)

- local/distant disease, principally in the lungs, mediastinum, pleura, liver and adrenal glands, can do brain too

- operable disease to check for distant metastases which may not be picked up on CT

- fibre-optic or rigid bronchoscopy allows visualisation of the bronchial tree, tumour biopsy and bronchial washings to be taken. Endo-bronchial Ultrasound (EBUS) can be used to biopsy lymph nodes within the mediastinum.

- trans-thoracic biopsy under radiological guidance is sometimes required for the biopsy of peripheral lung tumours, or distant metastatic disease e.g. liver metastases.

- neuron specific enolase (NSE) and lactate dehydrogenase (LDH) may provide useful indications of tumour activity. These are not routinely used.

- PFTs are important for assessing underlying lung disease / function --> show fitness for treatment

- to assess fitness pre-surgery to see if safe


lung cancer:
- management of SCLC (2)
- in which patients is prognosis better? (2)
- how does treatment vary to NSCLC? (1)
- which cancers cause SVCO? (4)
- is surgery done in SCLC? (1)
- what to tell patients ask if smoking caused their cancer? (1)
- what to tell them to do next? (1)

- if appears “limited stage” at diagnosis (i.e. encompassable within a high dose radiotherapy field) then radical radiotherapy + chemotherapy
- prophylactic cranial irradiation used with limited disease and those in extensive who respond to chemo

~80% of patients with SCLC will respond to combination chemotherapy (with complete response rates approaching 50%) but most relapse then die rapidly

- Eaten-Lambert syndrome concurrently because often discovered earlier
- high performance status

---> complications such as SVCO and MSCC = treat with chemotherapy rather than radiotherapy (in contrast to NSCLC!)

1st = NSCLC
2nd= SCLC
3rd= non-Hodgkin’s lymphoma
4rd= breast/ thymic/ mediastinal germ cell tumours

- SCLC = considered a systemic disease at presentation --> surgery inappropriate in many cases
(often occurs by accident i.e. it's resected and they realize it's SCLC)
- no evidence of improved outcome

- if they ask, say yes, smoking will have contributed but there are many other factors too such as genetics and bad luck

- stop smoking now.. it will reduce treatment side effects, improve the efficacy of treatment and decrease chance of recurrence


three uses for radiotherapy in SCLC? (3)
prognosis SCLC? (2)
prognostic factors (4)

remember SCLC is the awful one!!

1- treat primary tumor (concurrent with chemo)
2- prophylactic cranial irradiation (but can --> memory impairment, functional deficit and dementia) :(
3- palliative

- without treatment: 2-4months
- with treatment: 6-12 months

- extent of disease at presentation
- number of metastatic sites
- performance status, degree of weight loss
- biochemical abnormalities (elevated LDH or low sodium or albumin)

Patients with limited disease, a good performance status, and favourable biochemistry have a small but real chance of long-term survival (10-15%). Patients with extensive disease who are less fit are rarely cured but can obtain good palliation from chemotherapy.


management of NSCLC:
surgery? (3)

- possibility of cure
- mediastinal involvement is contraindication
- ~30% of NSCLC are suitable for surgery
- 3-5% mortality from pneumonectomy --> lobectomy/wedge resections recommended

In general:
SCLC= worse prognosis= metastasis at presentation= no surgery so have to use chemo/radio (the neoplastic one)
non-SCLC= better prognosis= surgery then chemo

Use of radiotherapy alone is complicated and not necessary to learn but interesting:
Giving radiotherapy at the same time as chemotherapy (concurrent chemo-radiotherapy) may also improve outcomes compared to giving chemotherapy first followed by radiotherapy (sequential chemo-radiotherapy). This is usually used in patients with Stage II-III disease.
Increasingly, early NSCLC located more peripherally in the lungs is treated by stereotactic ablative body radiotherapy (SABR). This delivers a small number (≤5) of very large doses of radiotherapy to a small, highly conformal volume around the lung tumour. This technique has rates of tumour control that are comparable to surgery and can be used in many patients who would not be fit enough for surgery.


NSCLC surgery:
when do you du adjuvant chemo?
when do you do adjuvant radiotherapy?

- adjuvant chemo improves survival if fit enough to tolerate it for pt. with nodal disease/larger tumors
- adjuvant radiotherapy if positive surgical margins


NSCLC: 3 adenocarcinoma, squamous cell and large cell
uses of targeted therapy? (1)
immunotherapy? (1)

(don't need exact points just have some understanding of these new emerging therapies)

- effective in clinical trials for advanced NSCLC
- in adenocarcinoma, pts. tested for EGFR and ALK mutations at diagnosis... if positive, can use TKIs (Tyrosine Kinase Inhibitors)
- only < 10% of pt.s are suitable but higher in some ethnic groups and non-smokers
- patients on these targeted therapies can be treated with second line targeted therapies (Osimertinib/Ceritinib) rather than the standard chemotherapy

- recently approved for advanced NSCLC if high PDL1 expression (a molecule involved in controlling the normal immune response)
- used neoadjuvant/adjuvant to chemotherapy

can extend life to around 2 years in some cases!


colorectal cancer:
familial risk factors?

- hereditary non-polyposis colon cancer (HNPCC) i.e. Lynch syndrome
- familial adenomatous polyposis (FAP)
- Gardner's syndrome

Specific gene defects associated with these conditions have been identified. For example, mutations in the APC gene (5q21-22) (familial adenomatous polyposis coli) and mutations in DNA mismatch repair genes (HNPCC)
--> you can test for it within families who present with lots and lots of cancer


breast cancer:
prevalence? (2)
risk factors:
oestrogen? (3)
genes? (3)
lifestyle? (3)
other? (2)

- 1 in 8 (15% of cancers in women)
- 1 in 870 in men
- survival rate increasing, 10 year survival 80%

no single cause:
uninterrupted oestrogen exposure
- early menarch, late menopause
- nulliparity/ first child at older age
- use of HRT (~2% increase)
- obesity

- P53 (linked to a few cancers)
--> family history important, younger members with ovarian/ bilateral breast cancer/ men with breast cancer --> refer to genetics team
(first degreee relative premenopausal is a concern)

- alcohol
- smoking
- diet

- chest wall/ mediastinal radiotherapy (ionising radiation)
- age

BRAC 2 linked to breast cancer but not ovarian! BRAC 1 is both!


what screening factors are important? (7)
what two ways are breast cancer detected? (2)
what ages are breast cancer screening and how often? (2)
name of cancers found in between screening? (1)

- cancer must be common
- pick up the cancer early
- early intervention--> increased cure rate
- tool must be used friendly
- can't discriminate e.g. if higher SES more likely to do it it's unethical as --> inequalities
- sensitive
- specific
- cost-effective
- must screen large population (in breast cancer 1 per 125 women who had screening)

1- NHS Breast Screening programme
2- symptoms --> GP 2 week wait or normal referral
go to clinic for a "triple assessment"

- 50-70 and screened every 3 years
- mammogram

- found in between are called INTERVAL CANCERS but they are rarer.


breast cancer:

- lump in axilla or breast (axillary or supraclavicular nodes)
- nipple inversion
- skin tethering
- bloody nipple discharge
- peau d'orange; very aggressive inflammatory breast cancer, short history of red, oedematous breast- often treated as mastitis --> 2 week referral; very often missed!
- symptoms of metastatic disease :(


breast cancer:
triple assessment (3)
what to do to assess metastasis? (3)
when is MRI performed? (1)

- clinical: full history and exam
- radiology: bilateral mammography (to detect multicentric tumours or synchronous primaries in the opposite breast)
- pathology; US and biopsy from lump and lymph node (FNA)

Cytological diagnosis should be confirmed by fine needle aspiration cytology (FNAC), needle biopsy, incisional or excisional biopsy.

if high risk of disseminated disease, perform:
- isotopic bone scan
- liver imaging
- US or CT scan

- MRI if discrepancy between clinical examination, mammogram and ultrasound findings, if breast density preludes accurate mammogram assessment and if the histology is lobular (as there is a higher frequency of multicentric disease)


breast cancer:
curative intent treatment? (2)
aims of palliative treatment? (3)
which type responds best to chemotherapy? (1)

- surgery
- adjuvant systemic treatment
- locoregional treatment (radiotherapy to the remaining breast)
- neo-adjuvant systemic treatment (chemo to shrink it)
- surgery

- symptom control
- maximise QoL
- improve survival

chemotherapy in breast cancer especially useful in local advanced disease or inflammatory breast cancer: ER negative/ HER2 positive disease responds most. No impact on overall survival.


breast cancer:
surgery types (4)
adjuvant treatments (3)
when would neo-adjuvant chemo be used? (3)

- wide local excision
- mastectomy

- axillary clearance (remove glands)
- sentinel node biopsy; if node-negative then get sentinel node out and examine the node and make sure no microscopic disease

- chemotherapy
- hormone therapy
- targeted therapies (Her 2)

neo-adjuvant chemo used to shrink the tumour so they can have wide local excision rather than mastectomy (patients choice)

1• Initial surgery is not possible due to the size of the tumour
2• To allow for breast conservation
3• Her2 positive or triple negative breast cancer (ER, PR and Her 2 negative) as high response rates are possible

Sentinel node biopsy involves injecting a tracer material that helps the surgeon locate the sentinel nodes during surgery. The sentinel nodes are removed and analyzed in a laboratory. If they are positive then patients will go on to have an axillary clearance or radiotherapy to the axillae.


breast cancer:
why is targeted therapy > chemotherapy? (2)

- chemotherapy isn't very targeted
- endocrine therapy is useful for estrogen sensitive (ER/PR+)

anti Her2 treatment good if tumour over expresses HER2 protein


breast cancer:
commonly used chemo treatments? (2)
less commonly used? (2)
how many cycles/ how long each session? (2)
what does chemotherapy need to balance? (4)

- EC (Epirubicin and Cyclophosphamide)
- Docetaxel

- FEC (5-FU, Epi and Cyclo)
- Paclitaxel

- oral chemotherapy used in palliative settings
- all work by causing DNA damage
- given in cycles every 3 weeks
- usually 6-8 cycles

- toxicity vs
- benefit vs
- patient's general health vs
- patient's wishes
(ultimately the choice is your patients!)


chemotherapy side effects:
general? (9)
organ specific? (6)

- fatigue
- hair loss
- N&V
- mucositis
- gastritis
- diarrhoea/const.
- myelosuppression-->neutropenic sepsis
- thrombocytopenia
- anaemia

each drug has organ specific side-effect (drug specific!)
- infertility
- second malignancies
- cardiotoxicity
- pulmonary toxicity
- nephrotoxicity
- neurotoxicity

consider drug combinations, is there an organ already compromised that we should avoid?

long term side-effects usually not reversible..


What does it mean if breast cancer is oestrogen recetor-positive?
where is oestrogen produced in premenopausal women? (1)
postmenopausal women? (4)
problems with aromatase inhibitors? (1) problems with tamoxifen? (2)
treatment to decrease oestrogen production? (3)

- oestrogen triggers it's growth by attaching to receptor
- block the receptor

- in ovaries pre-menopausal
- remove ovaries (oophrectomy)
- tamoxifen (sits on the receptor so the oestrogen can't fit in)

- no longer in ovaries, in adipose tissue, skin, liver, muscle and breast tissue
- aromatase inhibitors; anastrozole, letrozole, exemestane (blocks extra-ovarian oestrogen production)
- tamoxifen
(AIs usually preferred in post-menopausal, have fewer vascular and malignant effects but more probelsm w osteoperosis--> DEXA)

tamoxifen can be used in both!! but aromatase inhibitors only in post-menopausal or ovarian suppression

Tamoxifen therapy for 5 years, 20 mg/day, significantly reduces the annual risk of recurrence (by approximately 25%) and of death (17%) in the adjuvant setting. Increased thrombotic complications are reported and an increased risk of endometrial carcinoma.

if AI started and DEXA shows bone --> further recommendations depending on the results (such as lifestyle changes, Vit D and calcium supplementation or bisphosphonates).


Breast cancer:
side effects of hormonal therapy:
what do both tamoxifen and aromatase inhibitors cause? (4)
tamoxifen? (3)
aromatase inhibitors? (2)
two big differentials to consider in breathlessness with breast cancer? (2)

Both cause similar effects to menopause:
- vasomotor
- mood changes
- loss of libido
- body image

- vaginal discharge
- endometrial changes: benign/ malignant
- thromboembolic episodes- VTE/ stroke

- vaginal dryness
- decrease in BONE density
(- arthralgia and myalgia)

forms a large chunk of work for oncologists and GPs

- if on tamoxifen --> BEWARE as could be PE
- also beware for SVCO just incase!


Breast cancer:
what percent are HER2 positive? (1)
which therapies are given for this? (1)
how often given? (1)
route? (1)
risk to which organ? (1)
monitoring? (1)

- 15%

monoclonal Ab:
- trastuzumab (Herceptin)
hit the HER2 protein and kill it off

- given IV or subcut
- 3 weekly
NOT chemotherapy

- allergy
- can be CARDIOTOXIC --> check cardiac function and cardiac monitoring is critical


Breast cancer:
when is endocrine therapy useful? (1)
when is anti-HER2 used? (1)
when do you use chemo? (1)

- endorcrine--> if oestrogen (ER) positive

- if HER2 positive

chemo can be for almost all cancers
many not be appropriate in some circumstances e.g. if survival after surgery is 88%, but 89% with chemotherapy aswell it won't be worth having chemo too due to the side effects
(so done case-by-case basis)


measured in? (1)

- fractions

- Grays

- 15 treatments over 3 weeks (40Gy each time) for breast cancer


what type of breast cancer is immunotherapy useful in? (1)

triple negative (not expressive ER, PR or HER2)


breast cancer:
prognostic features? (4)
why is it important to think about prognosis when deciding management? (1)
which type of breast cancer does worst? (1)
which is best? (1)

1- Stage
2- Grade
3- Molecular markers:
- ER negative
- Her-2 positive
4- Age?

helps you decide what treatment modes to go down and how aggressive to be

- triple negative are worst

- ER positive tend to do best


breast cancer:
histology- what types? which is most common? (3)

1- infiltrating or invasive ductal carcinoma ~ 70-80%
2- lobular carcinoma ~10% of cases, is characterized by a higher incidence of multicentric tumours within the same or opposite breast
3- less common: medullary, colloid, comedo and papillary

GRADE 1 = well differentiated
GRADE 3 = poorly differentiated


when someone first receives a cancer diagnosis, how is treatment/ management plan decided? (1)
what tools aid decision making for this? (1)
breast cancer:
staging? (4)

discuss management plan in MDT

for breast cancer the standard treatment would be surgery first. However for a certain subset of patients neoadjuvant chemotherapy is considered (chemotherapy before surgery) such as...?

Tools such as Adjuvant online and the Oncotype DX test can aid in decision making. Oncotype DX is a genomic test designed to predict benefit from chemotherapy

Stage 0: Tis, N0, M0
Stage I: T1, N0, M0
Stage II: T2/3, N0, M0 or T0/1/2, N1, M0
Stage III: T or N > stage II, M0
Stage IV: Any T, Any N, M1


breast cancer:
what factors to consider when selecting adjuvant systemic therapy? (6)
what does ADJUVANT mean? (1)

• Hormone receptor status [oestrogen receptor (ER) status]
• HER-2 receptor status
• Menopausal status
• Tumour size and grade
• Nodal involvement
• Performance status

adjuvant is AFTER the primary treatment of surgery


breast cancer:
who is offered radiotherapy? (3)
how is radiotherapy given (which days)? (1)
who might get longer radiotherapy treatments? (2)
when is a large dose of radiotherapy used? (1)

1- adjuvant to conservative surgery for all patients to residual tissue i.e. rest of boob
(reduces locoregional cancer recurrence)

2- adjuvant to mastectomy to local chest wall if high risk of local recurrence
(e.g. deep resection margin involvement, large primary tumours (> 4cm), multiple axillary lymph nodes containing metastatic disease, and widespread lymphovascular tumour permeation)

3- may consider axillae of supraclavicular fossa irradiation

- standard treatment daily Mon-Fri for 3 weeks

- if <50 years old or close surgical margins give additional week

- large use in palliation to reduce bone pain


breast cancer:
therapeutic options for ER/PR positive disease? (2)
response to endocrine therapy depends on..? (3)

- Tamoxifen
- aromatase inhibitors (anastrazole or letrozole)
continued until documented evidence of disease recurrence
- ovarian ablation in premenopausal (surgically or radiotherapy induced) or by the use of luteinizing hormone releasing hormone (LHRH) agonists

• The dominant site of disease (highest in women with disease in soft tissue, less in those with bone metastases and less again in those with visceral metastases). This may simply reflect ER status
• An objective response to prior endocrine treatment.
• Greater duration of previous disease free interval.


prostate cancer:
prevalence? (1)
risk factors? (3)
genes? (3)
implications? (3)

- 1 in 8
- 50% occur in over aged 75

- age; >50
- FH; 2.5* if first degree relative
- ethnicity; Afro-carribean

- pTEN genes
- BRAC I role less clear but recent evidence shows rate of DNA repair pathway genetic defects is much higher than previously thought (12% in men with metastatic prostate cancer).

- radiation exposure, diet and anabolic steroids all implicated but not proven
may alter lvl of testosterone which controls growth and function of the prostate


prostate cancer:
histology? (1)
location? (1)
why isn't PSA screening done? (1)
can men request a PSA test at GP? which men? (1)
symptoms? (7)

- 95% adenocarcinoas
- posterior or peripheral parts

- no offical screening programme: evidence benefit < harm

- men >50 years old can request test after given written information

- LUTS; urinary symptoms (reduced flow/poor stream, increased frequency, dribbling nocturia); often co-existing BPH
- impotence
signs of metastatic cancer:
- anaemia
- bone pain
- weight loss
- general malaise
- fracture

Screening: over-diagnosis due to PSA tests --> prostate cancer found that doesn't need treatment --> unnecessary anxiety (would never cause them symptoms) ~75% with high PSA don't have cancer
- when PSA tests were invented, incidence of prostate cancer spiked but mortality didn't decrease substantially showing over-diagnosis


prostate cancer:
pathway if high PSA test in GP? (6)
what percent are negative after positive PSA? (1)
two types of biopsy? (2)
risks of transrectal? (3)
risk of transperineal? (1)
findings on DRE? (4)

1--> refer on 2 week wait to urology
2--> history and DRE
3--> MRI scan of prostate
4--> most then go on to have biopsy (80%) by intervention radiology
5--> consider isotope radionucleotide bone scan to see metastasis
6--> all findings go to MDT to decide if prostate cancer

75% who were found to have high PSA at their GP will not have prostate cancer after going through this whole pathway..

- transrectal TRUS
- transperineal

- rectal discomfort
- blood in urine/semen
- sepsis (3%) and hospitalization

- trans perineal biopsy tend to be safer, done under local and decreased risk of infection
(used to only be done under general anaesthetic --> not common place but now used more as under local)

- enlarged
- hard
- craggy gland (or nodule)
- obliteration of the median sulcus

MRI is CORONAL section of prostate (face-on)


prostate cancer:
what does grading depend on? (3)
what are they graded as? (3)
treatment options for low risk? (3)
additional investigation for immediate/high risk? (1)
treatment options for immediate/high risk? (2)
types of radiotherapy? (2)
risks of surgery? (2)
risks of radiotherapy? (1)
bracytherapy? (1)

- gleason

- graded as low, immediate or high risk

- LOW: active surveillance, surgery, radiotherapy
(if fit and young better to have treatment, if older AM probably best)

- IMMEDIATE/HIGH: bone scan (metastasis)
- surgery
- radiotherapy: EBRT and brachytherapy

radiotherapy is a radical therapy!

- incontinence
- impotence

- non-invasive and good option for co-morbidities as no direct intervention no but risk of long term bowel problems/ faecal incontinence, dysuria, rectal bleeding, impotence, diarrhoea

BRACHY:(type of radiotherapy)
- good option if fit with no comorbidity as it is invasive
- avoid if large prostate or significant urinary symptoms


metastatic prostate cancer:
treatment (4)
how does androgen deprivation therapy work? (1)
adverse effects of ADT? (5)

- androgen deprivation therapy
other systemic drugs in fitter patients
- chemotherapy
- abiaterone/enzalutamide
- palliative radiotherapy for persistent bony pain
- may offer surgery for urinary obstruction or prostatic symptoms

ADT: prostate cells and prostate cancer requires testosterone to divide
adrenal glands and tests: ADT blocks at level of angrogen

- hot flushes
- sexual dysfunction/ shrinkage penis and testes
- loss of muscle bulk/ strength
- memory effects and mood disturbance
- 10% weight gain and higher risk diabetes (metabolic syndrome)/ altered lipids
- osteoporosis/ higher fracture risk

5% increased absolute risk of CV mortality if known Hx of cardiovascular disease BUT only in observational studies


what is an isotope bone scan? (1)
how does Gleason score work? (1)

functional imaging:
- radiolabelled technetium
- taken up by osteoblasts
- at sites of bone remodelling e.g. sclerotic bone metastases in prostate cancer metastases.

- Several grading systems for prostate cancer exist. The Gleason system scores tumours (from 2 to 10) on the basis of histological patterns in the two most dominant areas of the tumour, (e.g. Gleason 4 + 3 means main area is 4 with the second area 3).


prostate cancer:
types of chemotherapy? (2)
how long? (1)

- docetaxel (in combintation with prednisolone)
- cabazitaxel
improves QoL and survival

- give 6 cycles in fit men


prostate cancer:
prognosis? (2)
poor prongnosis predictors? (3)

- Prostate cancer survival of men with low risk localised prostate cancer is excellent (99%) at 10 years whether they choose active surveillance, radiotherapy or surgery.

- Prostate cancer 10 year survival (all UK patients) is around 84%

- metastatic= 3.5 years median

Pattern of disease (bone metastases), aggressive pathology and younger age are associated with a poorer prognosis.


prostate cancer:
when are hormonal therapy used?
mechanism? (1)
types? (5)

- advanced disease or
- in conjunction with radiotherapy for localized disease

- inhibition of the growth-stimulatory effect of endogenous androgens may effectively treat prostatic cancer with a response rate of approximately 80%

1- Medical castration:
- LHRH; Luteinizing hormone-releasing hormone interferes with the release of gonadotrophins from the pituitary --> less testosterone
- given by monthly or 3 monthly subcutaneous or intra-muscular depot injections
- side effects: impotence, loss of libido and tumour flare
- tumour flare occurs on initiation of treatment (prior to the down regulation of gonadotropin) and is avoided by short-term concomitant anti-androgen therapy
- long-term --> increased cardiac risk and osteoporosis

2- GnRH (gonadotrophin-releasing hormone) antagonist
3- Oestrogen therapy; inhibit LHRH production from hypothalamus
4- anti-androgens
5- bilateral orchidectomy (done in countries with limited medical therapy)


colorectal cancer:
histology? (4)
spread is usually via...? (4)

epithelial: 90-95% adenocarcinoma (mucinous or signet ring).
rare others include:
- squamous cell carcinoma and adenosquamous carcinoma.
- carcinoid
- gastrointestinal stromal tumour
- primary malignant lymphoma

- invasion
- lymphatic
- venous
- trans-coelomic spread within peritoneal cavity


colorectal cancer:
symptoms? (4)
investigations? (5)
which staging used? (1)

- altered bowel habit
- weight loss
- rectal bleeding
- vague abdo pain

vary according to site of primary tumour and degree of spread

More occult tumours, typically of the right side of the colon and the caecum, can present with iron deficiency anaemia

- DRE; 3/4 of rectal can be felt
- direct visualisation with rigid sigmoidoscopy (to 25cm), flexible sigmoidoscopy and colonscopy allows biopsy or suspicious lesions
- double cosntrast barium enema les susually as no histology
- CT staging
- CT colonography= CT scan and insufflation of whole colon w gas to see synchronous polyps within bowl where colonoscopy not possible but doesn't allow biopsy
- CEA used to monitor disease

- Dukes


colorectal cancer:
what age has a worse prognosis? (1)

<40 years old= adverse prognostic factor (biologically more aggressive tumour?)


colorectal cancer:
Dukes staging (4)
5-year prognosis? (4)
how does treatment vary? (1)
which is the most active agent in colorectal cancer? (1)

- Dukes: A-D
A Invasion into but not through the bowel wall 80%
B Invasion through the bowel wall but not into nodes 50%
C Lymph node involvement 15-40%
D Distant metastases 5%

chemotherapy used in C, increases surival from 40-60% but not indicated in B although selected high-risk cases can be treated

5-FU is the most active agent in colorectal carcinoma with a response rate of approximately 25%.
Newer drugs such as Oxaliplatin and Irinotecan are now also in standard use.


colorectal cancer:
when is radiotherapy appropriate? (1)
why is radiotherapy rarely used in colon cancer? (2)

- primarily in rectal

NOT in colon cancer as
- the potential toxicity to adjacent organs
- the mobility of the tumours

Pre-operative (or rarely adjuvant) radiotherapy is indicated in high risk rectal carcinomas before (or rarely following) total resection. Local recurrences can be palliated with radiotherapy. Metastatic disease may also respond to palliative radiotherapy.


Where are the lung cancers commonly found?
1. adenocarcinoma
2. squamous cell
3. large cell


SCLC and squamous = BRONCHIAL
adenocarcinoma and large cell = PERIPHERALLY

commonly spread to lymph nodes under the carina --> stridor