OSCC Flashcards
1
Q
Where does the word “tumour” originate from?
A
latin - swelling
2
Q
What is the general nomenclature for benign tumours?
A
-oma to the cell type the neoplasm arises from
3
Q
What is the exception to the normal rule of naming benign tumours?
A
epithelial neoplasms
4
Q
How are benign epithelial neoplasms classified?
A
on their microscopic or macroscopic patterns
5
Q
Adenoma
A
benign gland patterned epithelial neoplasm
6
Q
Papilloma
A
benign epithelial neoplasm producing microscopic or macroscopic fingerlike fronds
7
Q
How are malignant epithelial origin neoplasms named?
A
-carcinoma
8
Q
How are malignant CT neoplasms named?
A
-sarcoma
9
Q
How are malignant epithelial neoplasms classified?
A
on their microscopic or macroscopic pattern
10
Q
What do the neoplastic cells resemble in squamous cell carcinoma?
A
stratified squamous epithelium
11
Q
What are the three exceptions in malignant nomenclature?
A
lymphoma, mesothelioma, melanoma
12
Q
Growth type of benign tumours
A
expansive
13
Q
Growth type of malignant tumours
A
infiltrating
14
Q
Growth speed of benign tumours
A
usually slow
15
Q
Growth speed of malignant tumours
A
usually rapid
16
Q
Do benign tumours often stabilise?
A
yes
17
Q
Do malignant tumours often stabilise?
A
no it would be exceptional
18
Q
Structure of benign tumours
A
typical
19
Q
Structure of malignant tumours
A
atypical (dedifferentiation - anaplasia)
20
Q
Mitoses in benign tumours
A
rare and typical
21
Q
Mitoses in malignant tumours
A
numerous and atypical
22
Q
Evolution of benign tumours
A
local
23
Q
Evolution of malignant tumours
A
local and general
24
Q
Local consequences of benign tumours
A
variable - compressions
25
3 local severe consequences of malignant tumours
infiltration, destruction, necrosis
26
General consequences of benign tumours
none unless secretory tumours/particular sites
27
In what phase are the general consequences of malignant tumours constant and severe?
generalisation phase
28
Which type of tumour is always fatal without treatment?
malignant
29
Do benign tumours tend to recur?
no
30
OSCC gender ratio
M 2.22:1 F
31
Three most common oral cancers
OSCC, NHL, mucoepidermoid carcinoma
32
Which continent has a high prevalence of oral cancer?
Asia
33
Black patients and oral cancer
detected later and greater mortality
34
what percentage of cancers are oral?
2%
35
what % of oral cancer is in over 55s?
78%
36
Most common oral cancer site
tonsils
37
2nd most common oral cancer site
tongue
38
3rd most common oral cancer site
base of tongue
39
where does OSCC originate from?
oral keratinocytes
40
what % of oral cancers are SCC?
over 90%
41
3 most common sites for OSCC?
tongue, FOM, gingiva
42
In countries where betel quid chewing is practiced, where are the 2 most common OSCC sites?
buccal mucosa and gingiva
43
How is early stage OSCC usually detected and why?
incidentally as tends to be asymptomatic
44
What are the 8 subtypes of OSCC?
1. verrucous carcinoma
2. basal SCC
3. papillary SCC
4. spindle cell SCC
5. Adenosquamous carcinoma
6. lymph-epithelial carcinoma
7. acantholytic SCC
8. carcinoma cuniculatum
45
Which subtypes of OSCC have a better prognosis?
verrucous carcinoma
| papillary SCC
46
which subtypes of OSCC have a worse prognosis?
spindle cell SCC
| adenosquamous carcinoma
47
which 3 subtypes have an exophytic verruco-papillary component?
verrucous carcinoma
carcinoma cuniculatum
papillary SCC
48
What are the 4 clinical appearances of OSCC?
OPMDs
ulceration
speckled
exophytic growth
49
OSCC appearance - OPMDs
flat/slightly raised red/white/mixed exophytic lesions
| may get changes in surface texture (smooth, granular, rough, crusted)
50
OSCC appearance - ulceration
solitary lesion that is not healing/responding to conservative management
usually presents with irregular and indurated margins
51
OSCC appearance - speckled
ill-defined mixed white-red lesions with granular aspects
52
OSCC appearance - exophytic growth
irregular overgrowth with a smooth or verrucopapillary (verrucous carcinoma) surface above normal mucosa
53
Late stage OSCC - what is the usual cause of pain?
ulceration
54
Late stage OSCC - what leads to trismus?
OSCC of buccal mucosa and involvement of the infra temporal fossa
55
Late stage OSCC - FOM symptoms
restriction of tongue mobility
progressive difficulty in mastication and speech
drooling of saliva
56
Late stage OSCC - gingiva
excessive mobility of involved teeth due to involvement of periosteum and possible spread to bone
57
Late stage OSCC - tongue base
```
sensation of fullness in throat
dysphagia
sensation of a lump in neck/throat
voice changes
ear pain
```
58
What 3 parts of the diagnostic pathway do you need for staging and grading?
pt history and exam
histopathology and clinical adjuncts
radiologic imaging
59
2 predictors of prognosis
staging and grading
60
Grading
cytologic differentiation of the cells - how much the cancer cells look like healthy cells under a microscope
61
Staging
where has the cancer spread?
62
5 morphologic features considered in grading
```
degree of keratinisation
nuclear polymorphism
number of mitoses
pattern of invasion
host response
```
63
Which morphologic feature is excluded from the Bryne grading system?
number of mitoses
64
what is the ideal pattern of invasion of a tumour?
pushing, well-delineated, infiltrating borders
65
Grade X
differentiation can't be assessed
66
Grade 1
well-differentiated
67
Grade 2
moderately differentiated
68
Grade 3
poorly differentiated
69
Grade 4
undifferentiated or anaplastic
70
Grades
X, 1, 2, 3, 4
71
What does a lower grade mean?
better prognosis
72
What does the grade predict?
how quickly the cancer will spread
73
What does TNM staging stand for?
Tumour, Node, Metastasis
74
TNM staging - T stages
T0-4
75
TNM staging - what does T describe?
size (cm) and location, how much the tumour has grown into nearby tissues
76
TNM staging - N stages
N0-3
77
TNM staging - what does N describe?
whether the cancer has spread to lymph nodes - regional or distant
78
TNM staging - M stages
M0 or M1
79
TNM staging - what does M describe?
whether cancer has spread to other parts of the body - distant metastasis
80
What does the 8th edition cancer staging not include?
non-epithelial tumours
81
what does T incorporate in 8th edition cancer staging?
DOI
82
what does N incorporate in 8th edition cancer staging?
ENE
83
Tumour Thickness
mucosal surface of tumour to deepest point of tissue invasion in a perpendicular fashion
84
Depth of Invasion
level of basement membrane adjacent to normal mucosa to deepest point of tumour invasion
85
What DOI is associated with a significantly increased risk of recurrence and nodal metastasis?
>10mm
86
When should elective neck dissection be considered?
for tumours <5mm deep
87
ENE
extension of metastatic cells through the nodal capsule into the perinodal tissue
88
what is the advantage of 8th edition cancer staging?
leads to identification if OSCC pts with a worse prognosis who might benefit from an improved post-op tx strategy
89
give some examples of where oral cancer can metastasise to
anywhere - lung, heart, vertebra, chest wall
90
What do you do before an imaging assessment?
establish the primary site and any neck metastasis clinically
have histological diagnosis
91
What is the role of radiology?
accurately stage the full extent and distant spread of disease with TNM system
92
What are the focus areas for imaging?
local extent of primary tumour
spread to loco regional cervical lymph nodes
detection of metastatic disease precluding cure and synchronous primary tumours of lung/upper aero-digestive tract
93
What is the main form of imaging used to detect the primary tumour?
CT
94
what is CT used for?
detecting primary tumour
| local bone infiltration
95
multi-detector CT (MDCT)
precisely determine boundaries of tumour
96
contrast-enhanced CT (CECT)
accurately determine LN metastases
97
what can't CT differentiate between?
recurrences, surgical scars and adverse reactions after radiation therapy
98
Give a form of imaging using ionising radiation
CT
99
give 2 examples of imaging without ionising radiation
MRI, US
100
give a form of functional imaging
Positron Emission Tomography combined with CT (PET-CT)
101
what can MRI determine the involvement of?
local STs, bone marrow, bones, vessels, nerves
| local LN and distant metastases
102
what is MRI better than CT/CBCT for?
assessment of STs
103
2 advantages of US
cheap and non-invasive
104
3 uses of US
evaluate superficial lesions
evaluate LNs
guide FNAB
105
what can colour doppler US be used for and what is the advantage of this?
to determine the type of blood vascularity in a lesion
| often increases the specificity of diagnosis
106
what is the advantage of PET-CT over CT or MRI?
may detect malignancy in structures which appear normal or are difficult to assess on CT/MRI e.g. small vol LN metastases
107
give 3 uses of PET-CT
look for the primary tumour site when metastases are found earlier (CUP)
detect recurrence of primary tumours
detect distant metastases of primary tumours
108
when is PET-CT recommended?
advanced cancer stages
109
8th edition cancer staging - 4 subsections
definition of primary tumour (T)
definition of regional LN (N, pN)
definition of regional LN (N, cN)
definition of distant metastases (M)
110
8th edition cancer staging - T stages
```
TX
Tis
T1
T2
T3
T4a
T4b
```
111
8th edition cancer staging - TX
primary tumour can't be assessed
112
8th edition cancer staging - Tis
carcinoma in situ
113
8th edition cancer staging - T1
< or = 2cm
| DOI < or = 5mm
114
8th edition cancer staging - T2
25mm
115
8th edition cancer staging - T3
210mm
OR
>4cm, DOI <=10mm
116
8th edition cancer staging - T4a
moderately advanced local disease
>4cm, DOI >10mm
OR
invaded adjacent structures only (superficial erosion of bone/socket alone by a gingival primary is not T4)
117
8th edition cancer staging - T4b
v advanced local disease - tumour invades masticator space, pterygoid plates, or skull base and/or encases ICA
118
8th edition cancer staging - NX
regional lymph nodes can't be assessed
119
8th edition cancer staging - N0
no regional LN metastasis
120
8th edition cancer staging - N1
1 ipsilateral
<=3cm
ENE -
121
8th edition cancer staging - N2a
single ipsilateral, 3
122
8th edition cancer staging - N2b
multiple ipsilateral <=6cm, ENE -
123
8th edition cancer staging - N2c
bilateral/contralateral, <=6cm, ENE -
124
8th edition cancer staging - N3a
>6cm, ENE -
125
8th edition cancer staging - N3b
any nodes and clinically overt ENE+
```
OR pN3b:
1 ipsilateral >3cm, ENE+
or
multiple ipsilateral/contralateral/bilateral ENE+
or
single contralateral, any size, ENE+
```
126
8th edition cancer staging - cM0
no distant metastasis
127
8th edition cancer staging - cM1
distant metastasis
128
8th edition cancer staging - pM1
distant metastasis, microscopically confirmed
129
8th edition cancer staging - what does U or L for N category mean?
indicates metastasis above the lower border of the cricoid (U) or below (L)
130
8th edition cancer staging - prognostic staging groups
```
0
1
2
3
4a
4b
4c
```
131
8th edition cancer staging - stage 0
Tis
N0
M0
132
8th edition cancer staging - stage 1
T1
N0
M0
133
8th edition cancer staging - stage 2
T2
N0
M0
134
8th edition cancer staging - stage 3
T3 N0 M0
or
T1/2/3 N1 M0
135
8th edition cancer staging - stage 4a
T4a N0/1 M0
or
T1/2/3/4a N2 M0
136
8th edition cancer staging - stage 4b
any T N3 M0
or
T4b any N M0
137
8th edition cancer staging - stage 4c
any T
any N
M1
138
how do involved LNs initially present?
soft
mobile
non-tender
139
how do involved LNs present at the advanced stage or in aggressive disease?
enlarged
firm/hard texture
usually non-tender fixation to adjacent tissue due to invasion of cells through the capsule
140
Lymph node levels
```
1a
1b
2a
2b
3
4
5a
5b
6
7
```
141
LN level 1a
submental
142
LN level 1b
submandibular
143
LN level 2a and b
upper jugular
144
LN level 3
mid jugular
145
LN level 4
lower jugular
146
LN level 5a and b
posterior triangle
147
LN level 6
anterior compartment
148
LN level 7
superior mediastinal
149
location of LN level 1a - submental
between anterior bodies of digastric muscles and hyoid bone
150
what do the submental (1a) nodes drain?
lower lip and chin
| secondary drainage for anterior tongue
151
location of LN level 1b - submandibular
from U to L margin of submandibular gland
medial to mandible
lateral to posterior body of digastric muscle
152
what do the submandibular (1b) nodes drain?
oral cavity
lower nasal cavity
submandibular gland
153
location of LN level 2 - upper jugular
from underside of lateral process of C1 to hyoid
medial to SCM
lateral to scalene muscles
154
what is LN level 2 divided into a and b by?
posterior border of IJV
155
what do the upper jugular (2) nodes drain?
```
nasal cavity
nasopharynx
oropharynx
larynx
hypopharynx
parotid gland
secondary drainage for oral cavity
```
156
location of LN level 3 - mid jugular
from bottom of hyoid to bottom of cricoid cartilage
medial to SCM
lateral to scalene muscles
157
what do the mid jugular (3) nodes drain?
```
nasopharynx
oral cavity
oropharynx
larynx
hypopharynx
```
158
location of LN level 4 - lower jugular
from bottom of cricoid to 2cm above sternoclavicular joint
medial to SCM
lateral to scalene muscle
159
what do the lower jugular (4) nodes drain?
```
hypopharynx
larynx
thyroid
cervical oesophagus
distal drainage from higher cervical levels
```
160
location of LN level 5 a and b - posterior triangle
from hyoid to transverse cervical vessels
medial to tail of SCM
lateral to anterior border of trapezius
161
what do the posterior triangle (5) nodes drain?
nasopharynx
oropharynx
thyroid
posterior sack
162
location of LN level 6 - anterior compartment
from lower edge of hyoid to upper edge of sternal manubrium
| between SCMs
163
what is LN level 6 divided into a and b by?
lower margin of cricoid cartilage
164
what does LN level 6 drain?
```
lower face
tip of tongue
FOM
anterior neck
hypopharynx
thyroid
larynx
cervical oesophagus
```
165
location of LN level 7 - superior mediastinal
from superior edge of manubrium sterni to upper border of arch of aorta
between left CCA and right innominate artery
166
what do the superior mediastinal (7) nodes drain?
nasopharynx
soft palate
tonsillar fossa
posterior pharyngeal wall
167
Predominant lymph node levels for metastasis - buccal
1b
| 100%
168
Predominant lymph node levels for metastasis - gingival
1a/b
| 70%
169
Predominant lymph node levels for metastasis - retromolar
1b/2a
| 62-80%
170
Predominant lymph node levels for metastasis - maxillary
1b/2a
| 60-70%
171
Predominant lymph node levels for metastasis - soft palate
1/2a (55%)
| but also 25% contralateral involvement
172
Predominant lymph node levels for metastasis - tongue
```
2b 8%
1/2a 75%
4 6-8%
contralateral 6-12%
more posterior = higher chance to involve the upper jugular and contralateral nodal metastasis, due to higher lymphatic interconnections posteriorly towards base of tongue
```
173
Predominant lymph node levels for metastasis - FOM
1/2a 75%
| contralateral 8-10%
174
in OSCC pts, when are level 4 (lower jugular) nodes only usually involved?
when other neck levels are positive for metastases
175
what feature of the primary tumour gives a greater risk of bilateral cervical node spread?
the closer to the midline the primary is
176
which areas does oropharyngeal cancer include?
```
base of tongue
inferior (anterior) surface of the soft palate and uvula
anterior and posterior tonsillar pillars
pharyngeal tonsils
lateral and posterior pharyngeal walls
```
177
staging for OPC non-HPV mediated (p16-)
same categories for oral and lip SCC
| - T, cN, pN, M, prognostic staging group
178
staging for HPV-mediated (p16+) OPC - T stages
```
T0
T1
T2
T3
T4
```
179
staging for HPV-mediated (p16+) OPC - T0
no primary identified (but identifiable neck node)
180
staging for HPV-mediated (p16+) OPC - T1
<=2cm
181
staging for HPV-mediated (p16+) OPC - T2
2
182
staging for HPV-mediated (p16+) OPC - T3
>4cm
OR
extension to lingual surface of epiglottis
183
staging for HPV-mediated (p16+) OPC - T4
moderately advanced local disease
(tumour invades the larynx, extrinsic tongue muscles, medial pterygoid, hard palate or mandible or beyond (mucosal extension to lingual surface of epiglottis from primary tumours of the base of the tongue and vallecula does not constitute invasion of the larynx))
184
staging for HPV-mediated (p16+) OPC - cN stages
```
cNX
cN0
cN1
cN2
cN3
```
185
staging for HPV-mediated (p16+) OPC - cNX
regional LNs cannot be assessed
186
staging for HPV-mediated (p16+) OPC - cN0
no regional LN metastasis
187
staging for HPV-mediated (p16+) OPC - cN1
>= 1 ipsilateral, less than or equal to 6cm
188
staging for HPV-mediated (p16+) OPC - cN2
contralateral or bilateral, less than or equal to 6cm
189
staging for HPV-mediated (p16+) OPC - cN2
LNs >6cm
190
staging for HPV-mediated (p16+) OPC - pN stages
pNX
pN0
pN1
pN2
191
staging for HPV-mediated (p16+) OPC - pNX
regional LNs cannot be assessed
192
staging for HPV-mediated (p16+) OPC - pN0
no regional LN metastasis
193
staging for HPV-mediated (p16+) OPC - pN1
less than or equal to 4 LNs
194
staging for HPV-mediated (p16+) OPC - pN2
>4 LNs
195
staging for HPV-mediated (p16+) OPC - M stages
cM0
cM1
pM1
196
staging for HPV-mediated (p16+) OPC - cM0
no distant metastasis
197
staging for HPV-mediated (p16+) OPC - cM1
distant metastasis
198
staging for HPV-mediated (p16+) OPC - pM1
distant metastasis, microscopically confirmed
199
staging for HPV-mediated (p16+) OPC - cTNM prognostic staging group 1
T0/1/2
N0/1
M0
200
staging for HPV-mediated (p16+) OPC - cTNM prognostic staging group 2
T0/1/2. N2. M0
or
T3. N0/1/2. M0
201
staging for HPV-mediated (p16+) OPC - cTNM prognostic staging group 3
any T. N3. M0
or
T4. N0/1/2/3. M0
202
staging for HPV-mediated (p16+) OPC - cTNM prognostic staging group 4
any T
any N
M1
203
staging for HPV-mediated (p16+) OPC - pTNM prognostic staging group 1
T0/1/2
N0/1
M0
204
staging for HPV-mediated (p16+) OPC - pTNM prognostic staging group 2
T0/1/2. N2. M0
or
T3/4. N0/1. M0
205
staging for HPV-mediated (p16+) OPC - pTNM prognostic staging group 3
T3/4
N2
M0
206
staging for HPV-mediated (p16+) OPC - pTNM prognostic staging group 4
any T
any N
M1
207
three aspects of multimodal approach to treatment
surgery
chemo
radio
208
OSCC stage 1 and 2 tx
surgery or radio
209
OSCC stage 3 and 4 tx
concomitant radio/chemo (+surgery) better outcomes than radio (+surgery)
210
what are definitive radio, concurrent CRT and sequential therapy usually limited to?
pts who are
- medically inoperable
- unresectable disease
- resectable disease where surgical resection cannot be accomplished with acceptable long-term functional consequences
211
what is the goal of surgery?
completely resect the primary tumour and any neck deposit, wherever achievable, to prevent recurrence and conserve high survival rate
212
why is surgery preferred over radio for stage 1/2?
reduced morbidity
213
stage 3/4 surgery
complete resection of primary tumour and neck nodes
214
why is it important to ensure negative resection margins?
increased risk of treatment failure in patients with positive surgical margins
215
how do you check for negative margins?
specimen examined and microscopic margins checked
216
give 3 examples of surgical techniques
open resection
transoral robotic surgery (TORS)
transoral laser microsurgery (TLM)
217
give 2 contraindications to open resection
T4b - invasion of the masticator space, pterygoid plates, skull base or carotid encasement
pt perception of QOL
218
what is the reason behind using minimally invasive surgery: TORS, TLM?
it mat provide improved functional outcomes with minimal surgical morbidity and enhance the pathologic staging
219
how does TORS work?
surgeon distant from patient controlling robotic unit
220
indications for minimally invasive surgery
T1-2 tumours of oropharynx but only if surgeon has good oral access
221
contraindications for minimally invasive surgery
retrognathia
class 2 malocclusion
limited cervical extension
SP tumour - higher rate of rhinolalia, velopharyngeal insufficiency and nasopharyngeal reflux
222
advantages of minimally invasive surgery
```
no external incision
no mandibulotomy or transmandibular access
decreased immediate post-op toxicity
shorter post-op hospitalisation time
faster fct recovery
enhanced visualisation - 3D+magnification of the field
elimination of physiologic tremors
movements can be scaled
fatigue reduction
training - teaching purposes
```
223
disadvantages of minimally invasive surgery
absence of tactile sensation - unable to feel tissue resistance or how tight a knot is
equipment size and weight
£££ - installation and annual maintenance
224
give the 4 types of neck dissection
comprehensive
selective
superselective
elective
225
comprehensive neck dissection
all LN levels of the neck are removed with/without 3 non-lymphatic structures (SCM, IJV, CN12)
226
selective neck dissection
not all LN levels are dissected
OSCC at least level 1-3
oropharyngeal SCC at least level 2-4
227
superselective neck dissection
dissection of only one or two contiguous LN levels to further decrease the morbidity of neck dissection
228
elective neck dissection
dissection of the appropriate nodal level, based on the risk of occult microscopic metastases
229
for OSCC what do you use to predict occult metastasis and guide neck dissection decision?
SLNB or DOI
230
what DOI is an accurate cut off value for performing an elective neck dissection in early stage OSCC?
DOI more than or equal to 4mm
231
what is a SLNB?
identifying and harvesting the initial node to which the primary tumour drains
high diagnostic accuracy
232
indications for a SLNB
to assess pts with biopsy-proven OSCC staged as early tumours with clinically (palpation) and radiologically (US, CT, MRI) N0 neck
assess bilateral N0 necks in primary tumours close to or crossing the midline
233
what can improve SLNB diagnostic sensitivity?
using immunohistochemistry
234
how does radiation therapy work?
uses high energy ionising radiation to disrupt the integrity of malignant cells through focal DNA damage, while doing as little harm as possible to normal cells
235
4 uses of radiation therapy
exclusive treatment of primary cancer
adjuvant therapy after surgery
adjuvant therapy before surgery
palliative therapy
236
radio - exclusive treatment of primary cancer
early stage cancer
| unresectable/advanced in combination with chemo
237
radio - adjuvant therapy after surgery
+/- chemo to control positive neck nodes and/or killing remaining cancer cells in + margins
238
radio - adjuvant therapy before surgery
+/- chemo to shrink size of tumour
239
radio - palliative therapy
to control symptoms of advanced OSCC e.g. pain, bleeding, dysphagia, and problems caused by bone metastases, and to give pt a better QOL
240
types of radiotherapy
external beam radiotherapy
| (internal) brachytherapy
241
how does EBRT work?
machine used to aim high energy rays/beams from outside the body into the tumour
focus the radiation on the exact location it needs to be, so normal tissues are affected as little as possible
242
normal treatment regime for EBRT
5 days a week for 6-7wks
243
2 examples of other EBRT schedules and their + and - s
hyperfractionation
accelerated fractionation
+may reduce the risk of cancer coming back in or near the place it started (local recurrence)
-tend to have more severe side effects
244
EBRT - hyperfractionation
total radiation dose in a larger number of doses e.g. 2 smaller doses per day
245
EBRT - accelerated fractionation
>or= 2 doses given each day so treatment completed faster
246
what is EBRT simulation technique for?
determine areas that will be radiated through a simulator
247
EBRT simulation technique procedure
supine on table, arms at sides, neck extended
immobilised by a thermoplastic head/shoulders mask to secure and gently hold head in place
head in neutral position
don't swallow during scanning
scan to identify target volumes
mark pt with tattoos in tx fields so they can be set up each day with precision, while allowing pt to wash without obscuring tx fields
248
name some types of EBRT
```
intensity modulated (IMRT)
3D conformal RT (3D-CRT)
image guided (IGRT)
volumetric modulated arc therapy (VMAT/Rapid arc)
intensity modulated proton therapy (IMPT)
stereotactic radio surgery (SRS)
stereotactic body RT (SBRT)
intraoperative RT (IORT)
```
249
what is IMRT?
high precision RT that uses computer controlled linear accelerators to deliver precise radiation doses to a malignant tumour or specific areas within the tumour
250
IMRT - what is the dose to target usually proportional to?
estimated tumour burden
251
advantages of IMRT
higher doses to be focused on the tumour
spares organs at risk (OAR)
(more individualised tx)
252
internal radiation therapy (brachytherapy)
hollow catheters placed into/around the tumour during surgery
left in place for several days while pt stays in hospital
radioactive materials are put into tubes for a short time each day
small radioactive pellets (rice) put right into tumour. give off low levels of radioactivity for several weeks and over time lose their strength
pellets just left in place and rarely cause any problems
253
when do short term RT side effects occur?
visible during/immediately after RT and may last for 2-3weeks after tx
254
short term RT side effects
```
oral mucositis
dental pain
taste loss
trismus (due to pain)
odynophagia
dysphagia
candidiasis
radiation dermatitis (RD)
ORN
```
255
when do long term RT side effects occur?
visible several weeks after RT and may last for long time or even permanently after tx
256
long term RT side effects
salivary gland hypofct
trismus (muscle fibrosis)
extensive dentition breakdown due to radiation caries (RC)
ORN (can develop over months or years after completion of RT)
257
what is ORN?
irradiated bone becomes devitalised and exposed through the overlying skin or mucosa without healing for 3m, without recurrences of tumour
258
why is the mandible more affected by ORN?
only supplied by inferior alveolar artery, whereas maxilla supplied by anterior, middle and posterior superior alveolar arteries
259
ORN staging classification
```
no universally used one
Marx
Epstein et al
Schwartz and Kagan
Notani et al
```
260
what % of ORN cases develop within the first 3 years after radiotherapy?
70-94%
261
risk factors for ORN
hyperfractionated irradiation regimen
high total dose (6000-7000cGy)
literature suggests chemo and radio increases incidence
pre-irradiation and post-irradiation dental extractions
poor OH and PDD
tobacco and alcohol use
262
ORN conservative tx
```
improve OH
antibiotics
minimal surgical debridement
hyperbaric 02 therapy
medical management: pentoxifylline, tocopherol
```
263
ORN surgical tx
sequestrectomy
saucerisation
segmental resection and free flap reconstruction
264
what is chemotherapy?
a drug tx to kill fast growing cancer cells that multiply much more quickly than most cells in the body
265
indications for chemotherapy
1. can use as the primary or sole tx for cancer
2. adjuvant therapy after surgery (+/- radio) to kill any residual cancer cells
3. adjuvant therapy before surgery (+/-radio) to shrink the size of the tumour
4. palliative therapy to relieve S+S of advanced OSCC and give pt a better QOL
266
which gender may benefit more from chemo in CST?
women
267
3 types of chemotherapy
adjuvant
induction
concomitant
268
adjuvant chemo
given after surgery for reducing the incidence of distant metastatic recurrence
269
induction chemo
given before definitive tx (radio/surgery)
| potentially reduce the risk of distant metastasis and the size of the primary tumour to improve loco regional control
270
concomitant chemo
given with surgery/radio to achieve radiosensitisation
271
give 2 indications for adjuvant chemotherapy
locally advanced disease HNSCC (stage 3-4b)
| recurrent or metastatic HNSCC (stage 4c)
272
adjuvant chemo for locally advanced stage 3-4b
platinum based chemo and radio
| - cisplatin, paclitaxel, 5-fluorouracil, carboplatin, cetuximab
273
adjuvant chemo for recurrent or metastatic stage 4c
cetuximab and platinum based chemo - cisplatin/carboplatin and 5-fluorouracil
or anti PD-1 immunotherapy plus chemo
- pembrolizumab and platinum and 5-fluorouracil
- nivolumab/pembrolizumab without chemo if pt has PD-LI+ recurrent or metastatic HNSCC
274
CRT
chemo given as a radiation sensitiser with the goal of reducing radiation resistance
275
chemo oral side effects
```
mucositis
infection
oral lichenoid reactions
hyperpigmentations
hyposalivation
altered taste
bleeding
MRONJ
SJS/TEN
```
276
treatment of early stage lip SCC
```
surgical resection
definitive radio if surgery not feasible/pt unfit for surgery
if deep (esp U lip) consider prophylactic selective neck dissection
```
277
post-surgical tx of early stage lip SCC
+ margins: reresection / radio
| primary tumour with perineural/lymphovascular invasion: radio adjuvant
278
treatment of locally advanced lip SCC
surgical resection
definitive concurrent radio and chemo if pt unfit for surgery or surgery not feasible
often need neck dissection
279
post-surgical tx of locally advanced lip SCC
+ margins: reresection and adjuvant radio/chemoradio
perineural/vascular/lymphatic invasion: adjuvant radio
ENE: adjuvant chemo radio
280
treatment of early stage oral cavity SCC
resection
definitive radio if surgery not feasible - consider conformed techniques and brachytherapy
neck dissection depends on site, extent and thickness
- SLNB for DOI >3mm and most stage 2 lesions
281
post-op adjuvant therapy for early and locally advanced stage oral cavity SCC
1+ LN - discuss radio
ENE - systemic therapy and radio
close or + margin - reresection/ (radio); tx with concurrent chemo radio
invasion - consider radio
282
treatment of locally advanced stage oral cavity SCC
resection
definitive concurrent radio and chemo radio if can't do surgery
ipsilateral/bilateral neck dissection
- if LNs involved, inc neck radio
283
treatment of early stage oropharyngeal SCC
clinical trials
definitive radio
surgical resection of primary tumour - minimally invasive techniques
consider elective nodal therapy
284
early stage and locally advanced oropharyngeal SCC post-op adjuvant therapy
CRT
| if positive margins reresection then radio
285
treatment of locally advanced stage oropharyngeal SCC
concurrent CRT
resection (but usually reserved for smaller primary tumours)
radio for neck +/- dissection
286
risk factors for oral cancer
predisposing factors
genetic susceptibility
OPMDs
oral microbiome
287
predisposing factors for oral cancer
social - alcohol and tobacco (smoked and smokeless)
diet - low fruit and veg
physical agents - UV light, radiation
chemicals - env and occupational exposures (arsenic, benzene, asbestos)
288
what effect do combined predisposing factors have?
synergistic effect
289
give a way in which alcohol causes cancer
ethanol---ADH--->acetaldehyde---ALDH--->acetate(energy)
if too much alcohol drunk, body can't process it fast enough so get build up of acetaldehyde - toxic and causes DNA damage
290
what infection in men may high alcohol lead to an increased risk of?
prevalent HPV infections
291
which foods may decrease the risk of oral cancer?
fruit and veg
| fish and omega 3 fatty acids
292
which foods may increase the risk of oral cancer?
high consumption of processed meat
293
is there a significant association between total/red/white meat and risk of oral cancer?
no
294
do dietary supplements have the same effect on risk reduction of cancer as foods?
no
295
oral hygiene as a risk factor for oral cancer
may also be a prognostic factor
aids the carcinogenic potential of other known carcinogens e.g. tobacco and alcohol
- increases carcinogenicity of known carcinogens
296
oral microbiome as a risk factor for oral cancer
candida associated with increased risk
| HPV
297
HPV manifestations
benign anogenital and cutaneous warts
respiratory papillomatosis
oral lesions
298
oral HPV manifestations
verruca - verruca vulgaris or common wart
condyloma - condyloma acuminatum
papilloma
not OPMDs
299
HPV genome structure - what 2 regions is it divided into?
E - early
| L - late
300
HPV genome structure - E region
45% of viral genome
encodes the proteins that are produced initially
E1,2,4,5,6,7 open reading frames
301
HPV genome structure - L region
40% of viral genome
encodes the proteins that are produced after synthesis of the proteins of the E region
L1,2 open reading frames
302
HPV genome structure - non-coding/designated long control (LCR) / upstream regulatory (URR) region
15% of viral genome
| involved in the control of viral gene expression
303
HPV genome structure - role of E proteins
destructs/inactivates TS protein
viral DNA replication
assembly and release of the viral particle
interaction with the epidermal GF
304
HPV genome structure - role of the L proteins
capsid protein in the viral particle
305
3 roles of the GDP in oral cancer
primary prevention
secondary prevention
overall health care of OSCC pt
306
primary prevention
educate pts about oral cancer and its risk factors
307
secondary prevention
early detection of OPMDs and OSCC - oral cancer screening
| referral if suspicious
308
GDP role in overall healthcare of OSCC pt
1 - pre-tx phase: be involved, be present at tumour board, make accurate and appropriate recommendations
2 - post-tx phase: help in alleviating pain and discomfort due to tx
3 - long-term followup: advise pt in maintaining good OH and attending regular dental visits
309
high risk HPV
16 and 18
310
how long does high risk HPV infection typically last?
12-18 months before eventually being cleared by immune system
311
when can dysplasia from HPV16 or 18 arise?
when the host immune system fails to clear and it persists for a long time
312
describe the oncogenic HPV function pathway if the immune system fails to clear it
viral E2 protein (a negative regulator of E6+7) function gets abrogated
over expression of main viral oncoprotein E6+7
subsequent inhibition of the TSPs p53 and pRb (retinoblastoma protein) pathways
leads to inhibition of interferon response, activation of telomerase, promotion of cell divisions, immortalisation and transformation
causes genetic instability with unregulated cell replication and accumulation of aberrant chromosomal mutations, which cause dysplasia of varying degrees
313
why can't early diagnosis of HPV-related OSCC be accurately established?
because clinical lesions of early HPV-related lesions are unknown
314
what does HPV+ OSCC have a significant association with?
history of suspicious Pap results of the cervix in females
315
what risk do unvaccinated pts for HPV have of developing OPC?
x19 risk
316
why is there a genetic susceptibility to cancer?
because carcinogenesis is a multistep process at both the phenotypic and genetic levels, resulting from the accumulation of multiple mutations
317
acquired (env) DNA damaging agents
chemicals
radiation
viruses
318
2 types of inherited mutations
genes affecting DNA repair
| genes affecting cell growth or apoptosis
319
why do you get mutations in genome of somatic cells?
failure of DNA repair and inherited mutations
320
3 effects of mutations in genome of somatic cells
activation of growth-promoting oncogenes
inactivation of TSGs
alterations in genes that regulate apoptosis
leads to
unregulated cell proliferation and decreased apoptosis
which leads to clonal expansion
321
from clonal expansion what contributes to tumour progression?
angiogenesis
escape from immunity
additional mutations
322
what 3 factors combine to to ensure a proper env for malignant development?
genetic events
risk factors
epigenetic mechanisms
323
what are epigenetic events?
"heritable phenotype changes that do not involve alterations in the DNA sequence"
324
give 3 examples of epigenetic events
DNA methylation
histone modifications
miRNAs
