CA.ORAL CAVITY FINAL.pdf

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About This Presentation

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Slide Content

CARCINOMA OF ORAL CAVITY AND
ITS MANAGEMENT
PRESENTER: DR. GOKULA KRISHNAN
MODERATOR: DR. BUDHI SINGH, ADDITIONAL PROFESSOR.

Synopsis
▪Incidence and epidemiology
▪Etiology & Premalignant
▪Anatomy
▪Molecular biology
▪Distribution
▪Patterns of spread
▪Clinical presentation
▪Diagnosis
▪Histology
▪Staging
▪Prognostics and predictive
factor
▪General management of SCC+
minor salaivarygland carcinoma.
▪Radical Management
oSurgical treatment
oRadiation treatment
oSystemic Chemotherapy
oMolecular therapy
oImmunotherapy
▪Toxicities
▪Surveillance
▪Management of recurrence
▪Palliative treatment
▪Conclusion

Incidence
Worldwide: (GLOBOCAN 2020)
•Global estimates suggest 3,77,713 (2%)new cases
and 1,77,757 (1.8%) deaths in 2020.
India:
•Lip and oral cavity cancers are the second most
common cancer in India, accounts for 1,35,929
(10.3%) new cases and 75,290 (8.8%) deaths in
both sexes, all ages.
•It is the most common cancer in indianmales
which accounts for 1,04,661 new cases (16.2%).
•In India, 20 per 100000 population are affected
by oral cancer.
GLOBOCAN 2020
BOTH SEXES
MALES

•Age of 50 to 70 years
•The commonest age is the fifth decade of life
•Incidence of oral cancer increases by age
•Incidence rate is 4 times as higher in males (16.2%) compared to females
(4.6%).
•Mostly it is diagnosed at later stages which result in low treatment outcomes.
•CANCER registration is not strictly followed in India, so the true incidence and
mortality may be higher, as many cases are unrecorded and loses follow up.
India
NCRP data

Epidemiology
Worldwide:
•Highest in Malanesia, South central
Asia and eastern Europe.
•Lowest in western Africa and
Eastern asia.
India:
•States like Uttar Pradesh, Jharkhand and Bihar in India witness more risk of
oral cancer.
MOST COMMON: CA.TONGUE f/b BUCCAL MUCOSA AND CHEEK (UP)
GLOBOCAN 2020

4.Etiology
Risk
factor
Non-modifiable:
1.Age
2.Ethinicity
3.Genetic syndromes
Modifiable:
1.Smoking (5-25 fold)
2.Alcohol+smoking (synergistic
effects)
3.Betal quid and gutka
4.Lifestyle/Diet
5.Poor Oral hygeine
6.Poor Dentition (sharp tooth)
7.Nuritional deficiencies
8.Infections
9.Low SE status
Emerging :
1.HPV
2.Immunosuppression
UV rays -carcinoma of the lip

5.Premalignant condition
Lesions Malignantrisk
Leukoplakia Homogeneous(1-18%)
Nonhomogeneous(>18%)
Erythroplakia 9%-Mildto moderate dysplasia
40%-CIN
51%-invasivecancer
Oral sub-mucosal
fibrosis
25%-Dysplasia
Carcinoma in situ

Anatomy
▪The oral cavity consists of,
1.Lips
2.Oral tongue
3.Floor of the mouth
4.Buccalmucosa
5.Alveolar ridge
6.Retromolartrigone
7.Hard palate.
Boundaries:
•Anterior: Skin–vermilion junction
•Superior: Junction between the hard and soft palate
•Inferior portion: Line of Circumvallatepapillae.

1.Lips
Extension :
The lips begin at the junction of the
vermilion border with the skin and
includes only the vermilion surface or that
portion of the lip that comes in contact
with the opposed lip.
Lymphatic drainage:
Upper lip:
•Preauricular, Periparotid, Ia, Ib
Lower lip:
•Medial part: Ia
•Lateral part: Ib

2.Oral tongue
Extension :
Anteriorlyfrom the circumvallatepapillae
to the undersurfaceof the tongue at the
junction of the floor of the mouth.
Lymphatic drainage:
•Tip: Ia
•Lateral: Ib, II
•Post portion: II
•Midline: Bilateral
•Sometimes directly to level-IV (skip mets)

3.Floor of mouth
Extension :
•Lower alveolar ridge to the undersurface
of the tongue.
•It overlies the mylohyoidand hyoglossus
muscles.
•Posterior boundary : base of the anterior
tonsillarpillar.
•Divided into right and left by the frenulum
and its contains the ostiaof the
submandibularand sublingual salivary
glands
Lymphatic drainage:
•Superficial mucosal system-crosses
midline and drains both I/L and C/L level
Ib
•Deep mucosal system-Ib, II.

4.Buccal mucosa
Extension :
•All mucous membrane lining the inner
surfaces of the cheek and lips from the
line of contact of the opposing lips
•Superiorly: Line of attachment of the
mucosa of the upper and lower
alveolar ridge.
•Posteriorly: Pterygomandibularraphe.
Lymphatic drainage:
•Periparotidlymphnodes
•Ia
•Ib

5.Alveolar ridge
Alveolar processes of the maxilla and
mandible and the overlying mucosa.
Lower alveolar ridge:
•Line of attachment of mucosa in the lower
GBS to the line of free mucosa of the floor
of the mouth.
•Posteriorly: Ascending ramusof the
mandible
Upper alveolar ridge:
•Line of attachment of mucosa in the
upper GBS to the junction of the hard
palate.
•Posteriorly: Upper end of the
pterygopalatinearch.
Lymphatic drainage:
•Ia, Ib, II
•Sometimes retropharyngeal LN.

6.Retromolar trigone
Extend:
•Triangular area overlying the ascending
ramusof the mandible.
•Base: Posterior most molar
•Apex: Maxillary tuberosity.
•Lymphatic drainage:
•II, Periparotidand Retropharyngeal LN.
7.Hardpalate
Extend:
•Inner surface of the superior alveolar
ridge to the posterior edge of the palatine
bone.
•Lymphatic drainage:
•Ib, II and Retropharyngeal LN.

Lymph node stations
Level Ia

Molecular biology
Phillip J.Hsuet al.

Distribution
Lips: lower-93%, upper-5%, Commissure-2%
•Tongue35%
•Floor of mouth30%
•Lower alveolus15%
10% •Buccalmucosa
8% •Upper alveolus/hard palate
•RMT2%

Patterns of spread
1.Local spread
2.Lymphatic spread:
•Most commonly involved lymph node stations: Levels I to IV.
•Level-II are most frequently involved.(Lindberg et al.)
•The retrostyloidspace is potentially at risk for involvement by metastatic disease when
upper level II nodes are grossly positive.
•The medial retropharyngeal nodes –rare
•The lateral retropharyngeal nodes are rarely involved in oral cavity cancer unless there is
oropharyngealinvolvement or a significant nodal burden.
Submental
(Ia)
Submandibular
(Ib)
Upper
Jugular (II)
Midjugular
(III)
Oral
tongue
9% 18% 73% 18%
FOM 7% 64% 43% 0
RMT 0 25% 63% 12.5%

Primary site(%)
Mobile
tongue
15.4
Lower gum25
Buccal
mucosa
0
Upper gum0
Floor of the
mouth
0
Number of ipsilateral
metastatic lymph nodes
(%)
None 0
Simple 26%
Multiple 50%
Level of ipsilateral
metastatic lymph nodes
%
No metastasis 0
Levels I–III 35
Level IV 75
Grade %
WD 7
MD 24
PD 33%

Patterns of spread
3.Distant metastasis: 15-20%
▪The risk is increases with the degree of lymph node involvement.
▪Patients with recurrent disease are also at higher risk for distant metastases.
▪Patients without clinically appreciable neck disease rarely fail distantly after
treatment.
Sites Percentages
Lungs 66%
Bones 22%
Liver 9.5%
Serve as a site for distant metastasis from
another anatomic primary tumour site.
Rare

1.Carcinoma lip:
▪M/C: lower lip
▪Non-healing ulcer with pain.
▪Anesthesiaof the lower lip and teeth may indicate involvement of
the mandibularcanal and inferior alveolar nerve.
2.Carcinoma oral tongue:
▪M/C: Lateral borders of the tongue
▪Usually presents as small ulcers and gradually invade the
musculature of the tongue.
▪Advanced lesions may be either ulcerative or exophytic.
▪Sometimes painful at early stages.
▪Cervical metastases occur early (30% to 40%) of patients
harbouring cervical lymph node metastases at diagnosis.
Clinical presentation

3.Carcinoma FOM:
▪M/C: Frenulum
▪Often infiltrative and may invade bone, the muscles of the
floor of the mouth, and the tongue.
▪Clinical fixation of the tumour to the mandible suggests
periostealinvolvement, which may occur early.
4.Carcinoma BM:
•M/C: Adjacent to the lower molars along the occlusalline
of the teeth.
•Rarely symptomatic early in its course.
•May be papillary or erosive and located near the dental
occlusalline
•Often associated with leukoplakia

5.Carcinoma Alveolus:
▪M/C: Edentulous areas or along the free margin of the
mandibularalveolus.
▪May present with pain while chewing, loose teeth, or ill-fitting
dentures in edentulous patients.
6.Carcinoma RMT :
•May present as exophyticgrowth pattern and limited
involvement of underlying bone or
•Infiltrate cortical bone and spread along regional tissue planes
to involve the pterygoidcomplex and parapharyngealspace.
•Produce trismusearly in the clinical course.
7.Carcinoma hard palate:
•Often painless.
•Irregularity in the mucosa or ill-fitting dentures.
•Non-healing ulcers of the hard palate, intermittent bleeding,
and pain

Diagnosis
History
Physical examination (visual and digital examination)
Routine blood investigation (CBC, RFT, LFT, Sr.Electrolytes)
Biopsy of the lesion and FNAC of lymph node/ Slide review
Endoscopy
Orthopantogram
X-ray chest PA view
USG neck
CECT BOS to T4
MRI Head and neck
PET-CT
HPVtesting

Physical examination
Inspection:
▪Entire oral cavity and teeth.
▪Neck
Palpation:
▪Help to bony involvement, tongue fixation, and
depth of involvement.
▪Bimanual palpation: the depth of tumour
invasion into musculature of the tongue and floor
of the mouth.
▪Neck node palpation
Core needle Biopsy of the lesion and FNAC of
lymph-node

Endoscopy
▪Routine indirect laryngoscopyexamination should be done.
▪Panendoscopyis also considered by many head and neck oncologists as
the optimal screening procedure in smokers.
▪Because the rates of synchronous and metachronoussecond primaries are
ranging from 8% to 21% in various literatures which was explained by the
‘‘field cancerization’’ hypothesis[Slaughter et al}.

X-rays
OPG:
▪Assessment of bone involvement
Chest x-ray PA view:
▪Exclude lung metastases
▪Second primary cancer.
Bony invasionSensitivitySpecificity PPV NPV
OPG
(Thashika
Kushrajet al.)
75% 100% 100%76%
CT 75% 100% 100%78%
SPECT 100% 14.3% 57% 100%
ThashikaKushrajet al.

USG
•Chaukaret al. reported that ultrasonographyis insufficient as a stand-alone
method for evaluating cervical lymph nodes (sensitivity 79%, specificity 69%)
•If USG combined with fine-needle aspiration may be superior to CT or MRI
for staging the neck in experience hands. [Van den Brekelet al.]
To evaluate:
1.Superficial lesions
2.Metastatic lymph nodes
3.Guide needle aspiration biopsies
(NAB).
4.To assess the lymph nodes following a
radical surgical resection with or
without adjuvant radiation therapy.

CT scan
1.Most commonly used modality to determine the,
1.Extent of soft tissue
2.Bony involvement
3.Occult disease in the neck
2.CT may be used to determine the extent of invasion into the deep musculature of the
tongue and adjacent structures.
Disadvantage:
▪CT cannot differentiate between recurrence, surgical scars and adverse reactions after
radiation therapy.
A Review of Literature by Paulina palaszet al.
Sensitivity Specificity
Tumourdetection 41-82% 82-100%
Bonyinvasion 63-80% 81-100%
Exclusionof LN mets 74% 85%
Cervical nodal mets 40-68% 75-82%
Recurrence 50% 80%

Supreetaaryaet al. TMH
Ca.tongue(T2)Ca.lip (T4a)
N3B (ENE+)
Masticarspace inv (T4b)Ca.BM (Masseterinv)
Ca.RMT (Mandible inv) N2CCa.UpperGBS

MRI
To determine the involvement of,
•Local soft tissues
•Bone marrow and bones (sensitivity 82%, specificity 66.7%)
•Vessels
•Nerves (PNI)
•To useful in Contrast allergy and significant dental artifact.
Ca.Tongue Ca.Tongue(myelohyoidinv) PNI-inferior alveolar nerve

PET-CT
▪To evaluate,
oPerineuralinvolvement
oSkull base involvement
oDistant metastases
•Clinical application of PET/CT is limited by the suboptimal detection of small
metastases.
▪The overall sensitivity and specificity of PET is superior to CT/MRI for evaluating
persistent or recurrent disease, particularly in patients who have received previous
radiotherapy.
•PET scan not be performed until 8 to 12 weeks post treatment to minimize the risk
of both FN and FP interpretations.
Sensitivity
[Liao et al]
Specificity PPV
[Maddipatlaetal]
NPV
Nodal
mets
77% 58% 83% 97%

Histology (AJCC 8
th
)
SCC-Most common-90%
oConventional SCC-WD/MD/PD
oAcantholyticSCC
oAdenosquamousSCC
oBasoloidSCC
oCarcinoma cuniculatum
oPapillary SCC
oSpindle cell SCC
oVerrucousSCC
oLymphoepithelialSCC
Adenocarcinoma< 10%:(minor
salaivaryglands)
oAciniccell ca
oMucoepidermoidcarcinoma
oAdenoidcysticcarcinoma-30 to
40%
oPolymorphousadenoca
oBasalcell carcinoma
oEpithelialmyoepithelialcarcinoma
oClearcell carcinoma
oMucinousadenocarcinoma
oOncocyticcarcinoma
oSalaivaryduct carcinoma
oMyoepithelialcarcinoma.
Others:
oMucosal melanoma-0.2 to 8%
oLymphoma-2%
oCarcinoma type cannot be
determined

AJCC 8
th
staging
Include only:
1.Squamouscell carcinoma
2.Minor salivary gland carcinoma
3.Neuro-endocrine carcinoma
Modifications: ( 7 to 8 thstaging):
▪T: The incorporation of DOI.
Extrinsic muscle invasion no longer used in T4.
▪N: The incorporation of ENE.
Essential features:
▪Includes-all of oral cavity plus mucosa of lip but not the external (dry) lip (dry
vermillion border).
▪DOI increases the T category by 1 for each 5 mm of tumour depth (until ≥ 10 mm)
▪Pathologic ENE+ will increase the nodal category by 1

▪It is not required for recurrent tumours or for metastatic tumours that are
resectedat a different time than the primary tumour.
▪Carcinomas of minor salivary glands are staged according to the
corresponding anatomic site of occurrence.
▪Reporting of surgical margins for carcinomas of the minor salivary glands
should follow those used for SCC of oral cavity.
Terminology:
▪TUMOUR THICKNESS
▪DEPTH OF INVASION
▪TUMOR BED VERSUS SPECIMEN MARGINS
▪ENE
▪WORST PATTERN OF INVASION 5

AJCC 8
th
staging
TX:Primary tumorcannot be assessed
Tis:Carcinoma in situ
T1:Tumor≤ 2 cm with depth of invasion (DOI)* ≤ 5 mm
T2:Tumor≤ 2 cm with DOI* > 5 mm and ≤ 10 mm or
Tumor> 2 cm and ≤ 4 cm with DOI* ≤ 10 mm
T3:Tumor> 4 cm or any tumorwith DOI* > 10 mm but ≤ 20 mm.
T4a:Moderately advanced disease:
ORALCAVITY: Tumorwith DOI* > 20 mm or
Tumorinvades adjacent structures only (e.g. through cortical bone of the mandible or maxilla or involves
the maxillary sinus or skin of the face).
LIP: Tumourinvades through cortical bone or involves inferior alveolar nerve , FOM or skin of face (Chin or
nose).
T4b:Very advanced disease:
Tumorinvades masticator space, pterygoidplates or skull base or encases the internal carotid artery
CLINICAL: (cN)
NX:Regional lymph nodes cannot be assessed
N0:No regional lymph node metastasis
N1:Single ipsilymph node, ≤ 3 cm sizeand (ENE)-.
N2a:Single ipsi. lymph node that is > 3 cm but ≤ 6 cm sizeand ENE-..
N2b:Multiple ipsil. lymph nodes, none > 6 cm sizeand ENE-.
N2c:Any bilateral or contralaterallymph node(s), none > 6 cm sizeand ENE-
N3a:Metastasis in a lymph node that is > 6 cm sizeand ENE-.
N3b:Metastasis in anynodes and clinically overt ENE(+).
PATHOLOGICAL: (pN)
N2a:Single ipsi. lymph node /contra-lateral lymph node that is ≤ 3 cm and ENE+ or
N3b:Metastasis in either
Single ipsilaterallymph node, > 3 cm and ENE+ or
Multiple ipsilateral, contralateralor bilateral lymph nodes, any with ENE+ or
Minor changes:29 December 2020, Kelly Magliocca, CAP

Staging
Distant metastasis:
•M0:No distant metastasis
•M1:Distant metastasis
T N M
Stage 0: Tis N0 M0
Stage I: T1 N0 M0
Stage II: T2 N0 M0
Stage III:T3 N0 M0
T1 -3 N1 M0
Stage IVA:T4a N0 -1 M0
T1 -4a N2 M0
Stage IVB:Any T N3 M0
T4b Any N M0
Stage IVC:Any T Any N M1

Management
▪Treatment decisions for all patients made in a multidisciplinary joint clinic with the
goal for maximizing survival and preservation of form and function.
▪Available treatment options are
•Choice of treatment modality, either singly or in combination, depends on the
stage and size of the tumuor, toxicity, performance status, comorbiddisease, and
patients convenience.
Surgical resection
Radiation
Combined modality treatment
±Molecular therapy

Treatment decision
Assess performance status and
stage of disease
Curative intent treatment
Palliative intent treatment
Supportive care
ST-IVB, IVC
Investigations
Pre-op work up
Pre RT work up
Referrals:
Dental prophylaxis
Speech therapy
Nutritional
Poor GC
Poor PS
Counseling and
symptomatic care
Advanced /
unresectable/
metastatic disease
Good GC
Good PS
Palliative treatment
Palliative RT
Palliative CT

Treatment outline
NCCN guideline

NCCN guideline

Surgical management
•Most commonly used treatment of choice for lesions of the oral cavity.
•Expeditious, effective, and associated with modest morbidity and good functional
outcome particularly for patients with small-to moderate-sized lesions.
•Goal:Tumour free resection margin and appropriate reconstruction for restoration of
form and function.
•Successful treatment relies on effective management of regional lymphaticsas well as
primary cancer

Assesment for resectability
Unresectable:
Primary disease:
▪Adequate surgical clearance is not achievable.
▪Extensive InfratemporalFossainvolvement
▪Extensive involvement of base skull.
▪Extensive induration/soft tissue disease till zygomaor hyoid.
Nodal Disease:
▪Clinically fixed nodes.
▪Infiltration of Internal /Common carotid artery.
▪Extensive infiltration of prevertebralmuscles, skull base.

Principles of resection
▪En bloc resection of primary tumour whenever feasible
▪In continuity neck dissection when direct extension of primary into neck
▪Third dimension (the base) should be taken carefully into account before excision.
•Adequate margin: 1.5 –2 cm (outcome of intra-operative positive margins followed by
immediate repeat resection revised to negative margins is associated with worse
survival compared to negative margins achieved with initial resection (31% vs. 49%,
respectively)[Scholl P et al.]
▪Clear margin: > 0.5 cm
•Close margin < 0.5 cm (LRC : Significantly improved with margins of 0.5 cm or greater vs
<0.5 cm (36% vs. 18%, respectively) [LoreeTR et al.]
▪Frozen section confirmation for margins may be done if the facility is available.
▪Contralateralneck should be addressed when the probability of bilateral / contralateral
metastases is high. Eg. Tumours crossing the midline / midline tumours.

Surgical management of primary
Trans-oral approach:
•Ca.Oraltongue/FOM/Buccalmucosa/Hard palate/Maxillary alveolar ridge.
Trans cervical: (lip-splitting incision/Visor flap with lingual release)
•ORAL TONGUE: Posterior extent /trismus/obstrucivedentition.
•Buccalmucosal resections.
Combined with mandibulectomy:
•Ca.RMT
•Marginal mandibulectomy: Small tumorswith periostealinvolvement.
•Segmental mandibulectomy: Pre-or intraoperativefindings of bone invasion,
tooth loss with low mandibularbone height, and bone that has previously been
irradiated.
TORS:
•Resectingmore posterior tumours without mandibulotomy.

Surgical management of neck
•High rate of cervical nodal metastasis associated with oral cavity cancers.
•Regional control and survival rates do not decrease with more selective
approaches if adjuvant therapies are used in high-risk patients. [Byers RM,
et al]
•There is a chance of 15.8% skip metastasis to level III or IV, without
involvement of levels I or II.[Byers RM],[Huang SH],[Shah JP et.al]
Neck node (CLINICAL/IMAGING) Neckdissection Levels
cN0 (20% probability of occult nodal disease)Elective neck dissection
(END)
SOHND(LEVEL-III)
Exception fororal
tongue (LEVEL I-IV)
cN+ Selective neck dissection
(SND)
Level I-IVor
Level I-V
1.cN3+
2.Disease extending into level V
3.Invading critical structures in the neck.
Radical and modified
neck dissection. (MRD)
LEVEL I-V

ELECTIVE NODAL DISSECTION vsDEPTH OF INVASION
•END is the standard of care.
•DOI is the best predictor for regional metastasis in the cN0 neck.
Sites Cut off Chance of occult metastasis
Oral tongue ≥ 4 mm 41.9% [SparanoA, et al]
FOM >1.5 mm 33% [Mohit-TabatabaiMA et.al]
Buccalcarcinomas,
Maxillary alveolar ridge
Hard palate
Depth has not been
extensively studied
9% (T4) [Huang SF, et al]

ELECTIVE NODAL DISSECTION VS OBSERVATION
▪70% of END are found to have pN0 at pathologic review and neck
dissection also morbid and costly.
Trail Comparison Results
Anil K. D’Cruz
(TMH)
END vsobservation
with TND (n-500)
(END vsobs):
3 yrOS: 80% vs60.5% (pN+)
Recurrence: 81 vs146
Deaths: 40 vs149
DFS: 69.5% vs45.9%
Adverse events: 6.6% vs3.3%
DOI: >3 mm predictor of regional metastasis
Anthony Po-Wing
Yuen etal.
END vsobservation(n-35) Recurrence: 6% vs37%
Node-related mortality: 22% VS 10%
ELECTIVE NODAL DISSECTION vsSLNB
▪A meta-analysis showed a pooled NPV of 96% in early-stage oral cavity tumors, with no
difference in regional recurrence between SLNB and END (6.7% vs6%). [no level I
evidence]

Carcinoma Oral cavity–RT±CT Indications
▪Adjuvant treatment-CMT
PORT alone indication:
oT1-T2N0 tumourswith adverse pathological features
oOne positive node without adverse features
PORT alone or consider CRT:
opT3 tumourswith adverse pathological features
opT4a disease
o≥2 Node positive
oLevel IV/V involved
oLVI
oPNI
oMandibularbone involvement
High risk features: CRT
oPositive margin: Re-resection /Chemoradiation
oENE+
▪Definitive treatment-Radical RT alone/CRT
▪Palliative treatment

Surgery+PORTvsRT alone
Trail stages Results
Robertson et al
Interim analysis
T2–T4/N0–N2(N-350)Surgery+PORTvsRT alone
2 yr LCR: 60%vs45%
Deaths: 2 VS 12
Survival:Extreme P-value of less than
0.001
MD Anderson Cancer Center[Phase III study] showed treatment
delay >6 weeks result decrease LRC.
Ideal time for PORT: within 4 to 6 weeks after completion of
surgery

▪N-521 pts, cN0
▪27.4 per cent of the patients the neck was
partially irradiated in conjunction with
treatment to the primary lesion.
▪In 26 per cent of the group nodal disease
subsequently developed.
▪Complete elective treatment of neck is
not advocated. Irradiation of tile proximal
lymphaticsis useful.

RT techniques
Conventional
•EBRT:
•Manual marking
•2D-Simulator based
•DRR based
Conformal
•EBRT:
•3DCRT
•IMRT
•Proton therapy
•Electron therapy
•Brachytherapy

Manual marking
Marking:
▪Patient is in supine position with extended neck and retracted shoulder.
▪Use head rest
▪B/L PARRALLEL OPPOSED
Subsites: [Ca.Lip/Oral tongue/FOM/Alveolus/Hard palate/ BM and RM(crossing midline)]
▪Superior: Upper border of zygomaticarch
▪Inferior: Early stage: Hyoid bone, Advanced stage: Inner border of clavicle
▪Anterior: 1 cm flash
▪Posterior: Tip of mastoid process (INTIAL PHASE), corresponding to ear lobule (CORD
OFF)
▪Energy: C0-60 /6-MV
Dose
prescription
Total dosePh-1 Ph-2 (Cordoff) Ph-3 (Boost)
Radical RT66Gy-70 Gy40Gy/20#/4
weeks
20Gy/10#/2 weeks6Gy Boost
PORT 60Gy 40Gy/20#/4
weeks
20Gy/10#/2 weeksIf Residual disease/high risk
feature: 6Gy Boost

Manual marking
Marking:
▪Patient is in supine position with extended neck and retracted shoulder.
▪Use head rest
▪ANTERO-LATERAL WEDGE PAIR
Subsites: [BM and RM(Well lateralized lesion)]
Anterior field:
▪Superior: Upper border of zygomaticarch
▪Inferior: Early stage: Hyoid bone, Advanced stage: Inner border of clavicle
▪Medial: Midline
▪Lateral: 1 cm flash
Lateral field:
▪Superior and inferior border same
▪Anterior: 1 cm flash
▪Posterior : Tip of mastoid (INTIAL)
Ear lobule (CORD OFF)
▪Energy: C0-60 /6-MV
Dose
prescription
Total dosePh-1 Ph-2 (Cord
off)
Ph-3 (Boost)
Radical RT66Gy 40Gy/20#/4
weeks
20Gy/10#/2
weeks
6Gy Boost
PORT 60Gy 40Gy/20#/4
weeks
20Gy/10#/2
weeks
If Residual
disease/high
risk feature:
6Gy Boost

2D-Simulation
▪Supine position with the neck extended and retracted shoulder.
▪A thermoplastic mask is used to immobilize patients during simulation and treatment.
▪Shoulder immobilization by using either a three-/four-point Aquaplastmask.
▪A bite block should be used to depress the tongue away from the hard palate
(Oral tongue and FOM lesions)
▪Some institutions use a cork and tongue blade or a custom intraoral stent for this purpose
▪For patients with a short neck, Retractors are used to depress the shoulders.
▪Post op scar/palpable lymph node marked with wire.

Conventional field borders
▪The Superior border: 1.5-to 2.0-cm above the border on the
tumorbed.
▪The inferior border: Thyroid notch, just above the true vocal
cords.
▪The posterior border:
1.Early stage disease (N0) -Mid-vertebral body level (ENI:I, II,
and III).
2.Advanced neck disease (N+) or positive level V lymph nodes-
Behind the C1 vertebral body spinousprocess (cover L-V)
▪Two lateral parallel–opposed fields are used.
▪The portals are then reduced at approximately 40 Gyto spare
high dose to the spinal cord.
▪If patients harborcervical lymph node metastases, or
high-risk disease, then the lower neck will also be
treated.

▪In this case, half-beam–blocked AP or opposed AP/PA fields are used
▪The superior border: Matched to the inferior border of the opposed lateral fields
at the level of the thyroid notch.
▪The inferior border: Inner border of clavicle
▪Anteriorly:Larynx block was used to protects the central larynx and spinal cord
overdose because of three-field overlap.
Low anterior neck

Dose and Fractionation
PORT:
▪Dose fractionation is 1.8 to 2.0 Gy/day.
▪Primary tumour with involved Lymph-node: 60 Gy/30#/ 6wks in 2 phases with
CORD OFF.
▪High risk (Close or positive microscopic margins or ENE)
–SIB to 66 Gy(e.g., 2.2 Gyper fraction over 30 fractions) or
–Sequential 6.0 Gylocalized boost
▪Gross residual disease, either further surgical resection or
focal boosting up to 70 Gy.
▪Low risk: (Clinically or pathologically uninvolved necks): 54 to 56 Gy
Radical RT alone:
▪66-70Gy/33-35#/ 6-7 wks in 2 phases with CORD OFF.
.

Electron Boost
▪Indications:
–Any residual lymph node after initial phase of radiotherapy in posterior
triangle.
▪Target volume is residual node + 1cm margin all around.
▪Electron field was matched with photon field.
▪An electron energy of 9 to 12 MeVis usually used depending upon the depth of
node from skin.
▪DOSE: 20Gy-26/10#-13#/2-2weeks

3DCRT
Steps:
1.Immobilization and positioning
2.CT simulation
3.Delineate target volumes and OARs (CONTOURING)
4.Planning
5.Dose prescription
6.Treatment

Immobilization and positioning
▪Patient has to be lie down in supine position with arms by side.
▪The shoulder has to be retract adequately.
▪3 or 5-clamp thermoplaticcast (orfitcast) to be used for immobilization of
head and neck.

CT Simulation
▪Patient has to be lie down in same position in CT simulator couch.
▪Intravenous contrast (inj. Omnipaque) should be utilized in patients with adequate
renal function to facilitates target volume delineation (LN).
•For oral tongue cancers, a bite block can be used during simulation and throughout
the course of treatment to elevate the hard palate and decrease dose to the superior
oral cavity.
•For cases in which the hard palate is target, a bite block can be employed to limit dose
to the tongue and inferior oral cavity.
▪CT scan from top of skull to carina with slice thickness of ≤3 mm.
▪After the CT scan , images was transferred to Treatment planning system and the
target has to delineate.
▪If available, MRI or PET scans obtained at the time of simulation can often be helpful
in defining target volumes.

IMRT
Target
volumes
Definition and description
CTV 66Primary: preoperative tumour volume can guide the targeting of CTV66.
Regions of soft tissue invasion, bone invasion, or microscopically
positive margins should be included in this volume
Neck nodes: regions of extracapsularextension
CTV 60Primary: preoperative gross disease and the entire operative bed
Neck nodes: preoperative gross disease and adjacent ipsilateralor
contralateralnodal regions at high risk for subclinical disease
CTV 54Ipsilateraland/or contralateraluninvolved nodal levels at low risk for
subclinical disease
1.Immobilization and positioning and
CT simulation same
2.Target volume delineation-PORT

Site-specific guidelines for clinical target delineation of oral
cavity cancers
Tumour site Stage Clinical treatment volume (CTV)
▪Oral tongue
▪Floor of the
mouth
T1–T4,N0▪Include the tumour bed, the entire oral tongue and
the base of the tongue.
▪For floor of the mouth lesions, consider including the
alveolar ridge, due to its proximity to the floor of the
mouth.
▪Both sides of the neck should be treated with
radiotherapy (even for well-lateralized T1–T2N0
lesions, if the depth of invasion is >4 mm), although
physician discretion can be used to determine if these
should be in the low-or high-risk CTV.
▪Consider ipsilateraland/or contralaterallevels I–IV
T1–T4,N1–3▪Sameas above
▪Consider ipsilateraland/or contralaterallevels I–V
Textbook of Nancy Y lee

1.Squamous cell carcinoma of the oral tongue, pathologic stage T2N1, status
post partial glossectomyand left neck dissection, with one positive lymph
node and multiple close margins
Textbook of Nancy Y lee

2.Squamous cell carcinoma of the floor of the mouth, pathologic stage
T2N2b, status post resection and right modified radical neck dissection
Textbook of Nancy Y lee

Site-specific guidelines for clinical target delineation of oral
cavity cancers
Tumour siteStage Clinical treatment volume (CTV)
Buccal
mucosa
T1–T4N0 ▪It is important to be generous with target volumes when
treating the inner cheek.
▪Include the tumorbed and the entire buccalmucosa.
▪Posteriorly, this should extend to retromolartrigone.
▪Superiorly, this should extend to near the inferior orbital rim
▪If the tumoris well lateralized, ipsilaterallevels I-IV alone can
be treated.
▪Otherwise, consider treating bilateral cervical lymph nodes
T1–T4N1–3Sameas above
Ipsilaterallevels I-IV should be treated within the neck.
Depending on pathologic findings and discussions with the
surgeon, consideration can be given to treating the
contralateralneck as well.
Textbook of Nancy Y lee

Squamouscell carcinoma of the buccalmucosa, pathologic stage
T4aN0 with minimal cortical bone invasion
Textbook of Nancy Y lee

Site-specific guidelines for clinical target delineation of oral
cavity cancers
Tumour siteStage Clinical treatment volume (CTV)
▪Retromolar
trigone
▪Hard palate
▪Gingiva
T1–T4N0 Include the preoperative tumorvolume and postoperative
tumorbed.
Consider covering ipsilaterallevels I–IV for all cases.
Treatment of the contralateralneck is at
the physician’s discretion.
T1–T4N1–3Sameas above
Treat the ipsilaterallevels I–IV for all cases and consider
treatment of the contralateralneck.
Textbook of Nancy Y lee

Adenoid cystic carcinoma of the right hard palate, pathologic stage T2N0. the
patient is status post bilateral partial maxillectomy, with extensive perineural
invasion and positive margins
Textbook of Nancy Y lee

SIB IMRT
T4N3bM0 squamouscell carcinoma of the floor of the mouth with
evidence of ENE

Target volume delineation-Radical treatment
Target
volumes
Definition and description
GTV 70 Primary: all gross disease on physical examination and imaging
Neck nodes: all gross disease and physical examination and imaging
CTV 70 Same as GTV 70 , although a 5 mm margin can be added if uncertainty
exists regarding the extent of gross disease
CTV 59.4Primary: encompass the entire CTV 70 with an additional margin of up
to 10 mm
Neck nodes: nodal levels with pathologic involvement and adjacent
ipsilateralor contralateralnodal regions at high risk for subclinical
disease
CTV 54 Ipsilateraland/or contralateraluninvolved nodal levels at low risk for
subclinical disease
Textbook of Nancy Y lee

Locally advanced squamouscell carcinoma of the floor of the mouth, clinical
stage T2N2c, who is not a surgical candidate
Textbook of Nancy Y lee

Dose prescription-PORT
▪The high-risk CTV (CTV66) :
•Receives 66Gy either as a SIB (2.2 Gyper fraction over 30 fractions) or
•as a sequential boost.
▪The intermediate-risk CTV (CTV60) :
•Receives 60 Gyin 2.0 Gyper fraction.
▪The low-risk CTV (CTV54–56):
•Receives 54 to 56 Gyas a simultaneous integrated boost in 1.8 to 1.87 Gyper
fraction.
Textbook of Nancy Y lee
Dose prescription-Definitive RT
PTV 70 : 70 Gy/33#/7 Weeks.
PTV 59.4: 59.4GY/33#/7 Weeks
PTV 54: 54GY/33#/7 Weeks

Critical structures QUANTEC CONSTRAINTS
Brainstem
Brain stem (+3 mm)
Max:<50Gy
Dose to 0.03 cc ≤ 52 Gyax< 50 Gy
Optic nerves Max < 54 Gy
Optic chiasm Max < 54 Gy
Spinal cord
Spinal cord (+5 mm)
Max < 45 Gyor 1 cc of the PTV cannot
exceed 50 Gy
Dose to 0.03 cc ≤ 48 Gy
Mandible Max < 70 Gyoutside high dose PTV, avoid
hot spots
Brachial plexus Max < 65 Gyoutside high dose PTV
Parotid gland a) Mean ≤26 Gyin one gland
(b) Or at least 20 cc of the combined volume
of both parotid glands will receive <20 Gy
(c) Or at least 50 % of one gland will receive
<30 Gy
Submandibulargland Mean dose <39 GY
Cochlea Max < 35 GY
Lens Max < 5 Gy
Glotticlarynx Mean < 45 Gy

Energy
▪Megavoltage beams with an energy range between 4 and 6 MV are most suitable.
▪Cobalt-60 remains acceptable in this region owing to the small lateral separation
distances in the head and neck area.
▪When higher energy beams are used, bolus material needed to bring dose to the
surface as required for tumours that extend to the skin.
▪Ideally, at least 95 % of the PTV for each dose level should receive the prescription
dose.
▪If contralaterallymph nodes are uninvolved, efforts should be made to spare the
contralateralparotid gland to help preserve salivary function.
▪The dose to the ipsilateralparotid gland and the submandibularglands can be
compromised for maximal coverage of the PTV.
▪For advanced tumors, coverage can be compromised to meet normal tissue
constraints if necessary.
Plan Assessment

Brachytherapy
Intent of treatment:
▪Radical :
oBrachytherapyalone as treatment in selected (early-stage) tumours of the
oral cavity with good results.
oDose prescription: 65 to 75 Gyover 6 to 7 days (LDR : 0.4 to 0.6 Gy/hour).
oRecently HDR and PDR brachytherapyare commonly used.
oThe most common technique is afterloadingwith 192Ir.
▪Boost: Used to boost the primary site either before or following EBRT
▪As salvage therapy in recurrent cases who have been irradiated before or
who are unfit for surgery

GEC-ESTRO recommendations-2009
1.Patient selection, the pre-treatment work up :
▪Easily accessible lesions
▪Early stage diseases (Ideal implant ≤ 5 cm)
▪Well localized tumorto organ of origin
▪No nodal or distant metastases
▪No local infections or inflammation
▪Proliferative/ ulcerative lesions preferred.
▪Favorablehistology-SCC
2.Patient care:
▪Pre treatment dental evaluation
▪Lead shielding can be used in lesions which close to the mandible to
avoid osteoradionecrosis.

GEC-ESTRO recommendations-2009
3.Treatment strategy:
▪When EBRT or NACT is combined with brachytherapy, the initial tumour
volume should always be considered, whatever the subsequent tumour
shrinkage.
▪The placement of radio-opaque markers (e.g., gold seeds) or tattoos can
be very helpful in delineating the tumour volume before any shrinkage
occurs.
▪Concomitant chemotherapy during brachytherapyis not recommended
for but useful for the treatment of recurrences.
▪Interval between EBRT and brachytherapyshould be as short as possible
and less than 2 weeks.
▪The total duration of radiation therapy within 8 weeks to limit tumour
cell repopulation..

GEC-ESTRO recommendations-2009
4. Target definition:
▪The GTV: The primary tumour volume defined by the clinical examination
and imaging techniques.
▪The CTV : GTV plus a safety margin 0.5–1 cm.
▪The PTV is not different from the CTV in a ‘‘perfect” implant.
▪The Treated Volume is encompassed by an isodosesurface corresponding
to the minimal target dose, the isodoseideally encompassing the CTV.
▪The skin should not be included in the CTV unless it is invaded by tumor,
and the skin dose should be minimized as much as possible.

GEC-ESTRO recommendations-2009
5.Implant technique:
▪Under GA
▪The brachytherapytechnique should be based on a classic system for
interstitial brachytherapy(Paris, Manchester or New York).
▪Guide needles can be inserted either freehand or template based.
▪Depending on the size of the lesion, a single plane, double plane, or volume
implant can be used to cover the tumorwith a 1-cm margin.
▪Catheters should be parallel and equidistant, ideally spaced at 1 to 1.5 cm.
▪Ultrasound or fluoroscopy guidance may be helpful when implanting
catheters.
▪Most LDR implant techniques can be used for HDR or PDR treatments.

GEC-ESTRO recommendations-2009
6.Dose and dose rate prescription:
▪LDR brachytherapy, delivering a high total dose is recommended to
secure local control, and to maintain the dose rate between 0.3 and 0.6
Gy/ h in order to minimize late side effects.
▪HDR brachytherapy, doses between 3 and 4 Gyper fraction have been
recommended with minimum of 6 h gap .
▪PDR brachytherapyhas biological advantages of LDR brachytherapywith
the technological advantages of the HDR afterloadingmethod.
▪Daytime PDR schedules were introduced by some authors to avoid
hospitalization and to reduce overall treatment costs.

GEC-ESTRO recommendations-2009
Anatomic
al site
Patient
selection
Implant
techniq
ue
MarginDose Result
Lip T1-3 RN 5–10 mm60–75 GyLDR-PDR LC: 90–95% N: 2–
10%
Buccal
mucosa
<4cm PT 5–10 mm65–70 GyLDR-PDR (25–
30 Gyboost if 45–50 Gy
ERT)
LC: 80–90% N: <10%
Mobile
tongue
T1-3 PT 5–10 mm65–75 GyLDR-PDR (25–
30 Gyboost if 40–45 Gy
ERT)
LR: >90% N: 10–20%
Floor of
mouth
T1-2N0RN or
PT
>5 mm 65 GyLDR-PDR (10–25
Gyboost if 46-50 Gy
ERT)
LR: >90% N: 10–30%
For salvage implants in a previously irradiated territory, a dose of 60 Gyis adequate.
HDR BT remain to be validated in prospective studies.

T2N0 SCC. lower lip (3.5cm size) with excellent cosmetic and functional status.
T2N0M0, SCC left lateral oral
HDR-BT: (25-Gy tumorboost)
Superficial T1 upper lip SCC
HBR-BT:Focalmucositis1 week after
treatment
Interstitial iridium 192 implant –HDR BT

The intraoral cone
▪Use: Boost the primary lesion
▪Selection citeria: Anterior oral cavity lesions in edentulous patients , palatal arch
sites and the size of the lesions up to 3 cm.
▪Treatment : either 100 to 250 kvpx-rays or electron beams in the 6 to 12 MeVrange.
▪Intraoral cone therapy requires careful daily positioning and verification by the
physician. For this purpose, the device is equipped with a periscope to visualize the
lesion.
▪The cone abuts the mucosa and is centereddirectly over the lesion.
▪It is used prior to external beam radiation so that the lesion can be adequately
visualized.
▪A major advantage of cone therapy is that it is highly focal to the tumorbed but non-
invasive.
▪Hence, when available, for suitable lesions, it may be preferred over brachytherapy.

Proton therapy
Uses:
•Unilateral head and neck irradiation-Select oral cavity cancers
Advantage:
•High LET
•Highly conformal dose distribution and also substantial organ sparing can be
achieved with the elimination of exit dose by BRAGG peak effect.
•Comparisons of proton beam therapy with IMRT have revealed reductions of
10 times or higher in radiation dose to critical midline and contralateral
organs, including parotid gland, submandibulargland, oral cavity, spinal cord,
and brainstem.
Disadvantage:
•Reduced dose to these normal organs resulted in decreased acute toxicities,
(mucositis, dysgeusia, nausea or vomiting, and fatigue ) but the grade 2 or
worse dermatitis was observed in patients due to the use of passive
scattering.

Proton therapy
.

Acute toxicity:
Common:
▪Fatigue
▪Hair loss
▪Skin reaction
▪Mucositis
▪Dryness of mucous membrane
▪Pain
▪Loss of taste
▪Malnutrition
Uncommon:
▪Candida infection.
▪Haematopoietic suppression.
Latetoxicity:
▪Permanent xerostomia.
▪Skin changes (atrophy of skin &
fibrosis).
▪Decaying of teeth.
▪Osteoradionecrosis.
▪Trismus.
▪Pharyngeal stenosis.
▪Transverse myelitis.
▪Radiation retinopathy, cataract.
▪Hypothyroidism, hypopitutarisim
▪Radiation induced malignancy-thyroid
cancer.
▪Carotid blowout syndrome/stenosis.
▪Oropharyngocutaneousfistula.
Toxicity

No SR Gr-1 SR
Gr-2 SR Gr-3 SR
SKIN REACTIONS
Gr-4 SR
MUCOSITIS
Gr-1 Mucositis Gr-2 Mucositis
Gr-3 Mucositis Gr-4 Mucositis

•Pooled data from randomized trials of patients with a
diagnosis of oral cavity, oropharynx, hypopharynx, and
larynx cancer who received chemotherapy in the
induction, concurrent, or adjuvant setting.
•Common randomized comparison between
radiotherapy and radiotherapy plus chemotherapy.
•Oral cavity patients comprised only 21% of the patient
population in the pooled analysis.
•The updated MACH-NC (1994 and 2000) report
published on 2009.
•Absolute survival benefit of 4.5% at 5 years with the
addition of chemotherapy, which is mainly driven by the
effect of concurrent chemoradiation(6.5% at 5 years).
Concurrent chemotherapy

•No clear evidence of a benefit for induction and adjuvant chemotherapies
•The subset analysis showed that the benefit of chemotherapy on survival did not differ
significantly between the group of trials with postoperative radiotherapy or curative
radiotherapy with conventional or altered fractionation.
•No significant difference was seen between mono-chemotherapy (Cisplatin> other
mono-therapies) and poly-chemotherapy.
•Decreasing effect of chemotherapy on survival with increasing age.
•Most of the randomised trials have used a dose of cisplatinof 100 mg/m2 , three times
throughout the course of radiotherapy (cumulative dose of 300 mg/m2)
•Induction chemotherapy provided a relatively more pronounced effect on distant
metastases, compared to concomitant chemotherapy.
•The benefit of the addition of chemotherapy to locoregionaltreatment is consistent in
all tumour locations of HNSCC [Update of MACH-NC: 2011]

Induction chemotherapy
Indications:
oCan given prior to RT to downstagingdisease in unresectabledisease.
oIt could treat subclinical distant metastatic disease without delay
oInduction chemotherapy could improve local regional control and organ
preservation
oInduction chemotherapy can provide prognostic information.
▪Early clinical trials found that cisplatin+ 5fluorouracil (PF, cisplatin-100 mg/m2,
and 5fluorouracil-1000 mg/m2/day continuous 24hour infusion for five days) given
every three weeks induced higher rates of complete response.
•Phase III experience now exists demonstrating the superiority of three-drug–
containing regimens (TPF-fluorouracil, cisplatin, and taxane) when compared to
fluorouracil and cisplatinalone(PF).
•3 large phase III studies [TAX324], [TAX323] , [GORTEC] demonstrated a survival
benefit favoringthe three-drug induction regimen response rates between 75%
and 100%, excellent survival, and high pathologic complete response rates at the
primary sites.

Controversies:
1.DeCIDE112 and PARADIGM (PHASE-III TRAIL):
▪Induction chemotherapy followed by concurrent chemoradiotherapyto
concurrent CRT alone failed to show a survival advantage with the
sequential treatment strategy.
▪The DeCIDEtrial had a 5% incidence of treatment-induced mortality in the
sequential arm compared to 0% in the CRT arm.
2.A meta-analysis : [Zhang L, et al.]
▪Decreased distant metastasis rate.
▪No statistically significant differences
in OS, PFS, (ORR), LRR.

Molecular therapies
•EGFR is up-regulated -90% of patients with squamouscell HNC and has
been associated with a poor prognosis.
•Indications:Recurrent/metastatic disease not amenable to local therapies.
•Benefit was greater in patients with oropharynxcancers, smaller primary
tumors, and more advanced nodal involvement.[Bonner et al]
Controversies:
•RTOG 0522: (Concurrent RT+Cisplatin+Cetuximabwith RT+ Cisplatin
alone)-No survival benefit.
•[VermorkenJB et al]:(Cis+5FU vsCis+5FU +Cetuximab) : addition of
cetuximabresutsin improvement in survival. [N EnglJ Med 2008;359]
▪Other drugs: Panitumumaband zalutumumab, Tirapazamine,

Immunotherapy
Indications:
•Recurrent/metastatic disease not amenable to local therapies.
•Refractory to platinum-based chemotherapy
FDA approved drug(2016):
▪KEYNOTE 012 (PHASE IB)-Pembrolizumab
▪CHECKMATE(PHASE III)-Nivolumab
OverallRR MedianOS Toxicity
KEYNOTE 012-
Pembrolizumab
18%
HPV+: 25%
HPV-: 14%
13 months 2 pts-Grade3 LFT
abnormalities
1 pt-Gr3 rash
CHECKMATE-
Nivolumab
13.3% 7.5 months 13%-Gr3 events

Follow up
History and physical exam (including complete H&N examination, including mirror and
fiberopticexam as indicated)
▪Year 1, every 1–3 mo
▪Year 2, every 2–6 mo
▪Years 3–5, every 4–8 mo; >5 y every 12 mo
▪Baseline imaging of primary and neck within 6 mo of therapy.
Serial reimaging as clinically indicated based on signs/symptoms, continued tobacco
use, and areas inaccessible to exam; routine imaging may be indicated in areas
difficult to visualize on exam
Chest imaging as clinically indicated for patient with smoking history for lung cancer
screening
TSH every 6–12 mo if neck irradiated
Ongoing dental evaluation focused on patient education, prevention/management of
caries,xerostomia, osteoradionecrosis, and oral candidiasis
Supportive care and rehabilitation
▪Speech/hearing and swallowing evaluation as clinically indicated
Surveillance

Management of recurrence
▪Recurrence rate: 25%–48% [Liao et al],[Jones KR],[Whitehurst JO,]
▪Despite the salvage treatment, survival remains poor with range of 15-67%.
Options:
•Salvage surgery
•Reirradiation(EBRT±IBT)
•Chemotherapy
▪[Liao et al] :
–DFS cutoffof > 10 months associated with improved OS compared with < 10
months DFS (54%v12%, respectively;P<.001).
–Early recurrences, either surgery or chemoradiotherapyhad similar outcomes.
–late recurrences, surgical salvage was superior to chemoradiotherapy
(84.4%v52%, respectively).

Siteof
recurrence
%
Local 57.9
Locoregional26.3
Regional 15.8
Stageof
recurrence
%
Stage I-II47.4
Stage III-IV52.6
Recurrenttumour
site
Salvagecure
rate
Local 33%
Locoregional 20%
Regional 0

Re-irradiation
Indications:
•Surgical salvage is unsuccessful
•Surgery is not feasible
Consider:
•Age
•Primary site
•Stage
•Field size
•Maximum energy
•Fractionation scheme
•Technique (conventional or conformal)
•Total dose
•Duration between radiotherapy and recurrence

▪13-year experience with patients reirradiated(1970 and 1988 ) by both EBRT alone or IBT +
EBRT with minimum follow-up of 3 years.
▪Improvement in local control: (50% vs29 %) for the IRT + EBRT series and the EBRT series,
respectively.
▪The improvement in local control was not reflected in a survival benefit. (actuarial overall
survival of 20 ~o at 5 years was observed in both series).
▪No treatment-related deaths occurred.
▪28% (4/16 of the EBRT series and 3/9 of the IRT + EBRT series) did experience severe side
effects.
Site Technique Totaldose to
primary tumour
(GY)
Totaldose to recurrent
tumour(GY)
Cumulativedoses
Oral cavity EBT alone
(1970-80)
30-80 57
mean
30-84 50 mean70-154107
FOM EBRT+IBT
(1985-1988)
60 (EBRT) 50 (EBRT)+30(IBT) 112

Palliative treatment
▪Palliative Radiotherapy
▪Palliative chemotherapy
▪Best supportive care

Palliative Radiotherapy
•Indications:Incurable cancers (ST-IVB/IVC), Poor PS 2 or 3
•Palliative RT Dose: 30GY/10#/2weeks or SFRT: 8GY/ 6GY
•QUAD SHOT: (Previously untreated patients)
o14Gy/4#/2# per day with 6h apart/2 days. Repeated at 4 weekly intervals for
a further two courses if there was no tumour progression.
o[June corryet.al] reported it was very well tolerated with minimal toxicity and
a good response rate (53%) with median OS: 5.7 months. It also improved QoL
(44%).
•Split-courseRT :
o20Gy/5#/1 week followed by a 2 week gap, and then a further 20Gy/5#/1.
oIt is an effective palliative regimen with acceptable toxicity. Symptomatic
improvement -79%at 4–6 weeks of follow-up with CR (39%) )and PR(33%).
[K.N.Kancherlaet al.]

Metronomic chemotherapy
Options:
•Single agent cisplatin
•Methotrexate
•Cetuximab
•Phase II trial comparing oral MCT [daily Celecoxib(200mg twice daily) and
weekly methotrexate(15mg/m
2
)] to i.vsingle agent cisplatin(IP)
(75mg/m
2
) given 3 weekly in ECOG PS 0–2status patients. [Vijay
MarutiPatilet al.]
mPFS mOS
Oral MCT 101 days 249 Days
Singleagent Cisplatin66 days 152 Days ((p=0.02)

CARCINOMA LIP
NCCN guideline 2020

CARCINOMA ORAL CAVITY
NCCN guideline 2020

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