1.
Meenakshi Mohan, Nithya
Jagannathan
Oncology Reviews 2014; 8:244
ORAL FIELD CANCERIZATION: AN UPDATE
ON CURRENT CONCEPTS

2.
Introduction
Liviu Feller, Johan Lemmer. Oral Squamous Cell Carcinoma: Epidemiology, Clinical Presentation and Treatment. Journal of Cancer Therapy, 2015, 3,
263-268
Oral cancer holds the
9th position in the
cancer incidence
ranking worldwide

3.
Estimated New Cancer Cases and Deaths Worldwide for Leading Cancer Sites by
Level of Economic Development, 2013. Source: GLOBOCAN 2013
Ahmedin Jemal et al, Global Cancer Statistics, CA CANCER J CLIN 2014;61:69–90
Estimated new cases Estimated deaths
1,30,900
74,500
3
Introduction

4.
`Nair K et al, Cancer: Current scenario, intervention strategies and projections for 2015 4

5.
In india,
Fourh most common cancer in
females
90% occur in patients over 45 years
of age
Introduction
COMMON SITES OF OCCURENCE

6.
Introduction
OScc-most
common oral
cancer worldwide
Over the last
decade its
incidence has
increased by
50%
Mainly occur
after fourth
decade of life
Affects men
than women
(M:F = 1.5:1)
Percentage of 5-
year survival for
patients with
OSCC varies
from 40-50%.
Liviu Feller, Johan Lemmer. Oral Squamous Cell Carcinoma: Epidemiology, Clinical Presentation and Treatment. Journal of Cancer Therapy, 2015, 3,
263-268

7.
 OSCC develops from exposure to different
carcinogens resulting in genetic or epigenetic
mutations.
 This type of cancer is particularly devastating to
patients because treatment entails excision of
facial structures essential for esthetics and
function.
Introduction

8.
INTRODUCTION
Squamous cell carcinoma- most common
Average survival rate: 5 years
Mortality rate
unchanged
Recurrence
Locally or remote site

9.
Process of
transformation of an
existing
precancerous lesion
into a malignancy.
FIELD CANCERIZATION
FIELD DEFECT
FIELD EFFECT
INTRODUCTION

10.
Anaplasia (from ancient Greek: ana, "backward" + plasis, "formation") is a condition of cells in which they have poor cellular
differentiation, losing the morphological characteristics of mature cells and their orientation with respect to each other and to endothelial
cells.
Oral cancer does not arise- isolated cellular
phenomenon
Anaplastic tendency - many cells - once
Multifocal development process - various rates -
within the entire field - response - carcinogen
TOBACC
O
INTRODUCTION

11.
Oral cancer developing in multifocal areas
of a pre-cancerous change
Abnormal tissues surrounding the tumor
Oral cancer often consisting of multiple
independent lesions that may coalesce
The persistence of abnormal tissue even
after surgery may explain secondary
primary tumor and recurrences
INTRODUCTION

12.
NON
CARCINOGENENIC
TAR FOUND IN
TOBACCO
COMBINE WITH OXYGEN
ON SLOW COMBUSTION
CARCINOGENIC TAR
EPOXIDE FORMS A
REACTIVE CARCINOGEN
COMBINES TO GUANINE IN DNA
HIGH CANCER
RISK!

13.
Criteria used to diagnose multiple carcinomas
the neoplasm must be
distinct and anatomically
separate. A multi-centric
primary neoplasm is
diagnosed when a
dysplastic mucosa is
present next to it
a potential second primary
carcinoma which represents
a metastasis or a local
relapse should be
excluded. It has to occur 3
years after the initial
diagnosis or it should be
separate from the first
tumor by at least 2 cm from
the normal epithelium
WARREN AND
GATES

14.
67- 96
MONTHS
PRE
MALIGNAN
T FIELD
INVASIVE
CARCINOM
A

15.
History of field cancerization
Slaughter
et al
Concept and
definition
(1953)
Lateral
cancerization
Carcinogen-
induced
mucosal
changes
Concept was
extended to
other organs
Analyzed the
tissues
adjacent to
squamous cell
carcinoma.The
first examined in
the aerodigestive
tract
due to a progressive
transformation of the
tissue adjacent to the
tumor rather than the
expansion of pre-existing
cancer cells into the
adjacent tissue
Oropharynx
esophagus
lungs stomach,
colon cervix
anus skin and
bladder

16.
Concept of field cancerization
Triggers sequential
cellular
transformations
that ultimately lead
to the replacement
of the normal
epithelium by a
proliferating field
Process of
carcinogenesis
initiates from
multiple genetic
and epigenetic
alterations in the
mucosa
Carcinogens
- large area -
damage a
large
proportion of
cells -
premalignant
states within -
surface
exposed.
Synergy
Formation of
multiple patches of
premalignant
disease
FIELD
CANCERIZATIO
N
higher-than-expected
rate of multiple local
second primary tumors
the clonal expansion of
premalignant daughter
cells in a particular
field

17.
Multiple squamous
cell lesions occur
independently of
each other.
This is due to the
exposure of the oral
cavity to
carcinogens in at
the same time
leading to multiple
genetic
abnormalities in the
entire area
1st
Multiple lesions arise due to the
migration of dysplastic and altered
cells with two different patterns as
follows:
(1) migration of malignant cells through
the saliva (micro metastasis);
(2) intra-epithelial migration of the
progeny of initially transformed
malignant cells.
2nd
Theories of field cancerization
POLYCLONAL MONOCLONAL

18.
HISTOLOGICALLY
In smokers and alcoholics: TAM- migrating tumor cells
In healthy individuals: Absent
CLONALITY
Two separate lesions are said to develop from a single clone when
they share common genetic alterations
This clonal relationship between several premalignant and malignant
lesions suggests that the tumor cells or the progenitor cells drift and
result in cancerization
in the absence of a clonal relationship between multiple lesions, it is
more likely that they derive from an independent event
INVESTIGATIONS

19.
The process of carcinogenesis begins with a stem cell
which develops one or more genetic and epigenetic
alterations. Subsequently a clone of genetically
altered cells forms a patch or a cluster.
Field cancerization model

20.
PATCH PHASE
EXPANDING
FIELD PHASE
PRECURSOR LESION
WITHIN FIELD
DEVELOPMENT OF
CARCINOMA
CARCINOMA
EXCISED
SECOND FIELD
TUMOUR
PATCH FIELDCARCINOMAMODEL

21.
SECOND PRIMARY TUMOR
 Despite advances in therapy long term survival of
head and neck cancer patients has not significantly
improved in the last 20 years.
 An important reason for this lack of progress is the
development of secondary primary tumor in the
upper aerodigestive tract.
 Patients at highest risk are those with early-stage
disease, when control of the first tumor, and
therefore survival, is greatest.
Jayam R. Oral field cancerization-A review. Journal of Indian Academy of Oral Medicine and Radiology 2010;22:201-5.

22.
 For SPT,
(a) Each of the tumors must present a definite picture of
malignancy
(b) Each must be distinct
(c) The probability of one being a metastasis of the other
must be excluded.
 Histological sections: To exclude the possibility of a
local recurrence - use a distance of at least 2 cm
between the first tumor and the SPT.
Warren and Gates(1932)
SECOND PRIMARY TUMOR
Jayam R. Oral field cancerization-A review. Journal of Indian Academy of Oral Medicine and Radiology 2010;22:201-5.

23.
DISTANT SECOND LESIONS
 The distance between two malignancies does not
necessarily predict clonality but distant, peripheral,
solitary, squamous lung lesions in conjunction with
HNSCC are thought to be metastases and
concurrent esophageal tumors are thought to be
separate primary tumors.
 While the probability of synchronous aerodigestive
tract tumors remains high with environmental
exposure, the relationship between them is often
predicted by the anatomic subset rather than
distance.
Alok A, Singh ID, Panat SR, Singh S, Kishore M. Oral Field Cancerization: A Review. Int J Dent Med Res 2014;1(3):98-104

24.
Markers in the determination of field cancerization.

25.
THERAPEUTIC IMPLICATIONS FOR FIELD
CANCERIZATION
It is a well-known clinical experience that even after surgical
removal of a tumor, there is a high risk for another tumor to develop
in the same anatomical area.
In some cases, the new tumor formation can be explained because
of the growth of incompletely resected carcinoma.
However, for the cases where the tumor had been removed, a
genetically altered field is the cause of new cancer.
The presence of altered fields of mucosa beyond the limits of
resection has been shown both histologically and on a molecular
basis.
Initial studies performed demonstrated that p53 mutations noted in
histologically normal margins could be detected in those patients
with known mutations in altered margins.

26.
Conclusions
The journey of a thousand miles must begin with a single step
The process of formation of oral
cancer results from multiple sites
of pre-malignant change in the
oral cavity (field cancerization).
The presence of a field with
genetically altered cells is a risk
factor for cancer.
To prevent field cancerization,
habitual ingestion of carcinogens
such as alcohol and cigarettes
should be stopped, and longterm
follow-up may be needed for
patients treated with radiotherapy,
chemotherapy, and teratogenic
drugs such as retinoids.
A good research in this field has a
strong potential to reveal new
diagnostic markers for early
detection, modalities to prevent
progression, and lastly ways to
combat development of second
primary tumor (or second field
tumors

27.
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6. Jayam R. Oral field cancerization-A review. Journal of Indian Academy of
Oral Medicine and Radiology 2010;22:201-5.
7. Liviu Feller, Johan Lemmer. Oral Squamous Cell Carcinoma: Epidemiology,
Clinical Presentation and Treatment. Journal of Cancer Therapy, 2015, 3,
263-268
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Thank you