Amelogenesis imperfecta, hypoplastic type - Dr Sanjana Ravindra
oral field cancerization - Dr Sanjana Ravindra
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Transcript of oral field cancerization - Dr Sanjana Ravindra
Meenakshi Mohan, Nithya Jagannathan Oncology Reviews 2014; 8:244
ORAL FIELD CANCERIZATION: AN UPDATE ON CURRENT
CONCEPTS
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
1,30,90074,500
Introduction
4`Nair K et al, Cancer: Current scenario, intervention strategies and projections for 2015
In india,Fourh most common cancer in females90% occur in patients over 45 years of age
Introduction
COMMON SITES OF OCCURENCE
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
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
INTRODUCTION Squamous cell carcinoma- most common
Average survival rate: 5 years
Mortality rate
unchanged
Recurrence
Locally or remote site
Process of transformation of an existing
precancerous lesion into a malignancy.
FIELD CANCERIZATION FIELD DEFECT FIELD EFFECT
INTRODUCTION
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 - carcinogenTOBACC
O
INTRODUCTION
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
NON CARCINOGENENIC
TAR FOUND IN TOBACCO
COMBINE WITH OXYGEN ON SLOW COMBUSTION
CARCINOGENIC TAREPOXIDE FORMS A REACTIVE CARCINOGEN
COMBINES TO GUANINE IN DNA
HIGH CANCER RISK!
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
67- 96 MONTHS
PRE MALIGNANT FIELD
INVASIVE CARCINOM
A
History of field cancerization
Slaughter et al
Concept and definition
(1953)Lateral
cancerization
Carcinogen- induced mucosal
changesConcept was extended to
other organs
Analyzed the tissues
adjacent to squamous
cell carcinoma.Th
e
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
Oropharynxesophaguslungs stomach, colon cervix anus skin and bladder
Concept of field cancerization
Triggers sequential
cellular transformations that ultimately
lead to the replacement of
the normal epithelium by a
proliferating field
Process of carcinogenes
is initiates from multiple genetic and epigenetic
alterations in the mucosa
Carcinogen
s - large area -
damage a large
proportion of cells -
premalignant states within - surface
exposed.
Synergy
Formation of multiple patches of premalign
ant 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
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
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
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
PATCH PHASE
EXPANDING FIELD PHASE
PRECURSOR LESION WITHIN FIELD
DEVELOPMENT OF CARCINOMA
CARCINOMA EXCISED
SECOND FIELD TUMOUR
PATCH FIELD CARCINOMA MODEL
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.
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.
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
Markers in the determination of field cancerization.
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.
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
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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