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      Oral Field Cancerization: An Update on Current Concepts

      review-article
      Author(s): ,
      Publication date (Electronic):
      Journal: Oncology Reviews
      Publisher: PAGEPress Publications, Pavia, Italy
      Keywords: cancerization, clone, field, patch, metastasis, tumor

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          Abstract

          There always exists a field with genetically altered cells with a high risk of developing premalignant and malignant lesions. It may often happen that an individual stem cell is genetically altered and can cause the formation of a clone or a patch which is likely to turn into a tumor. This explains the higher recurrence rates following tumor resections. It is essential to identify and to treat this field in order to have greater chances to prevent cancer and achieve a better outcome. This article reports concepts, theories and markers for the assessment of field cancerization.

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          Most cited references70

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          Epigenetic inactivation of SFRP genes allows constitutive WNT signaling in colorectal cancer.

          Hiromu Suzuki, D. Neil Watkins, Kam-Wing Jair … (2004)
          Aberrant WNT pathway signaling is an early progression event in 90% of colorectal cancers. It occurs through mutations mainly of APC and less often of CTNNB1 (encoding beta-catenin) or AXIN2 (encoding axin-2, also known as conductin). These mutations allow ligand-independent WNT signaling that culminates in abnormal accumulation of free beta-catenin in the nucleus. We previously identified frequent promoter hypermethylation and gene silencing of the genes encoding secreted frizzled-related proteins (SFRPs) in colorectal cancer. SFRPs possess a domain similar to one in the WNT-receptor frizzled proteins and can inhibit WNT receptor binding to downregulate pathway signaling during development. Here we show that restoration of SFRP function in colorectal cancer cells attenuates WNT signaling even in the presence of downstream mutations. We also show that the epigenetic loss of SFRP function occurs early in colorectal cancer progression and may thus provide constitutive WNT signaling that is required to complement downstream mutations in the evolution of colorectal cancer.
          Article 0 comments Cited 238 times – based on 0 reviews     Review now
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            A genetic explanation of Slaughter's concept of field cancerization: evidence and clinical implications.

            Boudewijn Braakhuis, Maarten P. Tabor, J. Kummer … (2003)
            The concept of "field cancerization" was first introduced by Slaughter et al. [D. P, Slaughter et al., Cancer (Phila.), 6: 963-968, 1953] in 1953 when studying the presence of histologically abnormal tissue surrounding oral squamous cell carcinoma. It was proposed to explain the development of multiple primary tumors and locally recurrent cancer. Organ systems in which field cancerization has been described since then are: head and neck (oral cavity, oropharynx, and larynx), lung, vulva, esophagus, cervix, breast, skin, colon, and bladder. Recent molecular findings support the carcinogenesis model in which the development of a field with genetically altered cells plays a central role. In the initial phase, a stem cell acquires genetic alterations and forms a "patch," a clonal unit of altered daughter cells. These patches can be recognized on the basis of mutations in TP53, and have been reported for head and neck, lung, skin, and breast cancer. The conversion of a patch into an expanding field is the next logical and critical step in epithelial carcinogenesis. Additional genetic alterations are required for this step, and by virtue of its growth advantage, a proliferating field gradually displaces the normal mucosa. In the mucosa of the head and neck, as well as the esophagus, such fields have been detected with dimensions of >7 cm in diameter, whereas they are usually not detected by routine diagnostic techniques. Ultimately, clonal divergence leads to the development of one or more tumors within a contiguous field of preneoplastic cells. An important clinical implication is that fields often remain after surgery of the primary tumor and may lead to new cancers, designated presently by clinicians as "a second primary tumor" or "local recurrence," depending on the exact site and time interval. In conclusion, the development of an expanding preneoplastic field appears to be a critical step in epithelial carcinogenesis with important clinical consequences. Diagnosis and treatment of epithelial cancers should not only be focused on the tumor but also on the field from which it developed.
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              Genetic progression model for head and neck cancer: implications for field cancerization.

              George W. Koch, J Califano, S Piantadosi … (1996)
              A genetic progression model of head and neck squamous cell carcinoma has not yet been elucidated, and the genetic basis for "field cancerization" of the aerodigestive tract has also remained obscure. Eighty-seven lesions of the head and neck, including preinvasive lesions and benign lesions associated with carcinogen exposure, were tested using microsatellite analysis for allelic loss at 10 major chromosomal loci which have been defined previously. The spectrum of chromosomal loss progressively increased at each histopathological step from benign hyperplasia to dysplasia to carcinoma in situ to invasive cancer. Adjacent areas of tissue with different histopathological appearance shared common genetic changes, but the more histopathologically advanced areas exhibited additional genetic alterations. Abnormal mucosal cells surrounding preinvasive and microinvasive lesions shared common genetic alterations with those lesions and thus appear to arise from a single progenitor clone. Based on these findings, the local clinical phenomenon of field cancerization seems to involve the expansion and migration of clonally related preneoplastic cells.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncol Rev
                Journal ID (iso-abbrev): Oncol Rev
                Journal ID (publisher-id): OR
                Title: Oncology Reviews
                Publisher: PAGEPress Publications, Pavia, Italy
                ISSN (Print): 1970-5565
                ISSN (Electronic): 1970-5557
                Publication date (Electronic): 30 June 2014
                Publication date Collection: 17 March 2014
                Volume: 8
                Issue: 1
                Electronic Location Identifier: 244
                Affiliations
                Department of Oral Pathology, Saveetha Dental College, Saveetha University , Chennai, India
                Author notes
                Department of Oral Pathology, Saveetha Dental College, Saveetha University, No 162, Poonamalle High Road, Vellapanchavadi, 600077 Chennai, India. +91.9884754910. dr.nithya@ 123456ymail.com

                Contributions: MM, collection of references and compilation of data; NJ, formatting, preparation and reviewing the article.

                Conflict of interests: the authors report no potential conflict of interests.

                Article
                DOI: 10.4081/oncol.2014.244
                PMC ID: 4419611
                PubMed ID: 25992232
                SO-VID: 546dc6fc-b61b-4db8-b1eb-f4f6e67f552f
                Copyright © ©Copyright M. Mohan and N. Jagannathan
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 17 December 2013
                Date revision received : 04 April 2014
                Date accepted : 27 April 2014
                Page count
                Figures: 2, Tables: 1, Equations: 0, References: 91, Pages: 7
                Categories
                Subject: Review

                Keywords: cancerization,clone,field,patch,metastasis,tumor
                Data availability:
                Keywords: cancerization, clone, field, patch, metastasis, tumor

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