Cutaneous field cancerization: clinical, histopathological and therapeutic aspects

Abstract

The concept of "field cancerization" was first introduced by Slaughter 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 studies support the carcinogenesis model in which the development of a field with genetically altered cells plays a central role. An important clinical implication is that fields often remain after the surgery for the primary tumor and may lead to new cancers, designated presently as "a second primary tumor" or "local recurrence," depending on the exact site and time interval. In conclusion, the development of an expanding pre-neoplastic 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. The most important etiopathogenetic, clinical, histopathological and therapeutic aspects of field cancerization are reviewed in this article.

Intense pustular reaction during treatment of actinic keratosis with ingenol mebutate

“…Koncepcja leczenia OZN (ang. field-directed therapy) wynika z uznanej w ostatnich latach teorii, że w keratynocytach tego obszaru występują zaburzenia genetyczne zwiększające potencjał rozwoju zmian nowotworowych [12,13]. W takiej formie leczenia znajdują zastosowanie: 5-fluorouracyl, imikwimod, terapia fotodynamiczna, tretynoina, diklofenak, pilingi chemiczne oraz niedawno wprowadzony na polski rynek ingenol mebutynianu.…”

Queratosis actínicas: un modelo de campo de cancerización

“…Se ha propuesto que desde la piel normal hasta el desarrollo de un CEC invasivo se acumularían alteraciones en 17p, 3p, 8p, 9p, 18q y 11q. Los principales genes alterados son p16 (INK4a, localizado en el cromosoma 9p21), p14 (ARF), p15 (INK4b) y p53 13,[16][17][18] .…”

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“…Los principales genes alterados son p16 (INK4a, localizado en el cromosoma 9p21), p14 (ARF), p15 (INK4b) y p53 13,[16][17][18] . Así, por ejemplo, se ha detectado pé rdida de heterozigosidad en los tejidos peritumorales hasta en un tercio de casos estudiados, incluso sin evidencia de alteraciones morfoló gicas, ni clínica ni histoló gicamente.…”